Wikipedia or Wikipediantic ? – wants your 3 pounds of flesh (WikiPEEdia, UR all INe)

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[WP:SOP] Statement of principles from Wikipedia founder Jimbo Wales, as updated by the community since then. 7.”)

Due & undue weight: [3]

“The relative prominence of each viewpoint among Wikipedia editors or the general public is not relevant & should not be considered,”

[WP:NPOV] “History of NPOV:” (Content # 6, Note 3)

(Neutral Point of View)
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TRANSLATION: Wikipedia editors, YOUR OPINION IS NOT RELEVANT
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MEANING: It is meaningless to attempt to slather your biased OPINION all over Wikipedia like butter on Texas toast, since supposedly, we only care about verifiable FACTS
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Wikipedia, what the problem is ?

Jimmy Donal Wales

Who ?

No, “The Who” is actually really British !

(as opposed to some “furreigner” who plops across the pond, wants to pound one of your pelts after a celebrity hunt, pops it in his bonnet, pip-pips about, and mounts it up on his rented wall along with what’s left of his balls)

I’m writing, of course, about “Jimbo,” the one who got away . . . Thankfully

The recipient of the write-up earlier this year in The New York Times [1] (Oh, pithy !!)
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Wales, who no longer runs the day-to-day operations of Wikipedia

“He applies his libertarian worldview to the Internet and has taken on institutions like the United States government
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You must be bloody well right joking me

(joking me ? Quit jokin’ me !)

JimCrow’s ’bout as “libertarian” as Fidel Castro with a gun in his hand and (f)lies between his teeth; from traveling with the windows down

Stephen Colbert shoulda seen that comin’ from a 8 mile away

Hey Stephen, Report’ THAT !!!
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“He grew up in Huntsville, Ala., the son of a teacher and a retail man
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And obviously, he didn’t “learnt” well

I think a refund’s in order

And here’s your free school Insolence to go with it

Happy eat in’

It is claimed that “HE” spends time:
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“traveling the world giving talks on free speech and Internet freedom
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seriously ?

Seriously ??

SERIOUSLY ???

Welcome to MizFitTV

What would “Jymboree” know about “free speech” and “Internet freedom,“ anyway ?

How many days did you serve your country in the United States military ?

Oh, you did NOT realize that while you were in San Diego, you could have signed that contract ?

After all, he’s no Vincent Kennedy McMahon”
(“HE” knows where “HIS” GRAPEFRUITS are)
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“B.D.F.L., or the Benevolent Dictator for Life”
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How ’bout:

Big
Disappointing
Fascist
Loser ?
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Argumentum ad Jimbonem” means dutifully following what Wales says, but there are even arguments about that”
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WP:NICETRY, but that’s “SHEEPLE”
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“One Wikipedia editor said, for instance, that Wales was no longer comfortable with the B.D.F.L. description”
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Jiminy Cricket !

Whazzamatta Jiminy?

Did “FASCIST” hit a bit too close to home ?
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“(There is, among some, a debate over what to call him)”

“Some users have also disputed the Latinized version of “Jimbo.”

“(Should it be “Jimboni” or “Jimbini”?)”
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Can you smell what “The Rock” is cookin’ ?

La-La-La-La-Laaaaaaawwww, JIMBRONI !!!!!!!

Get ready, and bend over, ’cause I’m gonna shine this thing up, turn it sideways, and shove it straight up your Candy AstroTurf hatch
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Introduction (statement of principles) [WP:SOP]

“This is a statement of principles from Wikipedia founder Jimbo Wales, as updated by the community since then”
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(Or if you go by The New York Times article, [1] Jimbroni is the co-founder” who tries to re-write history to make it appear that “HE” is the one-and-only Fascist Founder ?)
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“I should point out that these are my principles, such that I am the final judge of them”

This does not mean that I will not listen to you, but it does mean that at some ultimate, fundamental level, this is how Wikipedia will be run”
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No, actually, it DOES mean that he will NOT listen to you, as was the case when he ignored my 2/7/2013 appeal

In his defense, perhaps Kate Garvey has his balls
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Principles

1. “Wikipedia’s success to date is entirely a function of our open community”

“This community will continue to live and breathe and grow only so long as those of us who participate in it continue to Do The Right Thing

