“The Amazing Meeting” (I don’t think it means, what you think it says it means): 2 Intellectually and Ethically Challenged Individuals, Twaddle at TAM 2013

Gentlemen, I start your Insolence 😇
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(1:30) [1]
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The “motto” of “The Amazing (Not so Much) Meeting” is “Fighting Fakers,” which is apropos, since I doubt that “Orac” the “Check my Facts” Hack of Dr. David H. Gorski, grasps the irony, that when I read some of his blog articles, you could easily switch his name with the name of some individual he is flogging, and the proverbial shoe fits, and:
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(1:40)
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“This is a guy who sometimes fools even, you know, physicians”
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(I couldn’t have said it better, myself) 😊
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(2:47)
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He states:

“There is a long segment about “The Skeptics”

(applause) 😝
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(4:25)
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“His lawyer wrote a book”

“About a half of it is about Burzynski [4]
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6:00
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Gorski mentions that Burzynski noticed that there were higher levels of these chemicals in healthy people, than people with cancer
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Whereas, Burzynski is on record as having said [5]:

” . . . healthy people have abundance of these chemicals in blood
Cancer patients have varied to none

I did NOT know before now, that GorskGeek thinks that “none” is a “level” 😶
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He continues:

AS2.1 – which is a chemical called phenylacetic acid, which is a byproduct of metabolism that turns into phenylacetylglutamine by the liver

A10 – soluble is basically the same thing
It breaks down to PAG
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WOW !

I thought it was: AS2 1 😊

They are “basically the same thing” ? 😳

What does Burzynski say ? [6]

Phenylacetylglutaminate (PG) and Phenylacetate (PN) are metabolites of Phenylbutyrate (PB) and are constituents of antineoplaston AS2-1

PG and PN are naturally occurring in human body as result of metabolism of phenylalanine in liver and kidneys

formulation of antineoplaston AS2-1 is 4:1 mixture of synthetic PN and PG

A10 is 4:1 mixture of PG and iso-PG

That does NOT look like “basically the same thing” to me 😛

20131111-160455.jpg
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(6:50)
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Gorski founders on:

“And these are substances which were actually studied in the ’50’s and ’60’s and not found to be particularly, um, promising, but, he didn’t know that then”
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GorskGeek has #FAILED miserably to prove that on his blogs [7] 😄
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(8:00)
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Gorski comments about Burzynski’s “animal testing,” “species specific” claims:

“There are ways of getting around that”
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But Gorski, again, has #FAILED miserably to prove it [8] 😅
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(12:00)
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Gorski makes lame excuses about the NCI phase II clinical trial [9] 😖
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(12:50)
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Gorski claims Burzynski was indicted for insurance fraud in the 1997 case 😱
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GorskGeek, care to try and prove that one also ? [10] 😃
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(14:25)
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Gorski then states that out of 61 trials on clinicaltrials . gov, “most” are “closed or unknown”
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GorskGeek #FAILED again 😁

At the time it was:

1 – Not Yet Recruiting
(OPEN)(Phase 3)
1 – COMPLETED
2 – WITHDRAWN
(Withdrawn due to slow enrollment)
7 – WITHDRAWN
(This study has been withdrawn prior to enrollment)
(9=WITHDRAWN)
10 – Recruiting
(10=OPEN)
40 – Active, not recruiting –
(40=CLOSED)
61 =TOTAL
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(15:20)
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Gorski attempts to go all “legal eagle”:

“Listen to Burzynski’s lawyer!”

“You listen to Burzynski’s lawyer; and, and I swear I don’t understand, like why Burzynski would let him, let his lawyer say stuff this damning in his own book, but he does”

“So, get a load of some of these quotes, referring to one of the clinical trials, he says:”

“It was a joke”

“. . . there could not be any possibility of meaningful data coming out of the so-called clinical trial, it was all an artifice, that, you know, designed so that they could continue giving the treatment

“The FDA wanted all of his patients to be on an IND, so, that’s what we did”
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Gorski, attorney Rick Jaffe is an American, living in America NOT the formerly communist Poland

He can say whatever he wants

GorskGeek is NOT a lawyer 😓

And there’s an excellent reason why

Nor is he schooled in the proper usage of the English language

FACT:

” . . . the so-called clinical trial . . .”

Any human being with a modicum of intelligence about the English language, understands that the term “clinical trial” is singular, i.e. one

Burzynski’s lawyer is obviously referring to the CAN-1 clinical trial mentioned in Burzynski’s 11/25/1997 Securities and Exchange Commission (SEC) filing [11]

One trial that is retrospective is CAN-1 Clinical Trial
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CAN-1 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN

PATIENTS WITH REFRACTORY MALIGNANCIES

133 patients
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Clinical trial of patients treated by Dr. Burzynski through 2/23/1996

FDA has indicated it will not accept data generated by this trial since it was not a wholly prospective one
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Gorski continues his trend of #FAILURES when he mentions the additional types of treatments that Burzynski was offering, but he #FAILED to mention [12] 😂
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” … in 1997, his medical practice was expanded to include traditional cancer treatment options such as chemotherapy, gene targeted therapy, immunotherapy and hormonal therapy in response to FDA requirements that cancer patients utilize more traditional cancer treatment options in order to be eligible to participate in the Company’s Antineoplaston clinical trials”
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(18:20)
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Gorski addresses the case of Tori Moreno
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Kim Moreno states:

“We originally were at Miller’s Children at Long Beach Memorial and then went to City of Hope

“We also sent her MRI’s to Dr. Fred Epstein in New York to be looked at”

Gorski suggests that 3 different opinions could have misdiagnosed Tori Moreno

You can read an interview with Tori’s mother [13]
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(19:45)
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Gorski goes on to mention Burzynski patients going to Texas Children’s Hospital with hypernatremia issues
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Gorski, do you mean this ? [14]

The changing pattern of hypernatremia in hospitalized children

Department of Pediatrics, Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas, USA
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(20:00)
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Gorski mangles the case of Hannah Bradley, who had a grade 3 anaplastic astrocytoma brain tumor

GorskGeek makes excuses like “spontaneous remission”, but then provides no citation, reference, or link to a case of such a tumor having spontaneously exhibited remission [15]
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(20:40)
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Gorski states that antineoplastons are chemotherapy
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No, Gorski, antineoplaston are:

“…an unapproved drug, not ordinary “chemotherapy [16] 😣
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(21:53)
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Gorski claims in regard to Burzynski’s personalized gene-targeted therapy:

” . . . gives to the patient without regard for synergistic toxicity

“Boom, there you go”
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Gorski’s #FAIL rate continues, as Burzynski has stated that phase 2 and 3 publications are reviewed as part of this process [17]

Gorski, “BOOM, THERE YOU GO” ッ
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Gorski, you should hire out to the Democratic Party as their mascot, because you must be the biggest pompous ASS I’ve ever seen 😜

Gorski, my advice: don’t quit your day job, HACK 😷
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The #TAM2013 audience then has to suffer through 22:36 of the blatherskite of Robert J. (don’t call me Bobby) “Bob” Blaskiewicz Blatherskitewicz [2]

He blathers about the “dozen,” “17,” “16 dead,” “pancreatic cancer,” “Joseph, who was alive but died well within the life expectancy given his diagnosis,” “Joann, who was alive but died within a year of starting therapy,” “Irene S., who was dead within month,” “Maxine, who was already dead,” the “103 in 2011,” “63 in mid-June,” “17 on original 1999 site,” “about 3 added a year,” the “about 50 stories,” “1/10th of patient names gathered,” “Amelia S. – 7, tumor breaking up,” “Chase,” “Cody – 1994, 20 years ago, 2 visits, 6 weeks treatment breaking up,” “David,” “Janet, 3 – 5 yrs., oncologist, now dead, ovarian cancer,” “Pete took video down,” “8,000 patients,” “probable ischemic necrosis,” “13 yr. old, getting worse getting better, vomited – Marlene, nurse,” “Rory died 2005,” “Supatra, swelling, last wed., brain tumor,” “Side-effect, 2%, sodium load,” “Andrea, U.S. News and World Report, 30% chance recovery, glioblastoma, ANP in luggage, died on plane,” “Cathy wanted to be on ANP, Greg Burzynski, found out only brain tumor,” “Denise D. breast cancer,” and finally:
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(18:45)
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” … and light as many fires under his butt as we can
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Mentions Rick Jaffe’s book Galileo’s Lawyer

IT’S ALL ABOUT THE PATIENTS [4]
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All you need to know about Blaskiewicz is:

“White man speak with forked tongue” [18]
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The 3rd video is a panel discussion, which includes “man-crush” tag-team [3]

Robert Blaskiewicz and David Gorski
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(8:00)
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Bob says:

“Yeah, I’m not that type of doctor
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Bob, the correct answer for you, is:

“I’m NOT a doctor” QUACK
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(13:05)
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Gorski gabs that he’s a:

“Game of Thrones Geek”
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I just knew I was right, GorskGeek [19]
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(14:00)
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The only female panelist mentions “bureaucrats”, “wimps”, and “people without balls”
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2 out of 3 ain’t bad

She describes the Bob and David show to a T
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(15:00)
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The claim is made that a Burzynski physician appeared on the Burzynski Facebook page announcing results
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(16:00)
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Gorski #whines that the Texas Medical Board wasn’t successful in shutting Burzynski down because of “politics”
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LAUGHABLE
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(20:55)
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Gorski gives his usual excuse:

“He’s not an oncologist”
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GorskiGeek, that claim is as dead as apparently, quite a number of your brain cells [15]
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(34:40)
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Audience members are given the opportunity to speak, and this is the garbage served up:
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“Hi, this is Susan

Ah, don’t forget to mention that Wikipedia has been a major battlefield

We’ve had 23,000 views to the clinic’s page this last month, also rebutr . . .”
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“Control the flow of information”
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Gorski pipes up:

“What she said”
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(35:20)
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Blatherskitewicz chimes in:

“When it comes to Wikipedia can I just mention that is, that is, that that is so effective that Wikipedia was singled out in the most recent Burzynski movie
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Gorski chirps:

“Yes”
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Bob yacks:

“as being controlled by evil skeptics
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Gorski ejaculates:

“No, seriously”
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Bob bleats:

“No”

(applause)
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“You have to unleash the evil hoards of skeptics

“Wahahaha” 👿
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Dr. Stanislaw Burzynski on Wikipedia:

“Simply don’t pay attention to it, because it, it’s not true”

“You won’t be able to, do any, clinical research which we do, without convincing evidence, especially when you have the most powerful agency in the government which is against you

“So they would love to find something which is wrong with what we are doing”

“Ah, so the fact that they’ve, um, agreed that what we have has value, and they allow us to do phase 3 clinical trials it means that we are right”

“Because, uh, uh, nobody who didn’t have any, concrete evidence that it works, would be able to go as far”

“So whatever Wikipedia says, well, I don’t care for them

(laughing) [5]
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Enlightening ?

Inspiring ?

Amazing ?

Hypocrites

Apparatchiks [20]
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REFERENCES:
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[1]David Gorski – Why We Fight (Part I): Stanislaw Burzynski Versus Science-Based Medicine – TAM 2013 11/8/2013 (22:44)
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[2]Robert Blaskiewicz – Why We Fight (Part II): It’s All About The Patients – TAM 2013 11/8/2013 (22:36)
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[3] – Medical Cranks And Quacks
TAM 2013 JREF
11/8/2013 (42:42)
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[4]“Galileo’s Lawyer” Richard A. Jaffe, Esq.
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http://www.richardjaffe.com
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[5] – 11/9/2013 – Pete Cohen chats with Dr. Stanislaw Burzynski:
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https://stanislawrajmundburzynski.wordpress.com/2013/11/09/pete-cohen-chats-with-dr-stanislaw-burzynski/
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[6] – 6/2012 – Journal of Cancer Therapy, 2012, 3, 192-200 doi:10.4236/jct.2012.33028 Published Online June 2012, Pg. 192
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http://www.burzynskiclinic.com/images/stories/Publications/9219.pdf
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[7]Burzynski: Oh, RATS!!!:
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https://stanislawrajmundburzynski.wordpress.com/2013/07/26/the-lancet-oncology-peer-review-team-d-12-01519-fail-2/
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[8] – Critiquing: How Stanislaw Burzynski became Burzynski the Brave Maverick Doctor, part 1:
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https://stanislawrajmundburzynski.wordpress.com/2013/07/22/critiquing-how-stanislaw-burzynski-became-burzynski-the-brave-maverick-doctor-part-1/
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[9] – 9/19/2013 – Critiquing: National Cancer Institute (NCI) at the National Institutes of Health (NIH) CancerNet “fact sheet”:
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https://stanislawrajmundburzynski.wordpress.com/2013/09/19/critiquing-national-cancer-institute-nci-at-the-national-institutes-of-health-nih-cancernet/
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[10] – 9/25/2013 – Critiquing: National Council Against Health Fraud, Inc. – NCAHF News: JURY NULLIFICATION THWARTS BURZYNSKI CONVICTION:
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https://stanislawrajmundburzynski.wordpress.com/2013/09/25/critiquing-national-council-against-health-fraud-inc-ncahf-news-jury-nullification-thwarts-burzynski-conviction/
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[11] – 7/9/2013 – Burzynski: The Original 72 Phase II Clinical Trials:
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https://stanislawrajmundburzynski.wordpress.com/2013/07/09/burzynski-the-original-72-phase-ii-clinical-trials/
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[12] – 4/26/2013 – Burzynski: FDA requirements that cancer patients utilize more traditional cancer treatment options in order to be eligible to participate in the Company’s Antineoplaston CLINICAL TRIALS:
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https://stanislawrajmundburzynski.wordpress.com/2013/04/26/burzynski-fda-requirements-that-cancer-patients-utilize-more-traditional-cancer-treatment-options-in-order-to-be-eligible-to-participate-in-the-companys-antineoplaston-clinical-trials/
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[13] – Tori Moreno
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http://www.cancerinform.org/aburzinterview2.html
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[14] – 9/1999 – Pediatrics. 1999 Sep;104(3 Pt 1):435-9
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http://www.ncbi.nlm.nih.gov/m/pubmed/10469766/
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[15] – 11/2/2013 – Critiquing: Dr. Stanislaw Burzynski’s cancer “success” stories:
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https://stanislawrajmundburzynski.wordpress.com/2013/11/02/critiquing-dr-stanislaw-burzynskis-cancer-success-stories/
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10/25/2013 – Hannah Bradley – I Feel Empowered, In Control Of My Body: Four Women On Fighting Cancer With Alternative Therapies http://www.telegraph.co.uk/health/10383724/I-feel-empowered-in-control-of-my-body-four-women-on-fighting-cancer-with-alternative-therapies.html
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https://stanislawrajmundburzynski.wordpress.com/2013/10/25/hannah-bradley-i-feel-empowered-in-control-of-my-body-four-women-on-fighting-cancer-with-alternative-therapies-httpwww-telegraph-co-ukhealth10383724i-feel-empowered-in-control-of-my-body-fo/
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[16] – NOT ORDINARY CHEMOTHERAPY
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https://bulk.resource.org/courts.gov/c/F3/27/27.F3d.153.93-2071.html
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[17] – 9/4/2013 – University of Michigan, where is alum Dr. David H. “Orac” Gorski’s Grapefruits ?:
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https://stanislawrajmundburzynski.wordpress.com/2013/09/04/university-of-michigan-where-is-alum-dr-david-h-orac-gorskis-grapefruits/
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[18] – 10/13/2013 – Why “The Skeptics™” Perfessor Robert J. (don’t call me “Bobby”) “Bob” Blaskiewicz (@rjblaskiewicz) of University of Wisconsin, Eau Claire, “Fame,” is a Coward and a Liar:
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https://stanislawrajmundburzynski.wordpress.com/2013/10/13/why-the-skeptics-perfessor-robert-j-dont-call-me-bobby-bob-blaskiewicz-rjblaskiewicz-of-university-of-wisconsin-eau-claire-fame-is-a-coward-and-a-liar/
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[19] – 10/27/2013 – “The Skeptics™” Burzynski Bias, Censorship, Lies, and Alibi’s: September 28, 2013 “The Skeptics™” Burzynski discussion: By Bob Blaskiewicz – 2:19:51
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https://stanislawrajmundburzynski.wordpress.com/2013/10/27/the-skeptics-lie-lied-lies-liars-lying-burzynski-bias-censorship-lies-and-alibis-september-28-2013-the-skeptics-burzynski-discussion-by-bob-blaskiewic/
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[20] – 11/9/2013 – Wikipedia Articles:
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https://stanislawrajmundburzynski.wordpress.com/2013/09/11/burzynski-timeline/
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[19] – 1995 (6/6/1995) Dr. Michael A. Friedman to Burzynski (3 pgs.)

This page is linked to:
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Critiquing: Dr. Michael A. Friedman, Dr. Mark G. Malkin, Dr. Mario Sznol, Robert B. Lanman, Memorial Sloan-Kettering Cancer Center, Mayo Clinic, Department of Health & Human Services (HHS), Public Health Service, Quality Assurance and Compliance Section, Regulatory Affairs Branch (RAB), Cancer Therapy Evaluation Program (CTEP), Division of Cancer Treatment (DCT), National Cancer Center (NCI) at the National Institutes of Health (NIH), Stanislaw Burzynski: On the arrogance of ignorance about cancer and targeted therapies
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https://stanislawrajmundburzynski.wordpress.com/2013/09/08/critiquing-stanislaw-burzynski-on-the-arrogance-of-ignorance-about-cancer-and-targeted-therapies/
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[19] – 1995 (6/6/1995) – Michael A. Friedman, M.D., Associate Director, Cancer Therapy Evaluation Program (CTEP), Division of Cancer Treatment (DCT), National Cancer Institute (NCI), Department of Health and Human Services (HHS), Public Health Service, National Institutes of Health (NIH) 3 page letter to Burzynski

This letter is intended to respond to the major issues which have been raised in your recent correspondence of 4/20/1995 and 5/16/1995

Your accusations are serious and require comment

I will 1st address the questions you raised about individual patients participating in the NCI-sponsored antineoplaston studies

2 patients were treated at the National Cancer Institute

Patient .26-77-03-9 had evidence of focal glioblastoma multiforme on the biopsy reviewed at the NCI

A different specimen submitted to Dr. Rorke may or may not be relevant

This patient, however, had a brain scan 3 weeks prior to study entry

Patient .27-53-76-5 had a tumor which was 0.8 cm larger than the eligibility criteria dictated

Although pharmacologic data were obtained on both, neither patient is counted in an assessment of response

Both patients had objective tumor progression and are now off study

With respect to the other patients, I am including specific patient summaries from the treating investigators which address your other concerns; in particular, a response to your serious and unfounded statement that patient #196370 was treated in an unethical manner

Also contrary to your statement, you have been sent monthly clinical summaries of these patients since 7/1994 directly from Theradex

(see 3/9/1994 letter)

Having provided this information, I must convey my deep pessimism about the potential for continued interactions with you regarding these trials

Given recent events and your clearly articulated bias that the Mayo Clinic, Memorial Sloan Kettering Hospital and even the National Cancer Institute could not fairly test your product

(please see your letters of 10/26/1993 and 4/20/1995),

I now see a diminishing chance for a productive dialogue with you

Historically, the NCI has demonstrated pragmatism and flexibility in working with a wide variety of individuals and organizations to explore diverse interventions of potential benefit to the cancer patient

However, such a fruitful collaboration may simply not be possible with you

Pg. 2

The decision to suspend the NCI antineoplaston studies was reached by the investigators and the NCI and was explained in our letter of 5/12/1995

(see enclosed)

While we have frequently solicited your advice, we are in no way obligated to obtain your consent

Our interactions with you have been similar to those with pharmaceutical companies or other independent investigators

In the interest of testing antineoplastons, we have consistently considered your advice and recommendations but that in no way cedes control of these studies to you

(please refer to our letters of 7/15/1993, 10/20/1993, and 11/2/1993)

Your insistence on dictating the manner in which we conduct our review of these clinical trials is both presumptuous and inappropriate

The future of these trials rests entirely with the investigators and the NCI, since our primary obligation is to the American public

Recognizing your potential conflict of interest as the developer and the most visible proponent of antineoplastons, we could not responsibly act in any other manner

In contrast to the tenor of your unsupported statements, the NCI bases its position on scientific data

You have stated that you have a vast clinical experience with antineoplastons and we have generally been deferential to your demands despite the lack of substantive data

However, our scientific standards are broadly applied to all studies

The data and level of proof we require from you is much the same as that for other professional collaborators who make such claims

The 7 case records initially examined by the NCI hardly constitute a definition scientific result

It is naive and misleading for you to suggest that the experience of 2 of those patients who had tumors in excess of 5 cm provides adequate proof for all your contentions about tumor size, dose, etc., unless these were the only 7 brain tumor patients from your entire experience who had any hint of benefit

To be precise, in order to responsibly and properly assess your claims and accusations (as per your 4/20/1995 letter), we request that you provide the following information:

1. Exactly how many adult patients with primary brain tumors have you evaluated and treated with antineoplastons?

2. When analyzed by histological type, performance status, prior therapy, concurrent therapy (including chemotherapy), disease size and focality, how many adult brain tumor patients had objective responses?

Please characterize the quality and magnitude and duration of these responses

3. What dose, duration, schedule, and composition of antineoplastons did these patients receive?

Which of these patients benefited objectively?

What toxicities were encountered?

Do you have pharmacokinetic or pharmacodynamic data to support your contention that certain types of brain tumor patients require specific regimens?

4. For these patients, what statistical analyses relate patient or tumor characteristics with exact treatment regimen and outcome?

Pg. 3

If you provide such specific data, we can properly assess your claims

Lacking such information, we cannot

Moreover, your charges that patients received inappropriate care are not supportable without such detailed information

If, after careful consideration, the investigators at Memorial Sloan Kettering and Mayo Clinic do not reopen their studies, it is unlikely that the NCI will attempt to conduct further antineoplaston trials

Any unused antineoplaston material will, of course, be returned to you

Since we can make no judgement about the benefit or toxicity of antineoplastons at this time, we will be interested in the published outcome of peer reviewed studies that you or others may perform

If the NCI investigators choose to continue these studies, you will be so informed

In either circumstance, we will continue to sponsor clinical research of small molecules that may have differentiating properties (such as pure phenylacetate and phenylbutyrate)

cc:

Senator Joseph Biden
Senator Barbara Boxer
Senator Diane Feinstein
Senator Tom Harkin
Senator Barbara Mikulski
Congressman Berkley Bedell
Congresswoman Nancy Pelosi
Dr. Jan Buckner
Dr. Jay Greenblatt
Mr. Richard Jaffe
Dr. Wayne Jonas
Mr. Robert Lanman
Ms. Mary McCabe
Dr. Mark Malkin
Dr. Tony Murgo
Dr. Ralph Moss
Dr. David Parkinson
Dr. Edward Sondik
Dr. Mario Sznol
Dr. Dorothy Tisevich
Dr. Alan Trachtenberg
Mr. Frank Wiewel
Dr. Robert Wittes
——————————————————————

======================================
1993 (10/26/1993) – Burzynski to
1994 (3/9/1994) –
1994 (7/1994) – Burzynski to Theradex
1995 (4/20/1995) – Burzynski to
1995 (5/12/1995) – to Burzynski
1995 (5/16/1995) – Burzynski to
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Critiquing: Dr. David H. “Orac” Gorski and The Skeptics™ http://www.scienceblogs.com/Insolence

6/4/2013 Gorski made a remarkable admission:
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http://scienceblogs.com/insolence/2013/06/04/stanislaw-burzynski-versus-the-bbc/
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“Dr. Elloise Garside, a research scientists,

“echoes a lot of the questions I have, such as … ”

“Burzynski … antineoplastons … “:

what the scientific rationale is to expect that they might have antitumor activity” ?
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Gorski has claimed:
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6/7/2013 “Unlike Mr. Merola, I am indeed very concerned with getting my facts correct”
——————————————————————
http://scienceblogs.com/insolence/2013/06/07/i-want-my-anp/
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6/5/2013 “ … I do know cancer science”
——————————————————————
http://scienceblogs.com/insolence/2013/06/05/odds-and-ends-about-burzynski-clinic/
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11/2/2012 “Personally, having pored over Burzynski’s publications … “
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http://scienceblogs.com/insolence/2012/11/02/stanislaw-burzynski-fails-to-save-another-patient/
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5/8/2013 “I’ve searched Burzynski’s publications … “
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http://scienceblogs.com/insolence/2013/05/08/eric-merola-and-stanislaw-burzynskis-secret-weapon-against-the-skeptics-fabio-lanzoni-part-2/
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☆AnthonyJeselnik☆
🚫GorskonOrac🚫
You tweeted 12:44pm-3/30/13📄

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David Gorski (@gorskon) tweeted at 12:44pm – 30 Mar 13:
https://twitter.com/gorskon/status/318056135645073408
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Defend your tweet😅
#Burzynski—
(@FauxSkeptic) May 23, 2013

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David Gorski (@gorskon)
5/23/13, 9:32 AM

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@FauxSkeptic No need to defend my Tweet. The defense is in the link.
http://www.sciencebasedmedicine.org/index.php/stanislaw-burzynski-bad-medicine-a-bad-movie
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NO, Dr. Gorski, you have NOT “deconstructed his “evidence” in depth before”
Burzynski: Cancer Is Serious Business (Part I) consists of the documentary; as well as the documents on the movie web-site, which you have NOT “deconstructed … in depth before”

(What Gorski did is termed: “cherry-picking”)
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7/22/2013 I published the below article on my blog:
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Critiquing: In which Orac does Stanislaw Burzynski propagandist Eric Merola a favor…:
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https://stanislawrajmundburzynski.wordpress.com/2013/07/22/critiquing-in-which-orac-does-stanislaw-burzynski-propagandist-eric-merola-a-favor/
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“… because Gorski and others do NOT seem to understand how antineoplastons (ANP) A10 (Atengenal) and AS2-1 (Astugenal) work, I provide the relevant Burzynski publications and page #’s for them to review:
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It’s not like The Skeptics are going to help Gorski since they usually post inane comments that frequently go off topic on his Respectful Insolence blog
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Gorski, here’s:
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“the scientific rationale … to expect that (antineoplastons) might have antitumor activity”
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[1] 7/1971 Phenylacetic acid as potential therapeutic agent for treatment of HUMAN CANCER
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[2] 1976 Medium-sized peptides isolated from normal humans urine were tested for effect on DNA, RNA, and protein synthesis, and mitosis, in tissue culture of human myeloblastic leukemia, osteosarcoma, and HeLa cells
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active peptides produce up to 97% inhibition of DNA synthesis and mitosis in neoplastic cells in tissue culture

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[3] 1990 AS2-1 (AS)
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2 / 14.5% – Complete Remission
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3 / 21%- Partial Remission
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7 / 50%- Stabilization of disease with objective improvement
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2 / 14.5% – Progression
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1st patient enrolled in Complete Remission 17 months and off treatment 16 months
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[4] 4/1/1992 PHENYLACETATE-novel nontoxic inducer of TUMOR CELL differentiation
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Sodium PHENYLACETATE found to affect growth and differentiation of TUMOR CELLS in vitro at concentrations achieved in humans with no significant adverse effects
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Treatment of promyelocytic leukemia III.-60 cells resulted in rapid decline of myc oncogene expression followed by growth arrest and granulocyte differentiation
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results indicate PHENYLACETATE is effective in inducing tumor cell maturation and free of cytotoxic and carcinogenic effects, a combination that warrants attention to potential use in CANCER intervention
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Conclusions:
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Sodium PHENYLACETATE is investigational new drug approved for human use by U.S. Food and Drug Administration
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drug already established as safe and effective in treatment of hyperammonemia (2-4); we propose use may be extended to CANCER preventation and therapy
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[5] 9/15/1992 results suggest PHENYLACETATE, used alone or in combination with other drugs, might offer safe and effective new approach to treatment of some hematopoietic neoplasms and severe hemoglobinopathies
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NaPA, which has an unpleasant odor, can be substituted by its pro-drug, sodium PHENYLBUTYRATE (NaPB), for oral administration
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Upon ingestion by humans, PHENYLBUTYRATE undergoes @-oxidation to PHENYLACETATE
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Both NaPA and NaPB already proved safe for the treatment of infants and adults
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It seems important therefore to further evaluate the clinical relevance of our experimental data
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[6] 5/1993 nontoxic differentiation inducer, sodium PHENYLACETATE (NaPA)
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in vitro antineoplastic activity was observed with drug concentrations that have been achieved in humans with no significant toxicities, suggesting PA, used alone or in combination with other antitumor agents, warrants evaluation in treatment of advanced prostatic CANCER
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[7] 2/1994 sodium PHENYLACETATE can induce cytostasis and reversal of MALIGNANT properties of cultured HUMAN GLIOBLASTOMA CELLS, when used at pharmacological concentrations that are well tolerated by children and adults
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Systemic treatment of rats bearing intracranial GLIOMAS resulted in SIGNIFICANT TUMOR SUPPRESSION with no apparent toxicity to host
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data indicate PHENYLACETATE, acting through inhibition of protein prenylation and other mechanisms, may offer safe and effective novel approach to treatment of MALIGNANT GLIOMAS and perhaps other neoplasms as well
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[8] 4/1/1994 Phenylacetate has recently been shown to suppress TUMOR growth and promote differentiation in experimental models
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phase I trial of PHENYLACETATE conducted in 17 patients with advanced solid TUMORS
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99% of PHENYLACETATE elimination was accounted for by conversion to PHENYLACETYLGLUTAMINE, which was excreted in the urine
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1 of 6 patients with GLIOBLASTOMA MULTIFORME, whose steroid dosage has remained unchanged for duration of therapy, has sustained functional improvement for more than 9 months
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use of adaptive control with feedback for dosing of each patient enabled us to safely maintain stable PHENYLACETATE concentrations … which resulted in clinical improvement in some patients with advanced disease
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[9] 6/1/1994 PHENYLACETATE is naturally occurring plasma component that suppresses growth of TUMOR CELLS and induces differentiation in vitro
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Treatment with PHENYLACETATE extended survival … without associated adverse effects
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PHENYLACETATE, used at clinically achievable concentrations, prolongs survival of rats with MALIGNANT BRAIN TUMORS through induction of TUMOR differentiation
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role in treatment of BRAIN TUMORS and other CANCERS should be explored further
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[10] 9/1994 increasing incidence of melanoma and poor responsiveness of disseminated disease to conventional treatments call for development of new therapeutic approaches
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PHENYLACETATE, nontoxic differentiation inducer, can suppress growth of other NEUROECTODERMAL TUMORS, i.e., GLIOMAS, in laboratory models and HUMANS
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finding led us to explore efficacy of PHENYLACETATE and related aromatic fatty acids in MELANOMA
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PHENYLACETATE and PHENYLBUTYRATE found to a) induce selective cytostasis and maturation of cultured HUMAN MELANOMA CELLS, b) modulate expression of GENES implicated in TUMOR METATASIS (type IV collagenase and tissue inhibitor of metalloproteinases-2) and immunogenicity (HLA class I); and c) enhance efficacy of other agents of clinical interest
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in vitro ANTITUMOR activity observed with nontoxic, pharmacologic concentrations of PHENYLACETATE and PHENYLBUTYRATE, suggesting potential clinical use of drugs in treatment of MELANOMAS
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[11] 2/8/1995 (7/17/2006) PHENYLACETATE, a natural metabolite of phenylalanine which was originally described as a plant growth hormone, has recently gained attention as a possible differentiation inducer for a variety of HUMAN TUMOR CELL types
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Using the LA-N-5 cell line, we have determined that NaPA can stimulate the differentiation of neuroblastoma cells …
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NaPA and RA synergized in inducing differentiation, in that combination treatment resulted in cessation of cell growth along with morphologic and biochemical changes indicative of loss of malignant properties
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[12] 4/1995 (3/8/2013) PHENYLACETATE, an inducer of tumor cytostasis and differentiation, shows promise as relatively nontoxic antineoplastic agent
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PHENYLBUTYRATE, an odorless compound that also has activity in TUMOR models
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[13] 5/1995 Antineoplaston (Ap), new ANTITUMOR agent, clinically tested for effects on MALIGNANT BRAIN TUMORS
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1 – medulloblastoma
1 – pontine glioma
2 – anaplastic astrocytoma
2 – metastatic brain tumor
3 – glioblastoma (G,B)

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All underwent radiochemotherapy and surgical resection of tumors except:
1 – pontine glioma
2 – anaplastic astrocytoma
2 – metastatic brain tumor

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Complete Response:
1 – anaplastic astrocytoma
Partial Response:
1 – metastatic brain tumor
1 – pontine glioma
No change:
1 – anaplastic astrocytoma
1 – multiple brain metastasis
Progression of disease:
3 – glioblastomas
1 – medulloblastoma
showed continuous increase in tumor size

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Effects of Ap on malignant brain tumors considered due to synergy, since administered with other drugs and acceleration of tumor cellular differentiation
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Ap useful as approach to remission maintenance therapy for brain tumors
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[14] 6/15/1995 growth-inhibiting and differentiating effects of sodium PHENYLACETATE against hematopoietic and solid TUMOR CELL lines has aroused clinical interest in its use as an ANTICANCER drug
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1 – refractory malignant glioma had partial response
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1 – hormone-independent prostate cancer achieved 50% decline in prostate specific antigen level, maintained 1 month
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High grade GLIOMAS and advanced prostate cancer are reasonable targets for Phase II clinical trials
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[15] 7/1995 aromatic fatty acids phenylacetate (PA) and phenylbutyrate (PB) induce tumour cell differentiation in experimental models and currently in clinical trials
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close association between enhanced TGF-alpha production and melanoma cell differentiation suggests this growth factor, often linked to mitogenesis, may play a novel role in tumour differentiation by PA and PB
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[16] 9/27/1995 (7/17/2006) Alterations in expression of ras oncogenes are characteristic of wide variety of human neoplasms
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Accumulating evidence has linked elevated ras expression with disease progression and FAILURE of TUMORS to RESPOND to CONVENTIONAL THERAPIES, including radiotherapy and certain chemotherapies
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observations led us to investigate response of ras-transformed cells to differentiation-inducer PHENYLACETATE (PA)
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Using gene transfer models, we show PA caused cytostasis in ras-transformed mesenchymal cells, associated with increased expression of 2′,5′-oligoadenylate synthetase, an enzyme implicated in negative growth control
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PA also induced phenotypic reversion characterized by loss of anchorage-independent growth, reduced invasiveness and increased expression of collagen alpha type I, a marker of cell differentiation
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ANTI-TUMOR ACTIVITY of PA was observed in cases involving either Ha- or Ki-ras and was independent of mode of oncogene activation
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Interestingly, in contrast to their relative resistance to radiation and doxorubicin, ras-transformed cells were significantly more sensitive to PA than their parental cells
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profound changes in TUMOR CELL and molecular biology were associated with reduced isoprenylation of ras-encoded p21
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Our results indicate PA CAN SUPPRESS GROWTH of ras-transformed cells, resistant otherwise to free-radical based therapies, through interference with p21ras isoprenylation, critical to signal transduction and maintenance of MALIGNANT phenotype
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[17] 10/1995 investigated effects of a nontoxic differentiation inducer, PHENYLACETATE (PA), on NEUROECTODERMAL TUMOR-derived CELL lines
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PHENYLACETATE decreased transforming growth factor (TGF)-beta 2 production by medulloblastoma Daoy cells
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in vitro antiproliferative and differentiation inducing effects of PA suggest that this agent warrants further evaluation as a potential therapeutic modality for the treatment of MEDULLOBLASTOMAS and MALIGNANT GLIOMA in HUMANS
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[18] 10/12/1995 aromatic fatty acid PHENYLACETATE, a common metabolite of phenylalanine, shows promise as a relatively non-toxic drug for CANCER treatment
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slowly metabolized fatty acid alters tumor cell lipid metabolism causing … inhibition of protein prenylation critical to MALIGNANT growth
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data suggest PHENYLACETATE and analogues may act through common mechanisms to INHIBIT GROWTH of vastly divergent, undifferentiated CELL types, and provide basis for development of new agents for treatment of HUMAN MALIGNANCIES
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[19] 1995 Antineoplastons, firstly described by Burzynski, are naturally occurring peptides and amino acid derivatives which CONTROL NEOPLASTIC GROWTH
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toxicological study of Antineoplastons A-10 and AS2-1 in combination with other anticancer agents or radiation in 42 patients
46 tumors with terminal stage cancer
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Antineoplaston A-10 oral formulation
14 – patients
A-10 injectable formulation
25 – patients

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Antineoplaston AS2-1 oral formulation
33 – patients
AS2-1 injectable formulation
10 – patients