Doing The Right Thing takes many forms, but perhaps most central is the preservation of our shared vision for the neutral point of view policy and for a culture of thoughtful, diplomatic honesty
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The problem with this Wacky Tobacky “We are the (Wiki) World” WikiWhOReD Wonderland Jimbroni’s living in, is that “HE” has NOT been Doing The Right Thing since “HE” abdicated “his” “neutral point of view policy” and “culture of thoughtful, diplomatic honesty,” to “The Skeptics”

“The Skeptics,” who serve as gatekeepers of the Burzynski Clinic article, and who cite Dr. David H. Gorski a/k/a “Orac” aka GorskGeek as if he were a “reliable source”

“The Skeptics,” who bring new meaning to the term “Wikipedia Zero”

“The Skeptics,” who are Intellectual Cowards like their false god Gorski, the Closet Communist of Science-Based Medicine a/k/a Science-Basted Medicine aka Science-Based Mudicine (Spinning Bowel Movement), Wiki Wordsmith Wannabes, nut-jobbers, stale from their failure at the National Peanut Festival in Dothan, Alabama
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3. ““You can edit this page right now” is a core guiding check on everything that we do”

“We must respect this principle as sacred”
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Do the lies just dribble off your chin like phlegm?

You canNOT just go in and “edit” the Burzynski Clinic article “page right now”

That statement is pure, unadulterated Alabama B.S.

That’s NOT a “sacred principle,” it’s sacré “bull”
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7. “Anyone with a complaint should be treated with the utmost respect and dignity”
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Unfortunately, you do NOT practice what you preach, do you, HYPOCRITE ?
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“They should be encouraged constantly to present their problems in a constructive way”
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So that you can ignore the problem(s), right, Jimbroni ?
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“Anyone who just complains without foundation, refusing to join the discussion, should simply be rejected and ignored”
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THAT would automatically exclude all of “The Skeptics” now, wouldn’t it ?
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“We must not let the “squeaky wheel” be greased just for being a jerk
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Jimbroni, why have you allowed “The Skeptics” to choose from their “squeaky” wheel-house bag o’ tricks, get all “greased” up and jerk” so many people around in such a big CIRCLE-JERK, for so long?
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8. “Diplomacy consists of combining honesty and politeness

“Both are objectively valuable moral principles”

“Be honest with me, but don’t be mean to me”

“Don’t misrepresent my views for your own political ends, and I’ll treat you the same way”
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“Honesty” and “politeness” are really great buzzwords,” Jimbroni, but they are as foreign to your “Skeptics,” as “moral principles”
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A great example of the questionable “honesty” and “moral principles” of one of your apparatchiks, was demonstrated 2/3/2013, 6:56, when I sent an arbitration appeal e-mail to Wikipedia, advising, in part, that the e-mail listed on Wikipedia; as the one that blocked users should use, did NOT work, because there was NO “@” sign in it

There was a . (period) where the “@” sign belonged
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2/3/2013, 8:11 AM, Anthony (AGK) BASC
wikiagk@gmail.com
advised:

“Everything you have said in that e-mail demonstrates a misunderstanding or misreading of Wikipedia policy”
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Check the “time” and “place” where you are, so that you, too, can advise, that according to Wikipedia, pointing out to them that the e-mail they advise people to use, DOES NOT WORK; because there is no “@” sign in it (instead, there’s a . (period)), translates into meaning:
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“Everything you have said in that e-mail demonstrates a misunderstanding or misreading of Wikipedia policy”
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Core principles

Wikipedia:Simplified ruleset [WP:SR]

Wikipedia does not have its own views, or determine what is “correct”
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I wish I could LIE like that, but I have a conscience
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12/24/2012, Monday – 3:52 pm – 21:52 (UTC) –
“We are told that 2013 will be a big year, but apparently his plan is to release another bullshit movie not to publish useful research”

[User Talk:JzG|Guy] ([User JzG/help|Help!]) [2]

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“Bullshit movie” ?
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Does anyone other than me NOT think it a “coinkydink” that some “Guy” on Wikipedia, going by the name “Guy”, using the same 2 words (“Bullshit movie”) as a “Guy” on Twitter ?
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2. Founding principles:

“Neutrality is mandatory . . . “
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I call B.S.