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Major adverse effects that may have been related to agents used in combination with other conventional chemotherapeutic agents or radiation:
liver dysfunction
myelosuppression
general weakness
these effects weren’t seen when either Antineoplaston was administered alone

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Minor adverse effects observed in single use of either Antineoplaston A-10 or AS2-1:
reduced albumin
increased alkaline phosphatase
increased amylase
reduced cholesterol
peripheral edema
eosinophilia
fingers rigidity
excess gas
headache
hypertension
maculopapullar rash
palpitation
adverse effects didn’t limit to continuation of either agent

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Evaluation of usefulness of Antineoplastons in combination therapy based on imaging findings during course of treatment revealed DISAPPEARANCE or MEASUREABLE SHRINKAGE of TUMOR lasting more than one months:
15 tumors / 32.6%
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No increase in size of tumor for more than 3 months:
8 / 17.4%

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Mean survival time of patients SIGNIFICANTLY LONGER than patients with tumors showing progressive increasing
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Antineoplaston A-10 and AS2-1 LESS TOXIC than conventional chemotherapeutics and useful in maintenance therapy for CANCER patients
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[20] 2/1996 (11/23/2002)
sodium salt of PHENYLACETATE acid (NaPA) … acted synergistically with lovastatin to SUPPRESS MALIGNANT GROWTH

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used at pharmacologically attainable concentrations … compounds induced profound cytostasis and LOSS of MALIGNANT PROPERTIES
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results indicate targeting lipid metabolism with … aromatic fatty acid NaPA, may offer novel approach to treatment of MALIGNANT GLIOMAS
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[21] 5/1996 recently investigated as ANTICANCER AGENT because decreased growth and increased differentiation of variety of human NEOPLASMS, including PROSTATE CANCER in which a phase I trial has recently been completed
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PA’s GROWTH-INHIBITORY effects on a variety of cell lines
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PA MARKEDLY DECREASED rat PROSTATIC GROWTH and ductal morphogenesis at concentrations that have previously been well tolerated in patients
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Synthesis of DNA also significantly decreased per organ with PA
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In common with earlier studies, we found PA INHIBITS PROSTATIC GROWTH
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studies indicate there may be role for PA in treating BPH or elucidating mechanisms
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[22] 1996
Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which CONTROL NEOPLASTIC GROWTH

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These metabolites are water soluble and have ANTITUMOR EFFECT, they are further degraded to PHENYLACETIC acid
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Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid in ratio of 1 to 4 shown to have ANTITUMOR EFFECT in tissue culture study, then formulated as Antineoplaston AS2-1
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reported CYTOSTATIC INHIBITORY EFFECT of A10 on HUMAN HEPATOCELLULAR CARCINOMA CELLS and differentiation inducing effect of AS2-1 on various TUMOR CELLS suggest potential benefit for treatment of HUMAN HEPATOCELLULAR CARCINOMA since TUMOR recurs frequently despite initial successful treatment
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We report effects of Antineoplaston A10 and AS2-1 on cell proliferation, cell morphology, cell cycle, and DNA in human hepatocellular carcinoma cell lines
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BOTH AGENTS INHIBITED CELL PROLIFERATION and increased number of cells in G0 and G1 phases and Antineoplaston AS2-1 induced APOPTOSIS
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clinical experience of HEPATOCELLULAR CARCINOMA (HCC) patient whose TUMOR, after incomplete trancathere arterial embolization (TAE) for a 7cm 7cm HCC, has been stable for more than 15 months during which time he has been taking Antineoplaston AS2-1 continuously WITHOUT ANY SERIOUS ADVERSE EFFECTS
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[23] 8/23/1996 aromatic fatty acid PHENYLACETATE and analogs INDUCE TUMOR CYTOSTASIS and differentiation in experimental models
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studies using HUMAN PROSTATIC CARCINOMA, MELANOMA, and GLIOBLASTOMA cell lines showed a tight correlation between drug-induced cytostasis …
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results identify PHENYLACETATE and analogs as new class of aromatic fatty acids capable of activating hPPAR, and suggest nuclear receptor may mediate TUMOR cytostasis induced by these drugs
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[24] 9/1996 We examined hypothesis this postulate may not apply to evaluation of drugs such as PHENYLACETATE, a differentiating agent endowed with mechanisms of action different from those of classic cytotoxic chemotherapy
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Using HUMAN PROSTATIC CARCINOMA LNCaP cells as model, we show PHENYLACETATE induces PSA production despite inhibition of TUMOR CELL proliferation

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[25] 12/1996 PHENYLACETATE (PA) and related aromatic fatty acids constitute novel class of relatively nontoxic antineoplastic agents
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Using human breast carcinoma MCF-7 cells as model, we show PA-induced growth arrest associated with enhanced expression of cyclin-dependent kinase inhibitor p21Waf1/Cip1 …
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induction of p21WAF1/CIP1 mRNA by PA independent of cellular p53 status
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PA effectively induced p21WAF1/CIP1 mRNA and growth inhibition of wild-type mouse embryonal fibroblasts
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findings strongly support role for p21Waf1/Cip1 in PA-mediated inhibition of cell growth
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[26] 1996 Cytotoxic chemotherapies often give rise to multidrug resistance, which remains major problem in CANCER management
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In pursuit of alternative treatments for chemoresistant TUMOR CELLS, we tested response of multidrug-resistant (MDR) TUMOR CELL lines to aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB), 2 differentiation inducers currently in clinical trials
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Both compounds induced cytostasis and maturation of multidrug-resistant BREAST, OVARIAN, and COLON CARCINOMA CELLS with no significant effect on cell viability
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MDR cells generally more sensitive to GROWTH ARREST by PA and PB than parental counterparts
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PA and PB potentiated the cytotoxic activity of doxorubicin against MDR cells
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Taken together, our in vitro data indicate PA and PB, differentiation inducers of aromatic fatty acid class, may provide alternative approach to treatment of MDR TUMORS
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[27] 8/1997 aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB) are novel ANTITUMOR AGENTS currently under clinical evaluation
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ability to induce TUMOR differentiation in laboratory models and low clinical toxicity profile makes them promising candidates for COMBINATION with CONVENTIONAL THERAPIES
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In present studies, we characterized interactions between aromatic fatty acids and radiation, using as a model cell lines derived from CANCERS of PROSTATE, BREAST, BRAIN and COLON
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in vitro findings identify aromatic fatty acids PA and PB as new class of non-toxic modulators of radiation response, antagonistic effect of these compounds on radiation response needs further examination
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data strongly suggest that for PA or PB to have role in clinical radiotherapy, appropriate scheduling of combination therapies must take into account time-dependent effects in order to achieve clinical radiosensitization
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[28] 11-12/1997 Antineoplaston AS2-1 EXHIBITS CYTOSTATIC GROWTH INHIBITION of human hepatocellular carcinoma cells in vitro and showed minimum adverse effects in phase I clinical trial
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2 clinical cases of liver cancer (hepatocellular carcinoma and multiple liver metastases from colon cancer) in whom we believe antineoplaston A2-1 useful as maintenance therapy after transcatheter arterial embolization (TAE) and microwave coagulation necrosis (MCN)
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2 patients have continued to be in good condition for more than 2 years without limitation of normal activities
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Antineoplaston AS2-1 may be effective and useful as maintenance agent after TAE and MCN in patients with liver cancer
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[29] 1997 PHENYLACETATE and analogs represent new class of pleiotropic growth regulators that alter TUMOR CELL biology by affecting GENE EXPRESSION at both transcriptional and post transcriptional levels
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Based on findings, NaPA and NaPB entered clinical trials at NATIONAL CANCER INSTITUTE
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Ongoing phase I studies with NaPA, involving adults with PROSTATE and BRAIN CANCER, confirmed therapeutic levels can be achieved with no significant toxicities, and provide preliminary evidence for benefit to patients with advanced disease (Thibault et al., submitted)
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[30] 5 – 6/1998 Antineoplastons A10 and AS2-1 EXHIBIT GROWTH INHIBITION OF CANCER CELLS by diverse modes of action
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Observed ANTITUMOR RESPONSES within 2-3 weeks of combination treatment of chemoradiation therapy and antineoplastons A10 and AS2-1 in phase I clinical study conducted in Kurume University Hospital
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Reviewed 3 clinical cases of advanced cancer (multiple metastatic lung cancer, thalamic glioma and primary lung cancer) in which we believed antineoplaston A10 and AS2-1 may be contributing to RAPID ANTITUMOR RESPONSE
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Possible use of this combination for induction therapy in advanced cancer
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[31] 11-12/1998 Antineoplaston A10 injection (antineoplaston A10 I) exhibited CYSTOSTATIC GROWTH INHIBITION OF HUMAN HEPATOCELLULAR CARCINOMA (HCC) CELLS in vitro and showed minimum adverse effects in phase I clinical trial
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2 cases of advanced HCC treated with antineoplaston A10 I
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Both cases showed interesting responses to antineoplaston A10 I
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One showed massive coagulation necrosis of tumors after intra-arterial infusion of antineoplaston A10 I and other showed RESOLUTION of portal vein TUMOR thrombosis with systemic infusion of antineoplaston A10 I
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Usefulness of anti-neoplaston A10 I in terminal staged HCC is discussed
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[32] 3/1999 determine response rate, time to treatment failure, and toxicity of phenylacetate in patients with recurrent malignant glioma …
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Adult patients
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43 – enrolled 12/1994-12/ 1996
40 – assessable
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Reversible symptoms
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fatigue
somnolence
were primary toxicities
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only mild hematologic toxicity
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30 / 75% – failed treatment within 2 months
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7 / 17.5% – stable disease
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3 – 7.5% – response defined as more than 50% reduction in tumor
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Median time to treatment failure
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2 months
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35 – died
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median survival
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8 months
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PHENYLACETATE HAS LITTLE ACTIVITY at this dose schedule in PATIENTS with RECURRENT MALIGNANT GLIOMA
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Further studies with drug would necessitate evaluation of different dose schedule
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[33] 7/3/2000 Antineoplastons first described by Burzynski are naturally occurring peptides and amino acid derivatives, which CONTROL NEOPLASTIC GROWTH
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data suggest strong inverse association of urinary antineoplaston A-10 level with breast cancer
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finding was stimulus for further investigations of antineoplaston A-10 levels in some benign as well as other malignant diseases to determine utility of approach as predictive test for women at risk of developing breast cancer
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[34] 8/31/2000 Antineoplastons are naturally occurring CYTODIFFERENTIATING AGENTS
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Findings confirm presence of immune defects among patients with breast cancer and results should stimulate development of new strategies to induce and augment immunity for treatment of breast cancer
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Antineoplaston A-10 may provide rational basis for designing trials to employ its immune modulatory potentials as adjuvant therapy in breast cancer patients
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[35] 12/2000 4 new piperidinedione A10 analogs synthesized and tested for antimitotic activity on human breast cancer cell line against prototype A10 and antibreast cancer drug tamoxifen
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“3B” and “3D” were several-fold more potent ANTIPROLIFERATIVE AGENTS than A10 and tamoxifen and had significantly higher capacity to bind DNA than A10
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[36] 8/2001 No partial remission or complete remission was seen, but 7 patients had stable disease for more than 6 months while on drug
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PB may have role as cytostatic agent and should be additionally explored in combination with cytotoxics and other novel drugs
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[37] 2002 p53 tumor suppressor gene plays important role in protecting cells from developing undesirable proliferation
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Mutant p53 gene or malfunctioning p53 protein found in more than 50% of cancer cells impedes DNA repair or apoptosis induction
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May be why some cancers gain resistance to chemotherapy and radiation and become more resistant after frequent cancer treatments
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non-toxic p53 gene activator would induce cancer cell apoptosis and help damaged cancer cells to recover
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combination use of chemotherapeutics or radiation with non-toxic p53 gene activator will be crucial in cancer therapy, damaging DNA with chemotherapeutics or radiation on one hand and promoting apoptosis induction with p53 gene activator on the other
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Strategy would be most efficient for remission induction and maintenance CANCER therapy
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Antineoplastons are naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH
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Antineoplaston A10 and AS2-1 are chemically identified and synthesized antineoplastons PROVEN TO INHIBIT CANCER CELL GROWTH by arresting cell cycle in G1 phase and INHIBITING TUMOR GROWTH by reducing mitosis
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Agents thought to be good candidates for clinically easily applicable non-toxic p53 gene activators
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CASES OF ADVANCED CANCER RESPONDED WELL to combination treatment using chemotherapeutics and irradiation with antineoplaston A10 and AS2-1 in clinical trials being conducted in Kurume University Hospital
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[38] 3 – 4/2003 Phase II clinical trail to clarify whether antineoplaston AS2-1, mixture of sodium salts of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid at ratio of 1:4, prolongs recurrence-free interval of HCC patients who undergo frequent treatments for recurrence
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10 patients enrolled in trial
2 in stage I
6 in stage II
1 in stage III
1 in stage IV-B
at initial diagnosis

——————————————————————
10 / 100% – experienced 35 recurrence-free intervals
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Recurrence-free intervals during antineoplaston AS2-1 administration SIGNIFICANTLY LONGER than without
——————————————————————
Patients who experienced recurrence-free intervals with and without antineoplaston AS2-1 SHOWED LONGER INTERVALS during antineoplaston AS2-1 administration
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2 patients in stage I showed LONGER RECURRENCE-FREE INTERVALS than those in more advanced stages
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Antineoplastons AS2-1 couldn’t prevent recurrence of HCC but PROLONGED RECURRENCE-FREE INTERVAL between regional treatments and IMPROVED SURVIVAL RATE OF PATIENTS
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[39] 2003 Case of survival for nearly 8 years after treatment of unresectable multiple liver metastases from colon cancer, using microwave ablation and NONTOXIC ANTITUMOR AGENT, antineoplastons
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72-year-old man diagnosed with adenocarcinoma of ascending colon and 14 bilateral liver metastases underwent right hemicolectomy combined with microwave ablation of 6 metastatic liver tumors
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Antineoplaston A10 given intravenously, followed by oral antineoplaston AS2-1
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Computed tomography scans done 1 and 4 years after initial diagnosis showed recurrent tumors
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Patient underwent 2nd and 3rd microwave ablation of recurrent tumors, and has survived for nearly 8 years WITHOUT SUFFERING ANY SERIOUS ADVERSE EFFECTS
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Currently FREE FROM CANCER
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Demonstrates potential effectiveness of NONTOXIC ANTITUMOR AGENT, antineoplastons, for controlling liver metastases from colon cancer
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======================================
Burzynski has made it clear that PHENYLACETATE, by itself, does NOT achieve the results of antineoplastons (PHENYLACETATE, PHENYLGLUTAMINATE, PHENYLACETYLISOGLUTIMINATE, PHENYLBUTYRATE)
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[40] 2003
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Pg. 92
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Antineoplaston A10 and AS2-1 are synthetic derivatives of phenylacetate (PN) acid, glutamine and isoglutamine
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A10 is sterile solution of sodium phenylacetylisoglutiminate (isoPG) in 4 : 1 ratio
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Antineoplaston AS2-1 is sterile solution of sodium phenylacetate (PN) and phenylacetylglutaminate (PG) in 4 : 1 ratio
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Pg. 93
======================================
combination of antineoplaston A10 and AS2-1 used instead of single drugs
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Based on previous observations, combination treatment has provided better results than single drugs
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Pg. 97
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active ingredient of antineoplaston AS2-1 is PHENYLACETATE,
——————————————————————
Pg. 98
——————————————————————
known to modulate expression of ras oncogenes and tumor suppressor gene p53
——————————————————————
ras oncogene protein p21ras
——————————————————————
farneslyation of p21ras, which is inhibited by antineoplaston AS2-1
——————————————————————
Antineoplaston AS2-1 also activates p53 gene
——————————————————————
protein p53 activates p21 gene, which directs synthesis of p21WAF1/Cip1 protein
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Induction of p21WAF1/Cip1 suppresses human glioma cell proliferation
——————————————————————
proposed mechanism of action of 2 ingredients of antineoplaston A10, sodium phenylacetylglutamine (PG) and sodium phenylacetylisoglutimine (IsoPG), is inhibition of glutamine incorporation into proteins of neoplastic cells
——————————————————————
Antineoplaston A10 has demonstrated 5 effects related to therapeutic indication in patients with brain tumors: cytostatic, antimitogenic, antiproliferative and inhibitory effects, and differentiation of tumors
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[22-25]
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Initial clinical studies with antineoplaston therapy included testing of separate ingredients phenylacetate (PN) (antineoplaston AS5) and phenylacetylglutaminate (PG) (antineoplaston AS2-5)
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[26-28]
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studies failed to show marked anticancer activity of phenylacetate (PN) in malignant glioma, confirmed by phase II study by North
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Pg. 99
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American Brain Tumor Consortium
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[29]
——————————————————————
Based on results, further studies of phenylacetate (PN) as single agent in patients with malignant glioma were not recommended
——————————————————————
subsequent study by Buckner et al.
——————————————————————
[30]
——————————————————————
confirmed conclusion because patients receiving antineoplaston AS2-1 didn’t respond to treatment
——————————————————————
main difference between Buckner’s study is dosage of antineoplaston A10, which was approximately 50 times lower in Buckner’s study
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[31]
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2 patients who participated in our study (cases 3 and 8) developed recurrence on lower dosages of antineoplaston A10, but responded again with Complete Response (CR) when dosage of antineoplaston A10 was increased
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In these 2 patients, antineoplaston AS2-1 didn’t seem to have effect on 2nd response, which suggests antineoplaston A10 rather than antineoplaston AS2-1 is main active drug
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[41] 8/2005 Antineoplastons such as A10 include naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH OF CELLS
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Findings indicate antineoplaston A10 ANTITUMOR EFFECT could be utilized as effective therapy for breast cancer patients
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[42] 2006 Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which CONTROL NEOPLASTIC GROWTH
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Antineoplaston A10 (3-pehnylacetylamino-2,6-piperidinedion) is first chemically identified antineoplastons and when administered orally is hydrolysed in pancreatic juice to PHENYLACETYLGLUTAMINE and PHENYLACETYLISOGLUTAMINE in ration of 4 to 1
——————————————————————
These metabolites are water soluble and have ANTITUMOR EFFECT, are further degraded to PHENYLACETIC acid
——————————————————————
Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETYLISOGLUTAMINE in ratio of 4 to 1 formulated as Antineoplaston A10 injectable formulation
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Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid in ratio of 1 to 4 also shown to have ANTITUMOR EFFECT in tissue culture study, then formulated as Antineoplaston AS2-1
——————————————————————
Reported CYTOSTATIC INHIBITORY EFFECT of A10 on HUMAN HEPATOCELLULAR CARCINOMA CELLS and differentiation inducing effect of AS2-1 on various TUMOR CELLS suggest potential benefit for treatment of HUMAN HEPATOCELLULAR CARCINOMA since this TUMOR recurs frequently despite initial successful treatment
——————————————————————
BOTH AGENTS INHIBITED CELL PROLIFERATION and increased number of cells in G0 and G1 phases and Antineoplaston AS2-1 induced apoptosis, we also describe clinical experience of hepatocellula carcinoma (HCC) patient whose tumor, after incomplete trancathere arterial embolization (TAE) for 7cm 7cm HCC, has been stable for more than 15 months during which time he has been taking Antineoplaston AS2-1 continuously WITHOUT ANY SERIOUS ADVERSE EFFECTS
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[43] 1/2008 Novel mechanism through which all-trans retinoic acid (ATRA) and antineoplaston, ANTICANCER DRUG, CAUSED CELL GROWTH INHIBITION IN BREAST CANCER CELLS through effects on intracellular pathways
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Antineoplaston caused down-regulation of PKCalpha protein expression, resulting in INHIBITION of ERK MAPK phosphorylation, with resultant INHIBITION of Rb phosphorylation leading to G(1) arrest
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[44] 10/1/2010 As degradation product of Antineoplaston A10 in vivo, PHENYLACETYL GLUTAMINE showed ANTITUMOR ACTIVITIES
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Designed and radiosynthesized PHENYLACETYL GLUTAMINE derivative, achieved under mild reaction condition
——————————————————————
radiochemical purity of (S)-2-((S)-2-(4-(3-fluoropropyl)benzamido)-3-phenylpropanamido)pentanedioic acid ([18F]FBPPA) was 98%, and best radiochemical yield was up to 46%
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results revealed it might become potential PET imaging agent for DETECTING TUMORS
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References:
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[1] 7/1971
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Neish, W. J. P. Phenylacetic acid as a potential therapeutic agent for the treatment of HUMAN CANCER. Experientia (Basel), 27: 860-861, 1971
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[2] 1976
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Biological active peptides in human urine: III. Inhibitors of the growth of human leukemia, osteosarcoma, and HeLa cells
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S R Burzynski, …
Physiol Chem Phys 8(1):13-22 (1976), PMID .1066715
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[3] 1990
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BURZYNSKI, S. R., Kubove E., Burzynski, B. Treatment of hormonally refractory CANCER of the prostate with ANTINEOPLASTON AS2-1. Drugs Exp. Clin. Res., 16: 361-369, 1990
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[4] 4/1/1992
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SAMID, D., Shack, S., and Sherman, l.. T.
http://www.ncbi.nlm.nih.gov/pubmed/1372534/
Cancer Res., 52: 1988-1992, 1992
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Cancer Res. 1992 Apr 1;52(7):1988-92
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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
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SAMID D, Shack S, Ti-Sherman L PHENYLACETATE-A novel nontoxic inducer of TUMOR CELL differentiation. Cancer Res 52:1988, 1992
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[5] 9/15/1992
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SAMID, D., Yeh, A., and Prasanna, P. Induction of erythroid differentiation and fetal
hemoglobin production in HUMAN leukemic cells treated with PHENYLACETATE. Blood, 80: 1576-81, 1992
http://www.ncbi.nlm.nih.gov/pubmed/1381630/
SAMID D, Yen A, Prasanna P . Induction of erythroid differentiation and fetal hemoglobin production in HUMAN leukemic cells treated with PHENYLACETATE . Blood. 1992;80:1576
http://www.ncbi.nlm.nih.gov/m/pubmed/1381630/
Blood, 80: 1576-1581, 1992
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.abstract
Blood. 1992 Sep 15;80(6):1576-81
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.full.pdf
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD
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[6] 5/1993
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SAMID D, Shack S , Myers CE . Selective growth arrest and phenotypic reversion of prostate CANCER CELLS in vitro by nontoxic pharmacological concentrations of PHENYLACETATE . J. Clin. Invest . 1993;91:2288
http://www.ncbi.nlm.nih.gov/pubmed/8486788/
J Clin Invest. 1993 May;91(5):2288-95
http://www.ncbi.nlm.nih.gov/m/pubmed/8486788/
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC288233/