Neutrality is mandatory,” EXCEPT on the Burzynski Clinic article, controlled by “The Skeptics”
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4. “Ignore all rules (IAR):”

“Rules on Wikipedia are not fixed in stone”
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Especially when Jimbroni allows “The Skeptics”
to “dictator” the “rules”
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“The spirit of the rule trumps the letter of the rule

“The common purpose of building an encyclopedia trumps both”

“This means that any rule can be broken for a very good reason, if it ultimately helps to improve the encyclopedia”
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And “The Skeptics” are NOT required to provide ANY reason for having broken “any rule”
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“It doesn’t mean that anything can be done just by claiming IAR, or that discussion is not necessary to explain one’s decision”
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But do NOT expect Wikipedia to require anything from The Skeptics”
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Founding principles

1. “Neutral point of view (NPOV) as a mandatory editorial principle”
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EXCEPT when it comes to the Burzynski Clinic article
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12/26/2012 – I attempted to get Wikipedia to reference the interview which Burzynski’s attorney, Richard (Rick) A. Jaffe, and Lola Quinlan’s attorney; who posted it on his web-site, had given: [4]

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Please add re WP:NPOV that Burzynski’s attorney, Richard Jaffe has disputed Lola Quinlan’s claims:

“On February 1, 2012, Dr. Burzynski’s attorney, Richard Jaffe, disputed Lola Quinlan’s allegations on Houston’s KPRC News.”

Thank you very much.[[User: Didymus Judas Thomas 15:03, 12/26/2012 (UTC)
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So? [OR] Disputing it in the media probably means he doesn’t have a case. [/OR] In any case, a lawyer disputing the allegations against his client is not even news. — [[User: Arthur Rubin 15:24, 12/26/2012 (UTC)

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Arthur Rubin, I’m not sure what relevance your above post has re WP:NPOV since the article includes statements from attorneys representing both sides

17:51, 12/27/2012 (UTC) Didymus Judas Thomas

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12/24/2012, Monday – 3:54 pm (21:54.UTC) – “What they mean is that nobody else is doing any meaningful work on it, which necessarily means that it’s not considered in the least promising.”

[[User Talk:JzG|Guy]] ([User JzG/help|Help!])

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“Nobody else is doing meaningful work on it” ?

Ignores independent research done in Poland, Russia, Korea, Egypt, Japan, & China which specifically reference SRB’s publications in their publications re antineoplastons & phenylacetylglutamine (PG); which is AS2-5, & includes phase III trials published in China & continued research being published in China 12/17/2012?

FACTS:

1. I pointed out to Wikipedia, a 12/17/2012 scientific publication re antineoplastons, which referenced Burzynski @ 22. (antineoplaston AS21)

2. 7 days after this scientific journal was published, Wikipedia’a “Guy (Help!’s) ”response, Monday, 12/24/2012 @ 3:54 pm, is to advise me:

“What they mean is that nobody else is doing any meaningful work on it, which necessarily means that it’s not considered in the least promising.”

Guy (Help!) 3:54 pm, 12/24/2012, Monday

3. So, Wikipedia’s, Guy (Help!), defines an event having been published 7 days ago (12/17/2012 to 12/24/2012) as:

“…nobody else is doing any meaningful work on it…”

12/17/2012
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3524164
CDA-2 (cell differentiation agent 2), a URINARY preparation
http://po.st/g71N8P
CDA-2 and its main component PHENYLACETYLGLUTAMINE (PG or PAG)
Antineoplaston AS2-5 is PHENYLACETYLGLUTAMINE (PAG or PG)
http://redd.it/1dk974
Antineoplaston AS2-1 is a 4:1 mixture of phenylacetic acid (PA) and PHENYLACETYLGLUTAMINE (PAG or PG)
Antineoplastons AS2-5 and AS2-1 are derived from Antineoplaston A10
BURZYNSKI Reference: 22.
antineoplaston AS21
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0052117
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12/26/2012, Wednesday – 12:43 – “There is unlikely to be any dispassionate debate over ANPs while Burzynski continues with his unethical practices.”

JzG|Guy User:JzG/help|Help!

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Wikipedia: Judge, Jury, Executioner
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“The world, right now, considers Burzynski to be at best unethical and at worst a quack…”?

Since when did Wikipedia conduct a world-wide “opinion poll” re Burzynski ?

And if Wikipedia is correct, how did this happen ?