http://m.jci.org/articles/view/116457
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[7] 2/15/1994
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SAMID, D., Ram, Z., Hudgins, W. R., Shack, S., Liu, L., Waibridge, S., Oldfield, E. H., and Myers, C. E. Selective activity of PHENYLACETATE against MALIGNANT GLIOMAS: resemblance to fetal brain damage in phenylketonuria. Cancer Res., 54: 891-895, 1993
http://www.ncbi.nlm.nih.gov/pubmed/8313377/
Cancer Res. 1994 Feb 15;54(4):891-5
http://www.ncbi.nlm.nih.gov/m/pubmed/8313377/
Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
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[8] 4/1/1994
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A phase I and pharmacokinetic study of intravenous PHENYLACETATE in PATIENTS with CANCER
http://www.ncbi.nlm.nih.gov/pubmed/8137283/
Cancer Res 54(7):1690-4 (1994), PMID.8137283
http://www.ncbi.nlm.nih.gov/m/pubmed/8137283
Cancer Res April 1, 1994 54:1690
http://cancerres.aacrjournals.org/content/54/7/1690
Cancer Res. 1994 Apr 1;54(7):1690-4.
http://m.cancerres.aacrjournals.org/content/54/7/1690.abstract
Cancer Res . 1994;54:
http://cancerres.aacrjournals.org/content/54/7/1690
Clinical Pharmacology Branch, National Cancer Institute, NIH, Bethesda, Maryland
http://m.cancerres.aacrjournals.org/content/54/7/1690.full.pdf
A A Thibault, …, D D SAMID et al.
http://cancerres.aacrjournals.org/content/54/7/1690.full.pdf?sid=78d246d7-a4ee-4980-bdaf-b299dc98cbe8
Thibault A, Cooper MR, Figg WD, Venzon DJ, Sartor O, Tompkins AE, et al. (SAMID D)
↵1 This study was supported in part by a grant from Elan Pharmaceutical Research Co.
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[9] 6/1/1994
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Growth inhibition, TUMOR maturation, and extended survival in experimental BRAIN TUMORS in rats treated with PHENYLACETATE.
http://www.ncbi.nlm.nih.gov/pubmed/8187079/
Ram Z, SAMID D, Walbridge S, et al:
http://www.ncbi.nlm.nih.gov/m/pubmed/8187079/
Cancer Res 54:2934-2927, 1994
http://m.cancerres.aacrjournals.org/content/54/11/2934.abstract?ijkey=03bc67e581ef77536842806b949046916458d548&keytype2=tf_ipsecsha
Cancer Res. 1994 Jun 1;54(11):2923-7.
http://m.cancerres.aacrjournals.org/content/54/11/2923.abstract
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland
http://m.cancerres.aacrjournals.org/content/54/11/2923.full.pdf
Cancer Res. 1994 Jun 1;54(11):2923-7
http://cancerres.aacrjournals.org/content/54/11/2923
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[10] 1994
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Liu L , Shack S , Stetler-Stevenson WG , Hudgins WR , SAMID D . Differentiation of cultured HUMAN MELANOMA CELLS induced by the aromatic fatty acids PHENYLACETATE and PHENYLBUTYRATE . J. Invest. Dermatol . 1994;103:335
http://www.ncbi.nlm.nih.gov/pubmed/8077698/
J Invest Dermatol. 1994 Sep;103(3):335-40
http://www.ncbi.nlm.nih.gov/m/pubmed/8077698/
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
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[11] 2/8/1995
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PHENYLACETATE synergizes with retinoic acid in inducing the differentiation of human neuroblastoma cells.
http://www.ncbi.nlm.nih.gov/pubmed/7829265/
Int J Cancer. 1995 Feb 8;60(4):507-14
http://www.ncbi.nlm.nih.gov/m/pubmed/7829265/
Department of Pathology and Laboratory Medicine (Neuropathology), UCLA School of Medicine
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910600414/abstract
Int J Cancer 60:507-514, 1995
Int J Cancer. 1995 Feb 8;60(4):507-14.
International Journal of Cancer
Volume 60, Issue 4, pages 507–514, 8 February 1995
Article first published online: 17 JUL 2006
DOI: 10.1002/ijc.2910600414
Sidell N, Wada R, Han G, et al: (SAMID D)
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[12] 4/1995
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Disposition of PHENYLBUTYRATE and its metabolites, PHENYLACETATE and PHENYLACETYLGLUTAMINE.
J Clin Pharmacol 35:368-373, 1995 Abstract
http://www.ncbi.nlm.nih.gov/pubmed/7650225/
J Clin Pharmacol 35:368-373, 1995 Abstract
http://www.ncbi.nlm.nih.gov/m/pubmed/7650225/
The Journal of Clinical Pharmacology
Volume 35, Issue 4, pages 368–373, April 1995
http://m.jcp.sagepub.com/content/35/4/368.abstract?ijkey=74bff0d86ce76b404728762fe2a1bfde1641fa41&keytype2=tf_ipsecsha
J Clin Pharmacol. 1995 Apr;35(4):368-73
http://onlinelibrary.wiley.com/doi/10.1002/j.1552-4604.1995.tb04075.x/abstract;jsessionid=DFDEF1599D764E2845EC2897269C198B.d01t01
Article first published online: 8 MAR 2013
http://jcp.sagepub.com/content/35/4/368
Piscitelli SC, Thibault A, Figg WD, et al: (SAMID D)
DOI: 10.1002/j.1552-4604.1995.tb04075.x
Pharmacy Department, National Institutes of Health, Bethesda, Maryland, USA
http://m.jcp.sagepub.com/content/35/4/368.abstract?ijkey=74bff0d86ce76b404728762fe2a1bfde1641fa41&keytype2=tf_ipsecsha
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[13] 5/1995
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The effect of Antineoplaston, a new ANTITUMOR AGENT on MALIGNANT BRAIN TUMORS
http://www.ncbi.nlm.nih.gov/pubmed/7474850
Kurume Med J. 1995;42(3):133-40
http://www.ncbi.nlm.nih.gov/m/pubmed/7474850
Department of Neurosurgery, Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/3/42_3_133/_article
Tsuda H (Japan)
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/3/42_3_133/_article/references
Burzynski References: 1 – 2 and 4
SAMID Reference: 7 (who learned from Burzynski re PHENYLACETATE)
Lee (Japan) A-10 Reference: 3
Nishidi (Japan) A-10 Reference: 6
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/3/42_3_133/_pdf
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[14] 6/15/1995
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Phase I study of PHENYLACETATE administered twice daily to PATIENTS with CANCER. Cancer 75:2932-8, 1995
http://www.ncbi.nlm.nih.gov/pubmed/7773944/
Cancer 75(12):2932-8 (1995), PMID.7773944
http://www.ncbi.nlm.nih.gov/m/pubmed/7773944
A A Thibault, D D SAMID, … C E CE Myers
Cancer. 1995 Jun 15;75(12):2932-8
Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
Thibault A, SAMID D, Cooper MR, et al:
Thibault, A., SAMID, D., Cooper, M. A., Figg, W. 0., Tompkins, A. C., Patronas, N., Headlea, 0. J., Kohler, 0. A., Venzon, 0. J., and Myers, C. E. Cancer (Phila.), 75: 2932-2938, 1995.
http://onlinelibrary.wiley.com/doi/10.1002/1097-0142(19950615)75:12%3C2932::AID-CNCR2820751221%3E3.0.CO;2-P/abstract
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[15] 7/1995
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Transcriptional upregulation of TGF-α by PHENYLACETATE and PHENYLBUTYRATE is associated with differentiation of HUMAN MELANOMA CELLS
http://www.ncbi.nlm.nih.gov/pubmed/7578983/
Liu L., Hudgins W. R., Miller A. C., Chen L. C., SAMID D.
http://www.sciencedirect.com/science/article/pii/S1043466685700610
Cytokine, 7: 449-456, 1995.
Cytokine Volume 7, Issue 5, July 1995, Pages 449–456
Cytokine. 1995 Jul;7(5):449-56.
a Clinical Pharmacology Branch, National Cancer Institute, Armed Forces of Radiation Research Institute, Bethesda, Maryland, USA
b Radiation Biochemistry Department, Armed Forces of Radiation Research Institute, Bethesda, Maryland, USA
http://dx.doi.org/10.1006/cyto.1995.0061
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[16] 9/27/1995
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Increased susceptibility of ras-transformed cells to PHENYLACETATE is associated with inhibition of p21ras isoprenylation and phenotypic reversion. Int J Cancer 63:124-129, 1995
http://www.ncbi.nlm.nih.gov/pubmed/7558439/
Int J Cancer. 1995 Sep 27;63(1):124-9
http://www.ncbi.nlm.nih.gov/m/pubmed/7558439/
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD, USA
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910630122/abstract
Int J Cancer 63:124-129, 1995
Int J Cancer. 1995 Sep 27;63(1):124-9.
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910630122/references
International Journal of Cancer
Volume 63, Issue 1, Article first published online: 17 JUL 2006
DOI: 10.1002/ijc.2910630122
Shack S, Chen L-C, Miller AC, et al: (SAMID D)
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910630122/abstract
Shack, S., Chen, L-C., Miller, A. C., Danesi, A., and SAMID, D. Int. J. Cancer, 63: 124-129, 1995
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[17] 10/1995
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Stockhammer G, Manley GT, Johnson R, et al: (SAMID D) Inhibition of proliferation and induction of differentiation in medulloblastoma and astrocytoma-derived cell lines with PHENYLACETATE. J Neurosurg 83:672-681, 1995
http://www.ncbi.nlm.nih.gov/pubmed/7674018/
J Neurosurg. 1995 Oct;83(4):672-81
http://www.ncbi.nlm.nih.gov/m/pubmed/7674018/
Cotzias Laboratory of Neuro-Oncology, Memorial Sloan-Kettering Cancer Center, New York, New York, USA
http://thejns.org/doi/abs/10.3171/jns.1995.83.4.0672?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed&
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[18] 10/12/1995
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Cytostatic activity of PHENYLACETATE and derivatives against TUMOR CELLS:
Correlation with lipophilicity and inhibition of protein prenylation.
http://www.ncbi.nlm.nih.gov/pubmed/7488244/
Biochem Pharmacol. 1995 Oct 12;50(8):1273-9
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Biochem Pharmacol 50:1273-1279, 1995
http://www.sciencedirect.com/science/article/pii/0006295295020133
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD, USA
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[19] 1995
� � � � � � � � � � � � � � � �
Toxicological study on antineoplastons A-10 and AS2-1 in cancer patients
Kurume Med J. 1995;42(4):241-9
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Tsuda H
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Nishida et al. (Japan) A-10 Reference: 4 and 7
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Muldoon et al. A-10 Reference: 6
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[20] 2/1996
� � � � � � � � � � � � � � � �
Lipid metabolism as a target for BRAIN CANCER therapy:
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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland, USA
Prasanna P, Thibault A, Liu L, et al: (SAMID D)
� � � � � � � � � � � � � � � �
[21] 5/1996
� � � � � � � � � � � � � � � �
PHENYLACETATE is an inhibitor of prostatic growth and development in culture.
http://www.ncbi.nlm.nih.gov/pubmed/8627880/
J Urol 155:1762-1770, 1996
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J Urol. 1996 May;155(5):1762-70
Lipshutz JH, SAMID D, Cunha GR:
The Journal of Urology
Volume 155, Issue 5, Pages 1762-1770, May 1996
Department of Medicine, University of California, San Francisco, USA
� � � � � � � � � � � � � � � �
[22] 1996
� � � � � � � � � � � � � � � �
Inhibitory effect of antineoplaston A10 and AS2-1 on human hepatocellular carcinoma
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Kurume Med J. 1996;43(2):137-47
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Burzynski References: 1 – 3, 5 and 7
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article/references
SAMID Reference: 13 (who learned from Burzynski re PHENYLACETATE)
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_pdf
Nishida et al. (Japan) A10 Reference: 4 and 10
Muldoon et al. A10 Reference: 8
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[23] 8/23/1996
� � � � � � � � � � � � � � � �
Pineau T, Hudgins WR, Liu L, et al: (SAMID D) Activation of a human peroxisome proliferator-activated receptor by the ANTITUMOR agent PHENYLACETATE and its analogs. Biochem Pharmacol 52:659-667, 1996
http://www.ncbi.nlm.nih.gov/pubmed/8759039/
Biochem Pharmacol. 1996 Aug 23;52(4):659-67
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Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD, USA
http://www.sciencedirect.com/science/article/pii/0006295296003401
� � � � � � � � � � � � � � � �
[24] 9/1996
� � � � � � � � � � � � � � � �
The differentiating agent PHENYLACETATE increases prostate-specific antigen production by prostate cells
http://www.ncbi.nlm.nih.gov/pubmed/8827086/
Prostate 29:177-182, 1996
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Prostate. 1996 Sep;29(3):177-82
Walls R, Thibault A, Liu L, et al: (SAMID D)
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland, USA
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[25] 12/1996
� � � � � � � � � � � � � � � �
Gorospe M, Shack S, Guyton KZ, et al: (SAMID D)
Up-regulation and functional role of p21Waf1/Cip1 during growth arrest of HUMAN BREAST CARCINOMA MCF-7 cells by PHENYLACETATE. Cell Growth Differ 7:1609-1615, 1996
http://www.ncbi.nlm.nih.gov/pubmed/8959328/
Cell Growth Differ. 1996 Dec;7(12):1609-15
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Laboratory of Cellular and Molecular Biology, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, Maryland, USA
http://cgd.aacrjournals.org/cgi/reprint/7/12/1609.pdf
� � � � � � � � � � � � � � � �
[26] 5/1996
� � � � � � � � � � � � � � � �
Shack, S., Miller, A., Liu, L., Prasanna, P., Thibault, A., and SAMID, D.. Vulnerability of multidrug-resistant TUMOR CELLS to the aromatic fatty acids PHENYLACETATE and PHENYLBUTYRATE. Clin. Cancer Res., 2: 865-872, 1996
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Clin Cancer Res. 1996 May;2(5):865-72
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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892, USA
http://m.clincancerres.aacrjournals.org/content/2/5/865.abstract

http://m.clincancerres.aacrjournals.org/content/2/5/865.full.pdf
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[27] 8/1997
� � � � � � � � � � � � � � � �
Miller AC, Whittaker T, Thibault A, et al: (SAMID D)
Modulation of radiation response of HUMAN TUMOR CELLS by the differentiation inducers, PHENYLACETATE and PHENYLBUTYRATE. Int J Radiat Biol 72:211-218, 1997
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Int J Radiat Biol. 1997 Aug;72(2):211-8
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Armed Forces Radiobiology, Research Institute, Bethesda, MD, USA
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[28] 11-12/1997
� � � � � � � � � � � � � � � �
Antineoplaston AS2-1 for maintenance therapy in liver cancer
H Tsuda phase I clinical trial
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Oncol Rep. 1997; 4:1213- 1216
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Oncol Rep. 1997 Nov-Dec;4(6):1213-6
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Oncol Rep 4 (6):1213-6 (1997)
Oncology Reports
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KURUME UNIV,SCH MED,DEPT SURG,KURUME,FUKUOKA,JAPAN. KURUME UNIV,SCH MED,DEPT INTERNAL MED,KURUME,FUKUOKA,JAPAN. KURUME UNIV,SCH MED,DEPT RADIOL,KURUME,FUKUOKA,JAPAN
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[29] 1997
� � � � � � � � � � � � � � � �
PHENYLACETATE and PHENYLBUTYRATE as novel, nontoxic differentiation inducers
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DOI
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Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury 2
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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD USA
D D SAMID, W R WR Hudgins, … C E CE Myers
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[30] 5 – 6/1998
� � � � � � � � � � � � � � � �
Quick response of advanced cancer to chemoradiation therapy with antineoplastons
H Tsuda A10 and AS2-1 – I
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Oncol. Rep. 1998;5:597–600
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Oncol Rep. 1998 May-Jun;5 (3):597-600
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5 (3):597-600
Oncol Rep 5 (3):597-600 (1998)
Oncology Reports
Department of Anesthesiology, Kurume University, School of Medicine, Kurumeshi, Fukuokaken, Japan
� � � � � � � � � � � � � � � �
[31] 11-12/1998
� � � � � � � � � � � � � � � �
Antineoplaston treatment for advanced hepatocellular carcinoma
H Tsuda – A10 I – I
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Oncol Rep. 1998;5:1363-1367
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Oncol Rep. 1998 Nov-Dec;5 (6):1363-7
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Oncol Rep 5 (6):1363-7 (1998)
5 (6):1363-7
Oncology Reports, Spandidos Publications
Department of Radiology, Kumabe Hospital, Kurume University School of Medicine, Kurumeshi, Fukuokaken, Japan
� � � � � � � � � � � � � � � �
[32] 3/1999
� � � � � � � � � � � � � � � �
Phase II study of PHENYLACETATE in patients with recurrent MALIGNANT GLIOMA:
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J Clin Oncol. 1999 Mar;17(3):984-90
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(A10) – Potential utility of antineoplaston A-10 levels in breast cancer
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Cancer Lett 155:67-70, 2000
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Cancer Lett 155(1):67-70 (2000)
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DOI: 10.1016/S0304-3835(00)00408-0
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Cancer Letters, Elsevier Science
Department of Pharmacognosy, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

� � � � � � � � � � � � � � � �
[34] 8/31/2000
� � � � � � � � � � � � � � � �
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Cancer Lett 157: 2000
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Cancer Lett 157 (1):57-63 (2000)
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Cancer Lett. 2000 Aug.31;157(1):57-63
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Cancer Lett 157: 57-63, 2000
Cancer Letters – Elsevier
Cancer Letters, Elsevier Science
DOI: 10.1016/S0304-3835(00)00472-9
Department of Pharmacognosy, Faculty of Pharmacy, Mansoura University, Egypt

� � � � � � � � � � � � � � � �
[35] 12/2000
� � � � � � � � � � � � � � � �
(antineoplaston A10) – Novel piperidinedione analogs as inhibitors of breast cancer cell growth
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Arch Pharm (Weinheim), John Wiley & Sons, Inc.
Department of Medicinal Chemistry, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

� � � � � � � � � � � � � � � �
[36] 8/2001
� � � � � � � � � � � � � � � �
A phase Idose escalation and bioavailability study of oral sodium PHENYLBUTYRATE in patients with refractory solid tumor malignancies
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Clin Cancer Res 7(8):2292-300 (2001), PMID.11489804
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Clin Cancer Res. 2001 Aug;7(8):2292-300
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SAMID References: 2-3, 5-6, 15 and 22
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[37] 2002
� � � � � � � � � � � � � � � �
A novel strategy for remission induction and maintenance in cancer therapy
H Tsuda A10 and AS2-1
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Oncol Rep 2002;9:65–8
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Oncol. Rep. 2002;9:65-68
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Oncol Rep 9(1):65-8 (2002)
Oncology Reports, Spandidos Publications
Department of Anesthesiology, Kurume University, School of Medicine, Fukuoka-ken, Japan
� � � � � � � � � � � � � � � �
[38] 3 – 4/2003
� � � � � � � � � � � � � � � �
The preventive effect of antineoplaston AS2-1 on HCC recurrence
Hideaki H TSUDA Phase II Clinical Trial
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Oncol Rep. 2003 Mar-Apr;10(2):391-7
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Oncol Rep. 2003;10:391-397
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Spandidos Publications
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Oncology Reports 10: 391-397, 2003
Oncol Rep 10 (2):391-7 (2003)
Oncol Rep 2003;10:391–7
Department of Anesthesiology, Kurume Daiichi Social Insurance Hospital, Kushihara Kurumeshi, Fukuoka, Japan
� � � � � � � � � � � � � � � �
[39] 2003
� � � � � � � � � � � � � � � �
Long-term survival following treatment with antineoplastons for colon cancer with unresectable multiple liver metastases: report of a case
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Long-Term Survival Following Treatment with Antineoplastons for Colon Cancer with Unresectable Multiple Liver Metastases:
Report of a Case
Hideaki Tsuda A10 and AS2-1 – Phase II Clinical Trial
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Surg Today. 2003;33(6):448-53
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Surg Today 2003; 33:448–53
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Surg Today. 2003; 33:448-453
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Surgery Today, Springer
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DOI: 10.1007/s10595-002-2503-2
http://ci.nii.ac.jp/naid/10015483373
Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan
http://ci.nii.ac.jp/naid/10015483373
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� � � � � � � � � � � � � � � �
Antineoplaston induces G1 arrest by PKCα and MAPK pathway in SKBR-3 breast cancer cells
Hideaki H TSUDA Antineoplaston A10
http://www.ncbi.nlm.nih.gov/pubmed/16012735
Antineoplaston induces G1 arrest by PKCo and MAPK pathway in SKBR-3 breast cancer cells
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Oncology Reports, Spandidos Publications
Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan
� � � � � � � � � � � � � � � �
[42] 2006
� � � � � � � � � � � � � � � �
Inhibitory Effect of Antineoplaston A10 and AS2-1 on Human Hepatocellular Carcinoma
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Kurume Medical Journal
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� � � � � � � � � � � � � � � �
Preclinical studies of molecular-targeting diagnostic and therapeutic strategies against breast cancer
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Breast Cancer 15(1):73-8 (2008)
DOI: 10.1007/s12282-007-0015-y
http://link.springer.com/article/10.1007%2Fs12282-007-0015-y
Breast Cancer. 2008;15(1):73-8. doi: 10.1007/s12282-007-0015-y
http://www.springerlink.com/content/p724x34746l56v73
15(1):73-8
http://ci.nii.ac.jp/naid/10021288533
Breast Cancer: January 2008, Volume 15, Issue 1, pp 73-78
Department of Surgery, Kurume University, Fukuoka, Japan
Burzynski Reference: 12
Tsuda (Japan) Antineoplaston Reference: 13
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[44] 10/2010
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Antineoplaston A10 phenylacetyl glutamine (PG)
http://www.springerlink.com/content/tj0177485773007t
(S)-2-((S)-2-(4-(3-[18F]fluoropropyl)benzamido)-3-phenylpropanamido)pentanedioic acid labeled with 18F
http://link.springer.com/article/10.1007%2Fs10967-010-0633-2?LI=true
(S)-2-((S)-2-(4-(3-[18 F] fluoropropyl) benzamido)-3-phenylpropanamido) pentanedioic acid labeled with 18 F
http://www.springerlink.com/content/tj0177485773007t
Journal of Radioanalytical and Nuclear Chemistry, 2010, 286, 1, 135
http://link.springer.com/article/10.1007%2Fs10967-010-0633-2
October 2010, Volume 286, Issue 1, pp 135-140
http://link.springer.com/article/10.1007/s10967-010-0633-2/fulltext.html
DOI
10.1007/s10967-010-0633-2

http://onlinelibrary.wiley.com/doi/10.1021/js960120y/abstract
Burzynski References: 5. – 6.
http://www.springerlink.com/content/tj0177485773007t
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Burzynski: Oh, RATS!!!

After again showing how questionable the “research” of #ScienceBasedMedicine Dr. David H. “Orac” Gorski is:
https://stanislawrajmundburzynski.wordpress.com/2013/07/23/is-dr-david-h-orac-gorski-down-and-out-in-detroit-and-an-ethically-bankrupt-researcher-2/
and he is involved in the “War on Cancer,”(!!!) I decided to provide this more in-depth listing of Burzynski related scientific publications regarding animal, mice, and rat studies re: antineoplastons
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1983 – Burzynski SR, Hendry LB, Mohabbat MO, et al. Purification of structure determination, synthesis and animal toxicity studies of antineoplaston A10. In: Proceedings of the 13th International Congress of Chemotherapy. Vienna, Austria; 1983:17, PS. 12.4 11-4.
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1984 – Burzynski, S.R., Mohabbat MO, Burzynski B.
Animal toxicology studies on oral formulation of antineoplaston A10
Drugs Exptl Clin Res 1984;10:113-118
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1984 – Lee, S.S., Mohabbat, M.O., Burzynski, S.R.
Tissue culture and animal toxicity studies of antineoplaston A2
Drugs Exptl Clin Res 1984;10:607-610
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1985 – Lee, S.S., Mohabbat, M.O., Burzynski, S.R.
Tissue culture and acute animal toxicity studies of antineoplaston A2
Future Trends in Chemotherapy 1985;6:481-484
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1986 – Burzynski, S., Mohabbat. M., Lee, S.
Preclinical studies of antineoplaston AS2-1 in mice with oral administration
Drugs Exptl Clin Res 1986;132
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1986 – Burzynski, S. R., Mohabbat, M. O. , Le e, S. S. Pre clinical studies of antineoplaston AS2-1 and antineoplaston AS2-5
Drugs Exptl Clin Res 1986;12 (suppl1):11-16
http://www.ncbi.nlm.nih.gov/pubmed/3743376/
Drugs Exp Clin Res. 1986;12 Suppl 1:11-6.
http://www.ncbi.nlm.nih.gov/m/pubmed/3743376/
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1986 – Ashraf, AQ., Liau, M.C., Mohabbat, M.O., Burzynski, S.R.
Preclinical studies of antineoplaston A10 injections.
Drugs Exptl Clin Res 1986;12 (suppl 1):37-45.
http://www.ncbi.nlm.nih.gov/pubmed/3743379/
Drugs Exp Clin Res. 1986;12 Suppl 1:37-45.
http://www.ncbi.nlm.nih.gov/m/pubmed/3743379/
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1986 – Burzynski, S.R., Mohabbat M.O.
Chronic animal toxicity studies on antineoplaston A2.
Drugs Exptl Clin Res 1986;12 (suppl 1):73-75.
http://www.ncbi.nlm.nih.gov/pubmed/3743382/
Drugs Exp Clin Res. 1986;12 Suppl 1:73-5.
http://www.ncbi.nlm.nih.gov/m/pubmed/3743382/
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1987 – Lee, S.S., Mohabbat, M.O., Burzynski, SR
In vitro cancer growth inhibition and animal toxicity studies of antineoplaston A3
Drugs Exptl Clin Res 1987;13 (suppl1):13-16
http://www.ncbi.nlm.nih.gov/pubmed/3569011/
Drugs Exp Clin Res. 1987;13 Suppl 1:13-6.
http://www.ncbi.nlm.nih.gov/m/pubmed/3569011/
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1987 – Lee, S.S., Burzynski, S.R
Tissue culture and animal toxicity studies of antineoplaston A5
Drugs Exptl Clin Res 1987;13 (suppl 1):31-5.
http://www.ncbi.nlm.nih.gov/pubmed/3569013/
Drugs Exp Clin Res. 1987;13 Suppl 1:31-5.
http://www.ncbi.nlm.nih.gov/m/pubmed/3569013/
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1987 – Ashraf AQ, Liau MC, Kampalath BN, et al. Pharmacokinetic study of radioactive antineoplaston A10 following oral administration in rats. Drugs Exptl Clin Res. 1987;13(suppl 1):45-50.
http://www.ncbi.nlm.nih.gov/pubmed/3569015/
�
http://www.ncbi.nlm.nih.gov/m/pubmed/3569015/
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1988 – Ashraf, AQ., Kampalath, B.N., Burzynski, S.R
Pharmacokinetic analysis of antineoplaston A10 injections following intravenous administration in rats
Adv Exptl Clin Chemother 1988;6:33-39
http://www.encognitive.com/node/2449
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7/20/1988 – Chemopreventive effect of antineoplaston A-10 on urethane-induced pulmonary neoplasm in mice
http://www.ncbi.nlm.nih.gov/pubmed/3183462
Nihon Gan Chiryo Gakkai Shi. 1988 Jul.20; 23 (7):1560-5
http://www.ncbi.nlm.nih.gov/m/pubmed/3183462
23(7):1560-5 (1988)
Tsuda
N E
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1/20/1990 – A-10 Injection – The anticancer effect of antineoplaston A-10 on human breast cancer serially transplanted to athymic mice
http://www.ncbi.nlm.nih.gov/pubmed/2157780
Nihon Gan Chiryo Gakkai Shi. 1990 Jan 20;25(1):1-5
http://www.ncbi.nlm.nih.gov/m/pubmed/2157780
1st Department of Surgery, Kurume University School of Medicine
The Anticancer Effect of Antineoplaston A-10 on Human Breast Cancer Serially Transplanted to Athymic Mice, Journal of the Japan Society for Cancer Therapy 25(1):1-5 (1990)
Hashimoto K, Koga T, Shintomi Y, Tanaka M, Kakegawa T, Tsuda H, Hara H.
http://www.abstractboard.com/abstract/2157780/The-anticancer-effect-of-antineoplaston-A-10-on-human-breast-cancer-serially-transplanted-to-athymic.html
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1990 – Inhibitory effect of antineoplaston A-10 on breast cancer transplanted to athymic mice and human hepatocellular carcinoma cell lines. The members of Antineoplaston Study Group
Tsuda H (Japan) et al
http://www.ncbi.nlm.nih.gov/pubmed/2175003
Kurume Med J. 1990;37(2):97-104
http://www.ncbi.nlm.nih.gov/m/pubmed/2175003
Kurume Med J 37 (2):97-104 (1990)
http://www.jstage.jst.go.jp/article/kurumemedj1954/37/2/37_2_97/_article
Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/37/2/37_2_97/_article/references
Burzynski References: 1 – 8 and 11 – 14
http://www.jstage.jst.go.jp/article/kurumemedj1954/37/2/37_2_97/_pdf
The Kurume Medical Journal
http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.1992.tb01960.x/abstract
J-STAGE, Japan Science and Technology Information Aggregator, Electronic
http://ci.nii.ac.jp/naid/130000888719
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1991 – Inhibitory effect of orally administered antineoplaston A10 on the growth curve of human breast cancer transplanted to athymic mice
http://jglobal.jst.go.jp/public/20090422/200902015871267390
J Jpn Soc Cancer Ther 26:595-601, 1991
26:3:595-601:1991 03
Kurume Univ. School of Medicine
NISHIDA H, YOSHIDA H, KUBOTA H
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5/1992 – The inhibitory effect of the combination of antineoplaston A-10 injection with a small dose of cis-diamminedichloroplatinum on cell and tumor growth of human hepatocellular carcinoma
H TSUDA, et al (Japan)
http://www.ncbi.nlm.nih.gov/pubmed/1377669
The Inhibitory Effect of the Combination of Antineoplaston A-10 Injection with a Small Dose of cis-Diamminedichloroplatinum on Cell and Tumor Growth of Human Hepatocellular Carcinoma
http://www.ncbi.nlm.nih.gov/m/pubmed/1377669
Jpn J Cancer Res. 1992 May;83(5):527-31
http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.1992.tb01960.x/abstract
Jpn. J. Cancer Res. 83, 527-531
http://onlinelibrary.wiley.com/store/10.1111/j.1349-7006.1992.tb01960.x/asset/j.1349-7006.1992.tb01960.x.pdf?v=1&t=hd97ht7z&s=3481466c7830e5f8e2bb925a698de6f8155da747
Jpn J Cancer Res. 1992 May;83 (5):527-31
http://onlinelibrary.wiley.com/store/10.1111/j.1349-7006.1992.tb01960.x/asset/j.1349-7006.1992.tb01960.x.pdf;jsessionid=4ECD3F595A3971B5AB87763862867844.d03t02?v=1&t=hbmd55gj&s=a14b626a37db3ecd558109cee30dfe26c71827763862867844
Jpn J Cancer Res 83 (5):527-31 (1992)
http://onlinelibrary.wiley.com/store/10.1111/j.1349-7006.1992.tb01960.x/asset/j.1349-7006.1992.tb01960.x.pdf?v=1&t=hkfile3i&s=2756f110cf2202084cfc90a3715d8f1f9df7774c
Department of Anesthesiology, Kurume University, School of Medicine, Fukuoka-ken
http://onlinelibrary.wiley.com/store/10.1111/j.1349-7006.1992.tb01960.x/asset/j.1349-7006.1992.tb01960.x.pdf?v=1&t=hdcl29bl&s=dd78f02b92e0f5544c136e7b897a7d65bcf5dc71&systemMessage=Wiley+Online+Library+will+be+disrupted+on+23+February+from+10%3A00-12%3A00+BST+%2805%3A00-07%3A00+EDT%29+for+essential+maintenance
Article first published online: 26 AUG 2005
DOI: 10.1111/j.1349-7006.1992.tb01960.x
Japan Journal Cancer Research
Cancer Science, Wiley Online Library
Volume 83, Issue 5, pages 527–531, May 1992
Burzynski References: 1, 4 – 7 and 9
http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.1992.tb01960.x/references
Nishida (Japan) A-10 Reference: 2
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11/15/1995 – Sodium PHENYLACETATE Induces Growth Inhibition and Bcl-2 Down-Regulation and Apoptosis in MCF7ras Cells in Vitro and in nude mice
http://cancerres.aacrjournals.org/content/55/22/5156.abstract?sid=29b3d08f-4e59-473c-a804-10c68ed99112
Cancer Res. 1995 Nov 15;55(22):5156-60.
http://cancerres.aacrjournals.org/content/55/22/5156.full.pdf
Institut d’Oncologie Moléculaire et Cellulaire Humaine, Bobigny, France.
http://m.cancerres.aacrjournals.org/content/55/22/5156.full.pdf#page=1
References:
http://m.cancerres.aacrjournals.org/content/55/22/5156
1. SAMID, D., Shac, S., and Sherman, L. T. Phenylacetate: a novel nontoxic inducer of tumor cell differentiation. Cancer Res., 52: 1988-1992, 1992
http://www.naderlibrary.com/burzynski.screen3.htm
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9/2001 – Sodium PHENYLACETATE enhances the inhibitory effect of dextran derivative on breast cancer cell growth in vitro and in nude mice
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2375080
Br J Cancer. 2001 September; 85(6): 917–923.
doi: 10.1054/bjoc.2001.1993
PMCID: PMC2375080
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3/2005 Effects of antineoplaston AS2-1 against post-operative lung metastasis in orthotopically implanted colon cancer in nude rat
Hideaki TSUDA
http://www.ncbi.nlm.nih.gov/pubmed/15706406
Oncol Rep. 2005 Mar; 13 (3):389-95
http://www.ncbi.nlm.nih.gov/m/pubmed/15706406
Oncol Rep 13 (3): 389-95 (2005)
http://www.spandidos-publications.com/or/13/3/389
Oncology Reports, 3/2005, Volume 13 Number 3
Pages: 389-395 Oncology Reports, Spandidos Publications
Department of Surgery, Kurume University School of Medicine, Kurume City, Fukuoka, Japan
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7 – 8/27/2007 Induction of apoptosis in human hepatocellular carcinoma cells by synthetic antineoplaston A10
http://www.ncbi.nlm.nih.gov/pubmed/17695534
Induction of Apoptosis in Human Hepatocellular Carcinoma Cells by Synthetic Antineoplaston A10
http://www.ncbi.nlm.nih.gov/m/pubmed/17695534
Anticancer Res. 2007 Jul-Aug;27(4B):2427-31
http://ar.iiarjournals.org/content/27/4B/2427.short
Anticancer Res 27(4B):2427-31 (2007)
http://ar.iiarjournals.org/content/27/4B/2427.long
Anticancer Res. 7 – 8/2007; 27(4B):2427-31
http://ar.iiarjournals.org/content/27/4B/2427.full.pdf
Anticancer Research, Vol. 27, No. 4B, 2007, pp. 2427-2431
http://www.iiar-anticancer.org/main.php?pid=3398&id=2&ch=52&gch=&volume=27&issue=4B&show=details&page=2
Anticancer Research
HighWire Press
School of Pharmaceutical Sciences, Shandong University, Jinan, Japan
International Journal of Cancer Treatment
Burzynski References: 1, 3, 5, 13 and 15
Badria (Egypt) A-10 References: 2 and 20
Wang A10 Reference: 4
�
References:
�
Adam L, Crépin M, Savin C, Israël L. Sodium phenylacetate induces growth inhibition and Bcl-2 down-regulation and apoptosis in MCF7ras cells in vitro and in nude mice. Cancer Res. 1995 Nov 15;55(22):5156–5160.
�
Shack S, Miller A, Liu L, Prasanna P, Thibault A, SAMID D. Vulnerability of multidrug-resistant tumor cells to the aromatic fatty acids phenylacetate and phenylbutyrate. Clin Cancer Res. 1996 May;2(5):865–872.
�
SAMID D, Shack S, Myers CE. Selective growth arrest and phenotypic reversion of prostate cancer cells in vitro by nontoxic pharmacological concentrations of phenylacetate. J Clin Invest. 1993 May;91(5):2288–2295.
�
SAMID D, Hudgins WR, Shack S, Liu L, Prasanna P, Myers CE. Phenylacetate and
Phenylbutyrate
as novel, nontoxic differentiation inducers. Adv Exp Med Biol. 1997;400A:501–505.
�
SAMID D, Wells M, Greene ME, Shen W, Palmer CN, Thibault A. Peroxisome proliferator-activated receptor gamma as a novel target in cancer therapy: binding and activation by an aromatic fatty acid with clinical antitumor activity. Clin Cancer Res. 2000 Mar;6(3):933–941.
�
Thibault A, Cooper MR, Figg WD, Venzon DJ, Sartor AO, Tompkins AC, Weinberger MS, Headlee DJ, McCall NA, SAMID D, et al. A phase I and pharmacokinetic study of intravenous phenylacetate
in patients with cancer. Cancer Res. 1994 Apr 1;54(7):1690–1694.
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3/2005 – Effects of antineoplaston AS2-1 against post-operative lung metastasis in orthotopically implanted colon cancer in nude rat.
http://www.ncbi.nlm.nih.gov/pubmed/15706406
Matono K, Ogata Y, Tsuda H, Araki Y, Shirouzu K.
http://www.ncbi.nlm.nih.gov/m/pubmed/15706406
Oncol Rep. 2005 Mar;13(3):389-95
http://www.spandidos-publications.com/or/13/3/389
Oncology Reports
March 2005
Volume 13 Number 3
Department of Surgery, Kurume University School of Medicine, Kurume City, Fukuoka, Japan
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PUBLICATIONS BY STANISLAW RAJMUND BURZYNSKI AND ASSOCIATES
http://www.cancermed.com
——————————————————————
(former web-site screenshots)
http://www.circare.org/info/bri/burzynski_fdauntitled_promo_2012.pdf
——————————————————————
Stanislaw Rajmund Burzynski Publications:

https://stanislawrajmundburzynski.wordpress.com/2013/03/16/stanislaw-rajmund-burzynski-publications/

Phenylbutyrate (PB)

Dvorit D. SAMID learned about PHENYLBUTYRATE (PB) from Burzynski
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Antineoplastons AS2-1 and AS2-5 are DERIVED FROM A10
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Phenylacetylglutaminate (PAG or PG) and Phenylacetate (PN) are metabolites of PHENYLBUTYRATE (PB) and are constituents of antineoplaston AS2-1
� � � � � � � � � � � � � � � � �
National Cancer Institute (NCI)
at the National Institutes of Health (NIH) Antineoplastons
General Information:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page2
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Sodium PHENYLBUTYRATE (PB)
Year – Pubmed (110 entries)
1958 1st entry
1995 1st clinical trial
2001 Phase 1
2009 Phase 2
2012 Phase 3
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PHENYLBUTYRATE (PB)
19 (PHENYLBUTYRATE (PB + SAMID)
http://www.ncbi.nlm.nih.gov/m/pubmed/?term=Phenylbutyrate+Samid
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IV. Aetna considers SODIUM PHENYLBUTYRATE medically necessary for the treatment of acute promyelocytic leukemia and malignant glioma
http://www.aetna.com/cpb/medical/data/200_299/0240.html
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The FDA has approved SODIUM PHENYLBUTYRATE as a treatment to remove ammonia from the bloodstream in individuals with urea cycle disorders
� � � � � � � � � � � � � � � � �
SODIUM PHENYLBUTYRATE was given an orphan drug designation by the FDA for use as an adjunct to surgery, radiation therapy, and chemotherapy for treatment of individuals with primary or recurrent malignant glioma
http://www.anthem.com/medicalpolicies/policies/mp_pw_a050524.htm
� � � � � � � � � � � � � � � � �
Cumulative List of all Products that have received Orphan Designation: Total active designations: 2002 Effecive: (sic – Effective) 5/5/2009
http://www.fda.gov/downloads/forindustry/developingproductsforrarediseasesconditions/howtoapplyfororphanproductdesignation/ucm162066.xls
PHENYLBUTYRATE (PB) and SODIUM PHENYLBUTYRATE are listed alphabetically in the lower 1/4th of this document
� � � � � � � � � � � � � � � � �
Pubmed 110 entries
Sodium PHENYLBUTYRATE
“Sodium PHENYLBUTYRATE (aka PB) …”
� � � � � � � � � � � � � � � � �
If they’re going to include it in a phase 3 study, than it’s “fair game”
http://www.ncbi.nlm.nih.gov/m/pubmed/22961727
Hepatology
Early View (Online Version of Record published before inclusion in an issue)

Article first published online: 3 JAN 2013

DOI: 10.1002/hep.26058
http://onlinelibrary.wiley.com/doi/10.1002/hep.26058/abstract;jsessionid=34AE3D61DEEF5356F147DE74B26759F9.d01t03
Article:
http://onlinelibrary.wiley.com/doi/10.1002/hep.26058/full
References:
http://onlinelibrary.wiley.com/doi/10.1002/hep.26058/references
Cited by:
http://onlinelibrary.wiley.com/doi/10.1002/hep.26058/citedby

Hepatology. 2012 Sep 7. doi: 10.1002/hep.26058. [Epub ahead of print]
� � � � � � � � � � � � � � � � �
1990 – Treatment of hormonally refractory cancer of the prostate with antineoplaston AS2-1.
http://www.ncbi.nlm.nih.gov/m/pubmed/2152694/
BURZYNSKI, S. R., Kubove E., Burzynski, B.
Drugs Exp. Clin. Res., 16: 361-369, 1990.
� � � � � � � � � � � � � � � � �
1991 – Selective growth arrest and phenotypic reversion of prostate cancer cells in vitro by nontoxic pharmacological concentrations of phenylacetate.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC288233/
SAMID D., Shack S., Myers C.
J. Clin. Investig., 91: 2288-2295, 1991.
J Clin Invest. 1993 May; 91(5): 2288–2295.
doi: 10.1172/JCI116457
PMCID: PMC288233

References:

SAMID D, Flessate DM, Friedman RM. Interferon-induced revertants of ras-transformed cells:

resistance to transformation by specific oncogenes and retransformation by 5-azacytidine. Mol Cell Biol. 1987 Jun;7(6):2196–2200.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC365343/

http://www.ncbi.nlm.nih.gov/m/pubmed/2439904/
SAMID D, Shack S, Sherman LT. Phenylacetate:

a novel nontoxic inducer of tumor cell differentiation. Cancer Res. 1992 Apr 1;52(7):1988–1992.
http://www.ncbi.nlm.nih.gov/m/pubmed/1372534/

http://cancerres.aacrjournals.org/content/52/7/1988
SAMID D, Yeh A, Prasanna P. Induction of erythroid differentiation and fetal hemoglobin production in human leukemic cells treated with phenylacetate. Blood. 1992 Sep 15;80(6):1576–1581.
http://www.ncbi.nlm.nih.gov/m/pubmed/1381630/
Dover GJ, Brusilow S, SAMID D. Increased fetal hemoglobin in patients receiving sodium 4-PHENYLBUTYRATE. N Engl J Med. 1992 Aug 20;327(8):569–570.
http://www.ncbi.nlm.nih.gov/m/pubmed/1378939/
� � � � � � � � � � � � � � � � �
4/1/1992Phenylacetate:

A novel non-toxic inducer of tumor cell differentiation
http://www.ncbi.nlm.nih.gov/m/pubmed/1372534/
SAMID D, Shack S , Sherman L T
http://cancerres.aacrjournals.org/content/52/7/1988
Cancer Res 52:1988,1992
Cancer Res. 1992 Apr 1;52(7):1988-92.
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland.
↵1 Supported by Elan Pharmaceutical Corporation Grant G174ED.
Reference: 12 (SAMID, D.)
� � � � � � � � � � � � � � � � �
8/20/1992 – Increased fetal hemoglobin in patients receiving sodium 4-PHENYLBUTYRATE.
http://www.ncbi.nlm.nih.gov/m/pubmed/1378939/
Dover GJ, Brusilow S, SAMID D
N Engl J Med 327569, 1992
N Engl J Med. 1992 Aug 20;327(8):569–570.
� � � � � � � � � � � � � � � � �
9/15/1992 – Induction of erythroid differentiation and fetal hemoglobin production in human leukemic cells treated with phenylacetate.
http://www.ncbi.nlm.nih.gov/m/pubmed/1381630/
SAMID D, Yeh A, Prasanna P
Blood 80:1576, 1992
Blood. 1992 Sep 15;80(6):1576–1581.
Blood. 1992 Sep 15;80(6):1576-81.
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD.

References:

15. SAMID D, Shack S, Ti-Sherman L Phenylacetate-A novel nontoxic inducer of tumor cell differentiation. Cancer Res 52:1988, 1992
http://www.ncbi.nlm.nih.gov/m/pubmed/1372534/
Cancer Res. 1992 Apr 1;52(7):1988-92.
http://cancerres.aacrjournals.org/content/52/7/1988
20. SAMID D, Flessate DM, Friedman RM: Interferon-induced revertants of ras-transformed cells:

Resistance to transformation by specific oncogenes and retransformation by 5-azacytidine. Mol Cell Biol7:2196,1987
http://www.ncbi.nlm.nih.gov/m/pubmed/2439904/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC365343/
21. Rimoldi D, Srikantan V, Wilson VL, Bassin RH,SAMID D: Increased sensitivity of nontumorigenic fibroblasts expressing ras or myconcogenes to malignant transformation induced by 5-aza-2‘- deoxycytidine. Cancer Res 51:324,1991
http://www.ncbi.nlm.nih.gov/m/pubmed/1703037/

http://m.cancerres.aacrjournals.org/content/51/1/324.abstract

http://m.cancerres.aacrjournals.org/content/51/1/324.full.pdf

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34. Dover GJ, Brusilow S, SAMID D: Increased fetal hemoglobin in patients receiving sodium 4-PHENYLBUTYRATE. N Engl J Med 327569,1992
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� � � � � � � � � � � � � � � � �
5/1993 – Selective growth arrest and phenotypic reversion of prostate cancer cells in vitro by nontoxic, pharmacological concentrations of phenylacetate.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC288233/
SAMID D, Shack S, Myers CE:
J Clin Invest 91:2288, 1993
J Clin Invest. 1993 May; 91(5): 2288–2295.
doi: 10.1172/JCI116457
PMCID: PMC288233

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N Engl J Med 327569,1992
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33. D. SAMID
� � � � � � � � � � � � � � � � �
10/1/1993 – Enhanced fetal
hemoglobin production by phenylacetate and 4-PHENYLBUTYRATE in erythroid precursors derived from normal blood donors and patients with sickle cell anemia and P-thalassemia
http://www.ncbi.nlm.nih.gov/m/pubmed/7691251/
Fibach E, Prasanna P, Rodgers GP, SAMID D:
Blood 822203, 1993
Blood. 1993 Oct 1;82(7):2203-9.
Department of Hematology, Hadassah University Hospital, Jerusalem, Israel.

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19. SAMID D, Yeh A, Prasanna P Induction of erythroid differentiation and fetal hemoglobin production in human leukemic cells treated with phenylacetate. Blood 80:1576, 1992
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� � � � � � � � � � � � � � � � �
4/1/1994 Phase 1
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Clinical Pharmacology Branch, National Cancer Institute, NIH, Bethesda, Maryland
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J Clin Invest 91:2288, 1993
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11. SAMID. D., Ram, Z., Hudgins, W. R., Shack, S., Liu, L., Walbridge, S., Oldfield, E. H., Myers, C. E. Selective activity of phenylacetate against malignant gliomas:

resemblance to fetal brain damage in phenylketonuria. Cancer Res., 54: 891-895, 1994.
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Phenylacetate:

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16. Fibach E, Prasanna P, Rodgers GP, SAMID D:

Enhanced fetal
hemoglobin production by phenylacetate and 4-PHENYLBUTYRATE in erythroid precursors derived from normal blood donors and patients with sickle cell anemia and P-thalassemia
http://www.ncbi.nlm.nih.gov/m/pubmed/7691251/
Blood 822203, 1993
Blood. 1993 Oct 1;82(7):2203-9.
Department of Hematology, Hadassah University Hospital, Jerusalem, Israel.