Burzynski referenced by other Cancer researchers:

2011 – Phase II trial of tipifarnib and radiation in children with newly diagnosed diffuse intrinsic pontine gliomas
http://neuro-oncology.oxfordjournals.org/content/13/3/298.full
University of California—San Francisco

Children’s Hospital Boston, Massachusetts

St Jude Children’s Research Hospital, Memphis, Tennessee

Seattle Children’s Hospital, Seattle, Washington

Children’s Hospital of Philadelphia, Pennsylvania

Children’s Hospital of Pittsburgh, Pennsylvania

Children’s National Medical Center, Washington, DC

Cincinnati Children’s Hospital Medical Center, Ohio

Neuro Oncol (2011) 13 (3): 298-306
doi: 10.1093/neuonc/noq202

5.723 Impact Factor

25. ↵ Burzynski SR
Treatments for astrocytic tumors in children: current and emerging strategies
Paediatr Drugs. 2006;8:167-178
http://link.springer.com/article/10.2165%2F00148581-200608030-00003
Pediatric Drugs
May 2006, Volume 8, Issue 3, pp 167-178
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Rhode Island Red attempts to get away with misquoting me:
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“The other argument is that the secondary sources (i.e., respected cancer organizations, FDA, etc.) are not reliable because they are Burzynski’s “competitors”

[[User: Rhode Island Red]] 4:18 pm, Yesterday (UTC−6)
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What a Wipocrite (Wiki + Hypocrite)

Steve Pereira (SilkTork) is such a “WIPOCRITE,” that he claims:
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“the community were united that your contributions were biased”
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He conveniently; like a good little mini-Jimbroni would, ignores ALL of his fellow WIPOCRITES comments, which completely ignored:
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([WP:SOP] Statement of principles from Wikipedia founder Jimbo Wales, as updated by the community since then. 7.”)

Due & undue weight: [3]

“The relative prominence of each viewpoint among Wikipedia editors or the general public is not relevant & should not be considered,”

[WP:NPOV] “History of NPOV:” (Content # 6, Note 3)

(Neutral Point of View)
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1. 12/24/2012, Monday – 3:52 pm – 21:52 (UTC) – “We are told that 2013 will be a big year, but apparently his plan is to release another bullshit movie not to publish useful research”
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2. 12/24/2012, Monday – 3:54 pm (21:54.UTC) – “What they mean is that nobody else is doing any meaningful work on it, which necessarily means that it’s not considered in the least promising.”
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3. 12/26/2012, Wednesday – 12:43 – “There is unlikely to be any dispassionate debate over ANPs while Burzynski continues with his unethical practices.”
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4. 12/30/2012 8:58 “The world, right now, considers Burzynski to be at best unethical and at worst a quack…”?
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Am I NOT the only one convinced that “the community” was also “united” in something more than just their “goose-stepping ?
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Pereira, the imperfect ‘pedia Pimp tries to Wow his readers by waxing WikiWhOReD, by ignoring that ALL the previous BIASED opinion B.S. that his fellow-Facist forged ahead with, and which Wikipediantic history says means ABSOLUTELY NOTHING (say it again) because it is their BIASED OPINION and is ABSOLUTELY WORTHLESS, and it was as so much WikiLitter, well, he’s just facist-free speechless about that, as any Jimbroni AstroTurf Twerk should be
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To show exactly what zealots these WikiPimps are, just absorb this exchange:
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“The Burzynski Clinic Article has:

“…a Mayo Clinic study found no benefit….”

But that was not what the study concluded

See below:
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“CONCLUSION:

Although we could not confirm any tumor regression in patients in this study, the small sample size precludes definitive conclusions about treatment efficacy.”
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In the interest of Neutrality, please remove the reference to Mayo entirely or change to;
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“…a Mayo Clinic study found that “the small sample size precludes definitive conclusions about treatment efficacy.”
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Thank you very much

Didymus Judas Thomas 21:12, 12/10/2012
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“How is “found no benefit” not a a fair and pithy description of the Mayo Clinic study’s summary?”

Alexbrn 21:24, 12/10/2012
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“I feel this should be changed under WP:NPOV because not every reader is going to understand the “Fair & Pithy” reason I was provided

I feel that the average reader reading this will read it as meaning a study was done & completed with the necessary # of people for an effective study, when that was not the conclusion as pointed out in my above post

Thank you very much.”

Didymus Judas Thomas 11:02, 12/18/2012
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NO RESPONSE

That’s right !