28. Dover GJ, Brusilow SW, SAMID D:

Increased fetal hemoglobin in patients receiving sodium 4-PHENYLBUTYRATE
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N Engl JMed 327:569, 1992 (letter)
N Engl J Med. 1992 Aug 20;327(8):569-70.
� � � � � � � � � � � � � � � � �
7/1995 – Transcriptional upregulation of TGF-α by phenylacetate and PHENYLBUTYRATE is associated with differentiation of human melanoma cells.
http://www.ncbi.nlm.nih.gov/m/pubmed/7578983/
Liu L., Hudgins W. R., Miller A. C., Chen L. C., SAMID D.
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Cytokine, 7: 449-456, 1995.
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a Clinical Pharmacology Branch, National Cancer Institute, Armed Forces of Radiation Research Institute, Bethesda, Maryland, USA
b Radiation Biochemistry Department, Armed Forces of Radiation Research Institute, Bethesda, Maryland, USA
http://dx.doi.org/10.1006/cyto.1995.0061
� � � � � � � � � � � � � � � � �
8/23/1996 – Activation of the human peroxisome proliferator-activated receptor by the antitumor agent phenylacetate and its analogues.
http://www.ncbi.nlm.nih.gov/m/pubmed/8759039/
Pineau T., Hudgins W. R., Liu L., Chen L. C., Sher T., Gonzalez F. J., SAMID D.
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Biochem. Pharmacol., 52: 659-667, 1996.
Biochemical Pharmacology
Volume 52, Issue 4, 23 August 1996, Pages 659–667
Biochem Pharmacol. 1996 Aug 23;52(4):659-67.
∗ Laboratory of Molecular Carcinogenesis U.S.A.
‡ Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD U.S.A.
§ Experimental Therapeutics Program, University of Virginia Cancer Center, Charlottesville, VA, U.S.A.
http://dx.doi.org/10.1016/0006-2952(96)00340-1
This work was supported, in part, by funds from the Elan Pharmaceutical Research Corporation through a Cooperative Research and Development Agreement (CACR-0139).
� � � � � � � � � � � � � � � � �
9/1996 – The differentiating agent phenylacetate increases prostate-specific antigen production by prostate cancer cells.
http://www.ncbi.nlm.nih.gov/m/pubmed/8827086/
Walls R., Thibault A., Liu L., Wood C., Kozlowski J. M., Figg W. D., Sampson M. L., Elin R. J., SAMID D.
Prostate, 29: 177-182, 1996.
Prostate. 1996 Sep;29(3):177-82.
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland, USA.
� � � � � � � � � � � � � � � � �
10/25/1996 – Transcriptional upregulation of γ globin by PHENYLBUTYRATE and analogous aromatic fatty acids.
http://www.ncbi.nlm.nih.gov/m/pubmed/8937430/
Hudgins W. R., Fibach E., Safaya S., Rieder R. F., Miller A. C., SAMID D.
http://www.sciencedirect.com/science/article/pii/0006295296004765
Biochem. Pharmacol., 52: 1227-1233, 1996.
Biochem Pharmacol. 1996 Oct 25;52(8):1227-33.
Biochemical Pharmacology
Volume 52, Issue 8, 25 October 1996, Pages 1227–1233
a Clinical Pharmacology Branch, National Cancer Institute, and Laboratory of Chemical Biology, National Institute of Diabetes, Digestive Diseases and Kidney Diseases, National Institutes Of Health, Bethesda, MD, U.S.A.
b Department of Hematology, Hadassah University Hospital, Jerusalem, Israel
c Department of Medicine, State University of New York Health Science Center, Brooklyn, NY, U.S.A.
d Radiation Biochemistry Department, Armed Forces Radiation Research Institute, Bethesda, MD, U.S.A.
e University of Virginia Cancer Center, Charlottesville, VA, U.S.A.
http://dx.doi.org/10.1016/0006-2952(96)00476-5
☆
This work was supported by funds from the Elan Pharmaceutical Research Corp. and from the Israeli Science Foundation, administered by the Israel Academy of Sciences and Humanities.
� � � � � � � � � � � � � � � � �
1997 – The nuclear receptors PPARS as novel targets in differentiation therapy: activation by phenylacetate and PHENYLBUTYRATE .
SAMID D., Wells M., Kulkarni M., Lei L., Thibault A.
Anticancer Res., 17: 3927-3928, 1997.
� � � � � � � � � � � � � � � � �
8/2001 – A phase Idose escalation and bioavailability study of oral sodium PHENYLBUTYRATE in patients with refractory solid tumor malignancies
http://www.ncbi.nlm.nih.gov/m/pubmed/11489804
J Gilbert, S D Baker, … M A Carducci
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Clin Cancer Res 7(8):2292-300 (2001), PMID.11489804

Clin Cancer Res. 2001 Aug;7(8):2292-300

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http://www.sciencedirect.com/science/article/pii/0006295296004765
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http://www.sciencedirect.com/science/article/pii/0006295296003401
15. ↵ Walls R., Thibault A., Liu L., Wood C., Kozlowski J. M., Figg W. D., Sampson M. L., Elin R. J., SAMID D. The differentiating agent phenylacetate increases prostate-specific antigen production by prostate cancer cells. Prostate, 29: 177-182, 1996.
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� � � � � � � � � � � � � � � � �
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http://www.sciencedirect.com/science/article/pii/S1043466685700610
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http://www.sciencedirect.com/science/article/pii/0006295296004765
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http://www.sciencedirect.com/science/article/pii/0006295296003401
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� � � � � � � � � � � � � � � � �
4/2005 – Oral sodium PHENYLBUTYRATE in patients with recurrent malignant gliomas:

A dose escalation and pharmacologic study

Neuro-oncol. 2005 April; 7(2): 177–182 PMCID: PMC1871887

PDF:
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Mayo Clin Proc. 1999;74:137–145

12. Gore SD, SAMID D, Weng LJ

Impact of the putative differentiating agents sodium PHENYLBUTYRATE and sodium phenylacetate on proliferation, differentiation, and apoptosis of primary neoplastic myeloid cells

Clin Cancer Res. 1997a;3:1755–1762

17. Hudgins WR, Pineau T, Sher T, Gonzales FJ, Myers CE, SAMID D

Anticancer activity of phenylacetate and related aromatic fatty acids:

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J Clin Invest. 1993;91:2288–2295

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Selective activity of phenylacetate against malignant gliomas:

Resemblance to fetal brain damage in phenylketonuria

Cancer Res. 1994;54:891–895

21. Sidell N, Wada R, Han G, Chang B, Shack S, Moore T, SAMID D

Phenylacetate synergizes with retinoic acid in inducing the differentiation of human neuroblastoma cells

Int J Cancer. 1995;60:507–514
� � � � � � � � � � � � � � � � �
4/2005 – Oral sodium PHENYLBUTYRATE in patients with recurrent malignant gliomas:

A dose escalation and pharmacologic study

Neuro-oncol. 2005 April; 7(2): 177–182 PMCID: PMC1871887

PDF:
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http://www.ncbi.nlm.nih.gov/m/pubmed/9815560/

http://m.clincancerres.aacrjournals.org/content/3/10/1755.abstract

http://m.clincancerres.aacrjournals.org/content/3/10/1755.full.pdf

http://clincancerres.aacrjournals.org/content/3/10/1755
17. Hudgins WR, Pineau T, Sher T, Gonzales FJ, Myers CE, SAMID D

Anticancer activity of phenylacetate and related aromatic fatty acids:

Correlation with lipophilicity and capacity to activate nuclear receptor

Proc Am Assoc Can Res. 1994;35:391. (abstract 2332)

19. SAMID D, Shack S, Myers CE

Selective growth arrest and phenotypic reversion of prostate cancer cells in vitro by nontoxic pharmacological concentrations of phenylacetate

J Clin Invest. 1993;91:2288–2295
http://www.ncbi.nlm.nih.gov/m/pubmed/8486788/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC288233/

http://m.jci.org/articles/view/116457
20. SAMID D, Ram Z, Hudgins WR, Shack S, Liu L, Walbridge S, Oldfield EH, Myers CE

Selective activity of phenylacetate against malignant gliomas:

Resemblance to fetal brain damage in phenylketonuria

Cancer Res. 1994;54:891–895
http://www.ncbi.nlm.nih.gov/m/pubmed/8313377/

http://cancerres.aacrjournals.org/content/54/4/891
21. Sidell N, Wada R, Han G, Chang B, Shack S, Moore T, SAMID D

Phenylacetate synergizes with retinoic acid in inducing the differentiation of human neuroblastoma cells

Int J Cancer. 1995;60:507–514
http://www.ncbi.nlm.nih.gov/m/pubmed/7829265/
� � � � � � � � � � � � � � � � �
4/2007Phase I dose escalation clinical trial of PHENYLBUTYRATE sodium administered twice daily to patients with advanced solid tumors
Luis H LH Camacho, Jon J Olson, … Mark G MG Malkin
Invest New Drugs 25(2):131-8 (2007), PMID.17053987

Investigational New Drugs
April 2007, Volume 25, Issue 2, pp 131-138
http://www.ncbi.nlm.nih.gov/m/pubmed/17053987

http://link.springer.com/article/10.1007%2Fs10637-006-9017-4
References:

4. SAMID D, Shack S, Sherman LT

(1992)

Phenylacetate:

a novel nontoxic inducer of tumor cell differentiation

Cancer Res 52(7):1988–1992
http://www.ncbi.nlm.nih.gov/m/pubmed/1372534/
Cancer Res 52:1988,1992
Cancer Res. 1992 Apr 1;52(7):1988-92.
http://cancerres.aacrjournals.org/content/52/7/1988
5. DiGiuseppe JA, Weng LJ, Yu KH, Fu S, Kastan MB, SAMID D, et al

(1999)

PHENYLBUTYRATE-induced G1 arrest and apoptosis in myeloid leukemia cells:

structure-function analysis

Leukemia 13(8):1243–1253
http://www.ncbi.nlm.nih.gov/m/pubmed/10450753/
7. SAMID D, Hudgins WR, Shack S, Liu L, Prasanna P, Myers CE

(1997)

Phenylacetate and PHENYLBUTYRATE as novel, nontoxic differentiation inducers

Adv Exp Med Biol 400A:501–505
http://www.ncbi.nlm.nih.gov/m/pubmed/9547596/
20. Boudoulas S, Lush RM, McCall NA, SAMID D, Reed E, Figg WD

(1996)

Plasma protein binding of phenylacetate and PHENYLBUTYRATE, two novel antineoplastic agents

Ther Drug Monit 18(6):714–720
http://www.ncbi.nlm.nih.gov/m/pubmed/8946671/
24. Thibault A, SAMID D, Cooper MR, Figg WD, Tompkins AC, Patronas N, et al

(1995)

Phase I study of phenylacetate administered twice daily to patients with cancer

Cancer 75(12):2932–2938
http://www.ncbi.nlm.nih.gov/m/pubmed/7773944/
30. Stockhammer G, Manley GT, Johnson R, Rosenblum MK, SAMID D, Lieberman FS

(1995)

Inhibition of proliferation and induction of differentiation in medulloblastoma- and astrocytoma-derived cell lines with phenylacetate

J Neurosurg 83(4):672–681
http://www.ncbi.nlm.nih.gov/m/pubmed/7674018/
32. Ram Z, SAMID D, Walbridge S, Oshiro EM, Viola JJ, Tao-Cheng JH, et al

(1994)

Growth inhibition, tumor maturation, and extended survival in experimental brain tumors in rats treated with phenylacetate

Cancer Res 54(11):2923–2927
http://www.ncbi.nlm.nih.gov/m/pubmed/8187079/

http://m.cancerres.aacrjournals.org/content/54/11/2923.full.pdf

http://m.cancerres.aacrjournals.org/content/54/11/2923.abstract

http://cancerres.aacrjournals.org/content/54/11/2923
33. SAMID D, Yeh TJ, Shack S

(1991)

Interferon in combination with antitumourigenic phenyl derivatives: potentiation of IFN alpha activity in-vitro

Br J Haematol 79(Suppl 1):81–83
http://www.ncbi.nlm.nih.gov/m/pubmed/1931716/
34. Gorospe M, Shack S, Guyton KZ, SAMID D, Holbrook NJ

(1996)

Up-regulation and functional role of p21Waf1/Cip1 during growth arrest of human breast carcinoma MCF-7 cells by phenylacetate

Cell Growth Differ 7(12):1609–1615
http://www.ncbi.nlm.nih.gov/m/pubmed/8959328/
35. Bar-Ner M, Thibault A, Tsokos M, Magrath IT, SAMID D

(1999)

PHENYLBUTYRATE induces cell differentiation and modulates Epstein-Barr virus gene expression in Burkitt’s lymphoma cells

Clin Cancer Res 5(6):1509–1516
http://www.ncbi.nlm.nih.gov/m/pubmed/10389940/

http://m.clincancerres.aacrjournals.org/content/5/6/1509.abstract

http://m.clincancerres.aacrjournals.org/content/5/6/1509.long

http://clincancerres.aacrjournals.org/content/5/6/1509
36. Shack S, Miller A, Liu L, Prasanna P, Thibault A, SAMID D

(1996)

Vulnerability of multidrug-resistant tumor cells to the aromatic fatty acids phenylacetate and PHENYLBUTYRATE

Clin Cancer Res 2(5):865–872
http://www.ncbi.nlm.nih.gov/m/pubmed/9816242/

http://m.clincancerres.aacrjournals.org/content/2/5/865.abstract

http://m.clincancerres.aacrjournals.org/content/2/5/865.full.pdf

http://clincancerres.aacrjournals.org/content/2/5/865
37. SAMID D, Yeh A, Prasanna P

(1992)

Induction of erythroid differentiation and fetal hemoglobin production in human leukemic cells treated with phenylacetate

Blood 80(6):1576–1581
http://www.ncbi.nlm.nih.gov/m/pubmed/1381630/

http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.abstract

http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.full.pdf
38. Fibach E, Prasanna P, Rodgers GP, SAMID D

(1993)

Enhanced fetal hemoglobin production by phenylacetate and 4-PHENYLBUTYRATE in erythroid precursors derived from normal donors and patients with sickle cell anemia and beta-thalassemia

Blood 82(7):2203–2209
http://www.ncbi.nlm.nih.gov/m/pubmed/7691251/

http://m.bloodjournal.hematologylibrary.org/content/82/7/2203.abstract

http://m.bloodjournal.hematologylibrary.org/content/82/7/2203.full.pdf
� � � � � � � � � � � � � � � � �
4/2009Phase 2 study of sodium PHENYLBUTYRATE in ALS.
Merit E Cudkowicz, Patricia L Andres, … THE NORTHEAST ALS AND THE NATIONAL VA ALS RESEARCH CONSORTIUMS
Amyotroph Lateral Scler 10(2):99-106 (2009), PMID.18688762
Amyotroph Lateral Scler. 2009 Apr;10(2):99-106. doi: 10.1080/17482960802320487
http://www.ncbi.nlm.nih.gov/m/pubmed/18688762

http://informahealthcare.com/doi/pdf/10.1080/17482960802320487?noFrame=true

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1871887
� � � � � � � � � � � � � � � � �
10/1/2009 – A Phase I Dose-Finding Study of 5-Azacytidine in Combination with Sodium PHENYBUTYRATE in Patients with Refractory Solid Tumors
J Lin, J Gilbert, … M A Carducci
Clin Cancer Res 15(19):6241-6249 (2009), PMID.19789320, PMCID PMC2845396
Clin Cancer Res. 2009 Oct 1;15(19):6241-9. doi: 10.1158/1078-0432.CCR-09-0567. Epub 2009 Sep 29
http://www.ncbi.nlm.nih.gov/m/pubmed/19789320

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845396
References:

24. Robertson KD, Hayward SD, Ling PD, SAMID D, Ambinder RF

Transcriptional activation of the Epstein-Barr virus latency C promoter after 5-azacytidine treatment:

evidence that demethylation at a single CpG site is crucial

Mol Cell Biol. 1995;15:6150–9
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC230866/
� � � � � � � � � � � � � � � � �
7/2010Phase 2 comparison of a novel ammonia scavenging agent with sodium PHENYLBUTYRATE in patients with urea cycle disorders:

Safety, pharmacokinetics and ammonia control
http://www.ncbi.nlm.nih.gov/m/pubmed/20382058/
Brendan Lee, William Rhead, … Susan A Berry
Mol Genet Metab 100(3):8 (2010), PMID.20382058, PMCID PMC2905228
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905228/
Mol Genet Metab. 2010 Jul;100(3):221-8. doi: 10.1016/j.ymgme.2010.03.014. Epub 2010 Mar 23.
Baylor College of Medicine, Houston, TX, USA.

http://www.sciencedirect.com/science/article/pii/S1096719210001058
a Baylor College of Medicine, Houston, TX, United States
b Howard Hughes Medical Institute, TX, United States
c Pediatrics, Medical College of Wisconsin, Milwaukee, WI, United States
d Mount Sinai School of Medicine, New York, NY, United States
e Hyperion Therapeutics, Inc., South San Francisco, CA, United States
f Pharsight Corp., Montreal, Quebec, Canada
g Chiltern, Wilmington, NC, United States
h Division of Genetics and Metabolism, University of Minnesota, Minneapolis, MN, United States
http://dx.doi.org/10.1016/j.ymgme.2010.03.014

Antineoplastons: Phenylacetylglutaminate (PG or PAG), Phenylacetate (PN), and Phenylbutyrate (PB)

PHENYLACETYLGLUTAMINATE (PAG or PG) and PHENYLACETATE (PN) are metabolites of PHENYLBUTYRATE (PB) and are constituents of antineoplaston AS2-1
� � � � � � � � � � � � � � � �
Antineoplastons AS2-1 and AS2-5 are DERIVED FROM A10
� � � � � � � � � � � � � � � �
AS2-1 = 4:1 mixture of PHENYLACETIC ACID (PA) and PHENYLACETYLGLUTAMINE (PAG or PG)
� � � � � � � � � � � � � � � �
Antineoplaston AS2-5 = PHENYLACETYLGLUTAMINE (PAG or PG)
� � � � � � � � � � � � � � � �
National Cancer Institute (NCI) at the National Institutes of Health (NIH)
Antineoplastons
General Information: http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page2
� � � � � � � � � � � � � � � �
http://www.burzynskiclinic.com/scientific-publications.html
Review Articles on Clinical Trials:
�
1. 3/2004
�
Burzynski, S.R. The Present State of Antineoplaston Research. Integrative Cancer Therapies 2004;3:47-58.
http://www.burzynskiclinic.com/images/stories/Publications/994.pdf
Volume 3 Number 1 March 2004
DOI: 10.1177/1534735403261964
�
Pg. 48
�
Antineoplaston A2, which contributed to the highest number of complete responses in phase I clinical studies, was elected for final purification, isolation of active components, and structure determination.
Active ingredient identified as:
3-phenylacetylamino-2, 6-piperidinedione
and was named
antineoplaston A10. [27]
�
27. Burzynski SR, Hendry LB, Mohabbat MO, et al. Purification of structure determination, synthesis and animal toxicity studies of antineoplaston A10. In: Proceedings of the 13th International Congress of Chemotherapy. Vienna, Austria; 1983:17, PS. 12.4 11-4.
�
A10 has been reproduced by synthesis involving condensation of:
1-glutamine
with
phenylacetyl chloride
and subsequent cyclization of
phenylacetylglutamine (PG). [28]
�
28. Burzynski SR, Hai TT. Antineoplaston A10. Drugs of the Future. 1985;10:103-105.
�
Metabolism of A10 in human body yields:
phenylacetylglutamine (PG)
phenylacetylisoglutamine (isoPG)
phenylacetate (PN)
which were reproduced synthetically and formulated into:
antineoplaston
A10 injections (A10-I)
AS2-1
AS5
AS-25
[29-33]
�
29. Burzynski SR. Synthetic antineoplastons and analogs. Drugs of the Future. 1986;11:679-688.

30. Burzynski SR, Mohabbat MO, Lee SS. Preclinical studies of antineoplaston AS1-1 and antineoplaston AS2-5. Drugs Exptl Clin Res. 1986;12(suppl 1):11-16.
http://www.ncbi.nlm.nih.gov/pubmed/3743376/

http://www.ncbi.nlm.nih.gov/m/pubmed/3743376/
31. Burzynski SR, Khalid M. Antineoplaston A10 injections. Drugs of the Future. 1986;11:364-365.

32. Burzynski SR, Khalid M. Antineoplaston AS2-1. Drugs of the Future. 1986;11:361-363.

33. Burzynski SR. Antineoplaston AS2-5.. Annual Drug Data Report. 1986;8-319.
�
These formulations were submitted for basic research and phase I clinical studies. [34-44]
�
34. Burzynski SR, Mohabbat MO, Burzynski B. Animal toxicology studies on oral formulation of antineoplaston A10. Drug Exptl Clin Res. 1984;10:113-118.

35. Burzynski SR. Phase I clinical studies of antineoplaston AS2-5 injections. In: Ishigami J, ed. Recent Advances in Chemotherapy. Tokyo, Japan: University of Tokyo Press; 1985.

36. Burzynski SR, Burzynski B, Mohabbat MO. Toxicology studies of antineoplaston AS 2-1 injections in cancer patients. Drugs Exptl Clin Res. 1986;12(suppl 1):25-35.
http://www.ncbi.nlm.nih.gov/pubmed/3743378/

http://www.ncbi.nlm.nih.gov/m/pubmed/3743378/
37. Burzynski SR, Kubove E. Toxicology studies of antineoplaston A10 injections in cancer patients. Drugs Exptl Clin Res. 1986;12(suppl 1):47-55.
http://www.ncbi.nlm.nih.gov/pubmed/3743380/

http://www.ncbi.nlm.nih.gov/m/pubmed/3743380/
38. Lehner AF, Burzynski SR, Hendry LB. 3-phenylacetylamino-2,6-piperidinedione, a naturally-occurring peptide analog with apparent antineoplastic activity may bind to DNA. Drugs Exptl Clin Res. 1986;12(suppl 1):57-72.
http://www.ncbi.nlm.nih.gov/pubmed/3743381/

http://www.ncbi.nlm.nih.gov/m/pubmed/3743381/
39. Ashraf AQ, Liau MC, Mohabbat MO, et al. Preclinical studies of antineoplaston A10 injections. Drugs Exptl Clin Res. 1986;12(suppl 1):37-45.
http://www.ncbi.nlm.nih.gov/pubmed/3743379/

http://www.ncbi.nlm.nih.gov/m/pubmed/3743379/
40. Ashraf AQ, Liau MC, Kampalath BN, et al. Pharmacokinetic study of radioactive antineoplaston A10 following oral administration in rats. Drugs Exptl Clin Res. 1987;13(suppl 1):45-50.
http://www.ncbi.nlm.nih.gov/pubmed/3569015/

http://www.ncbi.nlm.nih.gov/m/pubmed/3569015/
41. Hendry LB, Muldoon TG, Burzynski SR et al. Stereochemical modeling studies of the interaction of Antineoplaston A10 with DNA. Drugs Exptl Clin Res. 1987;13(suppl 1):77-81.
http://www.ncbi.nlm.nih.gov/pubmed/3569020/

http://www.ncbi.nlm.nih.gov/m/pubmed/3569020/
42. Ashraf AQ, Burzynski SR. Comparative study of antineoplaston A10 levels in plasma of healthy people and cancer patients. Adv Exptl Clin Chemother. 1988;2:19-28.

43. Ashraf AQ, Kampalath BN, Burzynski SR. Pharmacokinetic analysis of antineoplaston A10 injections following intravenous administration in rats. Adv Exptl Clin Chemother. 1988;6:33-39.

44. Burzynski SR, Kubove E, Burzynski B. Phase I clinical studies of oral formulation of antineoplaston AS2-1. Adv Exptl Clin Chemother. 1988;2:29-36.
�
A10
A10-I
AS2-1
were selected for phase II studies.
2 initial phase II studies in
ASTROCYTOMA
and
HIGH-GRADE GLIOMA
began in
1988
and
1990
and were conducted outside investigational new drug (IND) process.
�
Since 1994 the FDA authorized 74 phase II studies with
A10
A10-I
AS2-1
under INDs
43,742
22,029
in advanced malignancies.
�
Pg. 49
�
Phenylacetate (PN)
is active ingredient of
antineoplaston AS2-1.
�
Phenylglutamine (PG)
is main ingredient of
A10-I.
�
Phenylglutamine (PG) exhibits antineoplastic activity across wide array of cancer cell lines.
�
Phenylglutamine (PG)
inhibits uptake of growth-critical amino acids, such as:
1-glutamine
and
1-leucine
in neoplastic cells.
�
Reduction in amino acid availability may contribute to drug’s antineoplastic activity.
�
Human glioma (U-87) cells rapidly take up Phenylglutamine (PG) by mechanism similar to facilitated diffusion.
�
Upon removal of Phenylglutamine (PG) from media, PG rapidly and completely effluxes from the cell.
�
Phenylglutamine (PG)
enters cells via stereospecific amino acid transporters for
1-glutamine.
�
Formulations of
Antineoplastons:
�
Antineoplastons
are a class of 12 antitumor agents.
�
Following synthetic antineoplaston formulations used in phase II studies.
�
Antineoplaston A10
capsules contain 500 mg of
3-phenylacetylamino-2, 6-piperidinedione.
�
Antineoplaston A10 injection
is mixture of sodium salts of
Phenylglutamine (PG)
and
Phenylacetylisoglutamine (isoPG)
in 4:1 ratio.
�
Available in 500 mL and 1000 mL (300 mg/mL) plastic bags.
�
Antineoplaston AS2-1
capsules containing 500 mg of 4:1
Phenylacetate (PN)
and
Phenylglutamine (PG).
�
Antineoplaston AS2-1 injection
is mixture of
Phenylacetate (PN)
and
Phenylglutamine (PG)
in 4:1 ratio.
�
Available in 250 mL (80 mg/mL) plastic bags.
� � � � � � � � � � � � � � � �
Interim Reports on Clinial Trials:
�
18. 6/2005
�
INTEGRATIVE CANCER THERAPIES
�
BT-12
�
CHILDREN WITH PRIMITIVE NEUROECTODERMAL TUMORS (PNET)
�
CAN-01
�
CAN-1
�
PATIENTS WITH REFRACTORY MALIGNANCIES
�
Burzynski, S.R., Weaver, R.A., Janicki, T., Szymkowski, B., Jurida, G., Khan, M., Dolgopolov, V.
�
Long-term survival of high-risk pediatric patients with PRIMITIVE NEUROECTODERMALTUMORS treated with Antineoplastons A10 and AS2-1
http://www.ncbi.nlm.nih.gov/pubmed/15911929
Integrative Cancer Therapies 2005;4(2):168-177
http://www.ncbi.nlm.nih.gov/m/pubmed/15911929
Integr Cancer Ther. 2005 Jun;4(2):168-77
http://www.burzynskiclinic.com/images/stories/Publications/1220.pdf
DOI: 10.1177/1534735405276835
http://m.ict.sagepub.com/content/4/2/168.long?view=long&pmid=15911929
Antineoplastons (ANP) A10 and AS2-1, which are synthetic analogs of naturally occurring derivatives of glutamine, isoglutamine, and phenylacetic acid, have shown an increasing spectrum of activity in primary brain tumors. [1]
�
Review Articles on Clinical Trials:
�
1. 3/2004
�
Burzynski, S.R. The Present State of Antineoplaston Research. Integrative Cancer Therapies 2004;3:47-58.
http://www.burzynskiclinic.com/images/stories/Publications/994.pdf
Volume 3 Number 1 March 2004
DOI: 10.1177/1534735403261964
� � � � � � � � � � � � � � � �
IV. Aetna considers SODIUM PHENYLBUTYRATE medically necessary for the treatment of acute promyelocytic leukemia and malignant glioma
http://www.aetna.com/cpb/medical/data/200_299/0240.html
� � � � � � � � � � � � � � � �
The FDA has approved SODIUM PHENYLBUTYRATE as a treatment to remove ammonia from the bloodstream in individuals with urea cycle disorders
� � � � � � � � � � � � � � � �
SODIUM PHENYLBUTYRATE was given an orphan drug designation by the FDA for use as an adjunct to surgery, radiation therapy, and chemotherapy for treatment of individuals with primary or recurrent malignant glioma
http://www.anthem.com/medicalpolicies/policies/mp_pw_a050524.htm
� � � � � � � � � � � � � � � �
Cumulative List of all Products that have received Orphan Designation: Total active designations: 2002 Effecive: (sic – Effective:) 5/5/2009
http://www.fda.gov/downloads/forindustry/developingproductsforrarediseasesconditions/howtoapplyfororphanproductdesignation/ucm162066.xls
PHENYLBUTYRATE (PB) and SODIUM PHENYLBUTYRATE are listed alphabetically in the lower 1/4th of this document
� � � � � � � � � � � � � � � �
Sodium Phenylbutyrate (PB)
Year – Pubmed (110 entries)
1958 1st entry
1995 1st clinical trial
2001 Phase 1
2009 Phase 2
2012 Phase 3
� � � � � � � � � � � � � � � �
Phenylacetate (PN)
Year – Pubmed (29,686 entries)
1883 1st entry
1994 Phase 1
1999 Phase 2
2013 latest
� � � � � � � � � � � � � � � �
Antineoplaston(s)
Year – Pubmed (88 entries)
1976 1st entry
1986 Phase 1
1999 Phase 2
2003 Phase 2 preliminary
2004 Phase 2 preliminary
2012 latest
� � � � � � � � � � � � � � � �
National Cancer Institute (NCI) at the National Institutes of Health (NIH)
Antineoplastons (PDQ®) Overview:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page1

http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/patient
General Information:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page2
History:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page3
Laboratory/Animal/Preclinical Studies:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page4
Human/Clinical Studies:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page5
Adverse Effects:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page6
Summary of the Evidence for Antineoplastons:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page7
Changes to This Summary:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page8
About This PDQ Summary:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page9
Questions and Answers About Antineoplastons:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/patient/page2
Current Clinical Trials:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/patient/page3
Changes to This Summary:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/patient/page4

Burzynski and AACR (American Association for Cancer Research)

ANTINEOPLASTON
ANTINEOPLASTONS
AS2-1

2005 and 2004 References on AACR:

Molecular mechanisms of G1 cell arrest and induction of apoptosis augmented by treatment with ANTINEOPLASTON AS2-1 in colon cancer cells

[Proc Amer Assoc Cancer Res, Volume 46, 2005]

Experimental and Molecular Therapeutics 18:

Cell Cycle Mechanisms of Anticancer Drug Action

Abstract #2294

Keiko Matono, Yutaka Ogata and Kazuo Shirouzu

Kurume University School of madicine, Kurume City, Japan
http://www.aacrmeetingabstracts.org/cgi/content/abstract/2005/1/538-c

Antitumor effect of biochemical defense modifier ANTINEOPLASTON AS2-1 against colon cacer through G1 and G2 cell arrest

[Proc Amer Assoc Cancer Res, Volume 45, 2004]

Experimental and Molecular Therapeutics 27:

Natural Products

Abstract #2976

Keiko, M.
Matono Keiko

Kurume University, Kurume City, Japan
http://www.aacrmeetingabstracts.org/cgi/content/abstract/2004/1/688-a

PHENYLBUTYRATE
and
PHENYLACETATE

Cited by BURZYNSKI

2004 Reference on AACR:

PHENYLBUTYRATE and PHENYLACETATE Induce Differentiation and Inhibit Proliferation of Human Medulloblastoma Cells

Laboratory of Molecular Neuro-oncology

Cancer Genomics Program

Texas Children’s Cancer Center, Baylor College of Medicine, Houston, Texas

Clin Cancer Res 2004;10:1150-1159

doi: 10.1158/1078-0432.CCR-0747-3 Clin Cancer Res February 1, 2004 10; 1150

Clinical Cancer Research

(Cited by 55)
Abstract:
http://m.clincancerres.aacrjournals.org/content/10/3/1150.abstract
Article:
http://m.clincancerres.aacrjournals.org/content/10/3/1150.full
PDF:
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Cited Articles by 48 articles, 20 of which you can access:
http://clincancerres.aacrjournals.org/content/10/3/1150.full.html#ref-list-1
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PHENYLBUTYRATE

2001 (SAMID who learned from BURZYNSKI – 6 References) Reference on AACR:

A Phase I Dose Escalation and Bioavailability Study of Oral Sodium PHENYLBUTYRATE in Patients with Refractory Solid Tumor Malignancies

Divisions of Medical Oncology and Experimental Therapeutics, Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland

NIH, Bethesda, Maryland

Clinical Cancer Research
http://m.clincancerres.aacrjournals.org/content/7/8/2292.full
2. ↵ … SAMID D.

Transcriptional upregulation of TGF-α by PHENYLACETATE and PHENYLBUTYRATE is associated with differentiation of human melanoma cells

Cytokine, 7: 449-456, 1995

Cytokine
Volume 7, Issue 5, July 1995, Pages 449–456
http://www.sciencedirect.com/science/article/pii/S1043466685700610
3. ↵ … SAMID D.

Transcriptional upregulation of γ globin by PHENYLBUTYRATE and analogous aromatic fatty acids

Biochem. Pharmacol., 52: 1227-1233, 1996

Biochemical Pharmacology
Volume 52, Issue 8, 25 October 1996, Pages 1227–1233
http://www.sciencedirect.com/science/article/pii/0006295296004765
5. ↵ SAMID D. …

Selective growth arrest and phenotypic reversion of prostate cancer cells in vitro by nontoxic pharmacological concentrations of PHENYLACETATE

J. Clin. Investig., 91: 2288-2295, 1991

6. ↵ … SAMID D.

Activation of the human peroxisome proliferator-activated receptor by the antitumor agent PHENYLACETATE and its analogues

Biochem. Pharmacol., 52: 659-667, 1996

Biochemical Pharmacology
Volume 52, Issue 4, 23 August 1996, Pages 659–667
http://www.sciencedirect.com/science/article/pii/0006295296003401
15. ↵ … SAMID D. (Dvorit Samid)

The differentiating agent PHENYLACETATE increases prostate-specific antigen production by prostate cancer cells

Prostate, 29: 177-182, 1996

Article first published online: 7 DEC 1998

DOI: 10.1002/(SICI)1097-0045(199609)29:33.0.CO;2-B

The Prostate
Volume 29, Issue 3, pages 177–182, September 1996
http://onlinelibrary.wiley.com/doi/10.1002/(SICI)1097-0045(199609)29:3%3C177::AID-PROS3%3E3.0.CO;2-B/abstract;jsessionid=733C54B7B855391DFBB8C8E7F8EEA65D.d02t02
Cited by:
http://onlinelibrary.wiley.com/doi/10.1002/(SICI)1097-0045(199609)29:3%3C177::AID-PROS3%3E3.0.CO;2-B/citedby
20. ↵ SAMID D. …

The nuclear receptors PPARS as novel targets in differentiation therapy: activation by phenylacetate and phenylbutyrate

Anticancer Res., 17: 3927-3928, 1997

D SAMID (Who learned from BURZYNSKI)

PHENYLACETATE

Cited by BURZYNSKI

1996 Reference on AACR:

Up-regulation and functional role of p21Waf1/Cip1 during growth arrest of human breast carcinoma MCF-7 cells by PHENYLACETATE

Cell Growth and Differentiation, Vol 7, Issue 12 1609-1615, 1996
American Association of Cancer Research

… D SAMID …

Laboratory of Cellular and Molecular Biology, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, Maryland, USA
http://cgd.aacrjournals.org/cgi/content/abstract/7/12/1609
S. R. BURZYNSKI …

Long-term Survival of High-Risk Pediatric Patients With Primitive Neuroectodermal Tumors Treated With ANTINEOPLASTONS A10 and AS2-1

Integr Cancer Ther, June 1, 2005; 4(2): 168 – 177

Integrative Cancer Therapies
http://ict.sagepub.com/content/4/2/168.abstract
S. R. BURZYNSKI

The Present State of ANTINEOPLASTON Research (1)

Integr Cancer Ther, March 1, 2004; 3(1): 47 – 58

doi: 10.1177/1534735403261964 Integr Cancer Ther March 2004 vol. 3 no. 1 47-58

Integrative Cancer Therapies
http://m.ict.sagepub.com/content/3/1/47.abstract

Sodium PHENYLACETATE

Cited by BURZYNSKI

1995 Reference on AACR:

Sodium PHENYLACETATE Induces Growth Inhibition and Bcl-2 Down-Regulation and Apoptosis in MCF7ras Cells in Vitro and in Nude Mice

Institut d’Oncologie Moléculaire et Cellulaire Humaine, 129 av. de Stalingrad, Bobigny

Université Paris Nord, 74 rue Marcel Cachin, Bobigny

Service d’Anatomie Pathologique

Clinique Universitaire de Cancérologie, 125 av. de Stalingrad, Bobigny, France

[Cancer Research 55, 5156-5160, November 15, 1995]

1995 American Association for Cancer Research
http://hwmaint.cancerres.aacrjournals.org/cgi/content/abstract/55/22/5156
S. R. BURZYNSKI …

Long-term Survival of High-Risk Pediatric Patients With Primitive Neuroectodermal Tumors Treated With ANTINEOPLASTONS A10 and AS2-1

Integr Cancer Ther, June 1, 2005; 4(2): 168 – 177

Integrative Cancer Therapies
http://ict.sagepub.com/content/4/2/168.abstract

S. R. BURZYNSKI

The Present State of ANTINEOPLASTON Research (1)

Integr Cancer Ther, March 1, 2004; 3(1): 47 – 58

doi: 10.1177/1534735403261964 Integr Cancer Ther March 2004 vol. 3 no. 1 47-58

Integrative Cancer Therapies
http://m.ict.sagepub.com/content/3/1/47.abstract

Cited by BURZYNSKI

2002 Reference on AACR:

Hypermethylation of HIC-1 and 17p Allelic Loss in Medulloblastoma

Departments of Pediatric Hematology/Oncology
and Pediatric Neurosurgery,
Children’s Research Institute, Children’s National Medical Center, Washington, D.C.

[Cancer Research 62, 3794-3797, July 1, 2002]

2002 American Association for Cancer Research

Molecular Biology and Genetics
http://hwmaint.cancerres.aacrjournals.org/cgi/content/full/62/13/3794
S. R. BURZYNSKI …

Long-term Survival of High-Risk Pediatric Patients With Primitive Neuroectodermal Tumors Treated With ANTINEOPLASTONS A10 and AS2-1

Integr Cancer Ther, June 1, 2005; 4(2): 168 – 177

Integrative Cancer Therapies
http://ict.sagepub.com/content/4/2/168.abstract