“NO RESPONSE” from the “mini-b” (a/k/a “mini-brain”), wannabe Fascists who are so zealous about using their alleged “Fair and Pithy” “found no benefit” WikiWhOReD; which they utilize in an effort to deceive those who are NOT smarter than a fifth-grader

These WikiPimps are so certain of the righteousness of their evangelical cause, that they do NOT even have the “GRAPEFRUITS” to use what the study’s conclusions actually said, and let the chips fall where they may

There are a lot of “chips” falling at Wikipedia

“BULL CHIPS”

JIMBRONI, you’re no Maggie Thatcher

You can’t even wear her pants
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Margaret Thatcher: “The Iron Lady”

Jimbroni: “No iron in the pants”
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Jimbroni’s list of Facist, mini-Hitler, Monty Pythonesque Women’s underwear wearing Wannabes on Wikipediantic:

1. Alexbrn
2. fluffernutter
3. NE Ent
4. Choyoołʼįįhí:Seb az86556 (Seb az86556)
5. Tom Morris
6. Guerillero
7. Dave Dial
8. John
9. Nstrauss
10. Yobol
11. Drmies
12. foxj
13. Ironholds
14. Rhode Island Red
15. Anthony (AGK) BASC wikiagk@gmail.com
16. Steve Pereira (Silk Tork) silktork@gmail.com
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WikiWhOReD (Wiki + Word + Whore): Pimping a word. Attempting to deceive someone by means of misdirection with words
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The South will rise again, just not in Jimbroni’s pants
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Happy Friday the 13th, Wikipediantic
======================================
REFERENCES:
======================================
[1] – 6/27/2013Jimmy Wales Is Not an Internet Billionaire (By AMY CHOZICK):
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http://mobile.nytimes.com/2013/06/30/magazine/jimmy-wales-is-not-an-internet-billionaire.html
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[2] – 12/24/2012, Monday – 3:52 pm – 21:52 (UTC) – [User Talk:JzG|Guy] ([User:JzG/help|Help!])
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http://en.wikipedia.org/w/index.php?title=Talk:Burzynski_Clinic&diff=next&oldid=529537854
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[3] – 12/26/2012Lola A. Quinlan:
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http://en.wikipedia.org/w/index.php?title=Talk:Burzynski_Clinic&diff=prev&oldid=529836971
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http://en.wikipedia.org/w/index.php?title=Talk:Burzynski_Clinic&diff=next&oldid=529836971
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Houston’s KPRC News:
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http://m.click2houston.com/news/Houston-cancer-doctor-draws-new-complaints-from-patients/-/16714936/8581480/-/hmrbjk/-/index.html
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Lola A. Quinlan’s attorney’s web-site:
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http://www.jag-lawfirm.com/burzynski-suit-kprc-02012012.html
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[4] –
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http://en.wikipedia.org/w/index.php?title=User_talk:Didymus_Judas_Thomas&diff=next&oldid=528610760
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These mini-b’s went so far as to allege all sorts of sockpuppetry

Wikipediantic, why don’t you list all the dates and times I was supposedly doing all of these activities; and don’t forget to include all the time I spent blogging, on Twitter, making comments on articles, etc., and once you have all that data compiled, explain how one individual could do all that in a 24-hour day

That’s right Wikipediantic

I’m challenging you to put up or shut up your cornholio

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“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:
——————————————————————
(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) 😊
——————————————————————
(2:47)
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He states:

“There is a long segment about “The Skeptics”

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

“About a half of it is about Burzynski [4]
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6:00
——————————————————————
Gorski mentions that Burzynski noticed that there were higher levels of these chemicals in healthy people, than people with cancer
——————————————————————
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” 😶
——————————————————————
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
——————————————————————
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 😛

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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”
——————————————————————
GorskGeek has #FAILED miserably to prove that on his blogs [7] 😄
——————————————————————
(8:00)
——————————————————————
Gorski comments about Burzynski’s “animal testing,” “species specific” claims:

“There are ways of getting around that”
——————————————————————
But Gorski, again, has #FAILED miserably to prove it [8] 😅
——————————————————————
(12:00)
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Gorski makes lame excuses about the NCI phase II clinical trial [9] 😖
——————————————————————
(12:50)
——————————————————————
Gorski claims Burzynski was indicted for insurance fraud in the 1997 case 😱
——————————————————————
GorskGeek, care to try and prove that one also ? [10] 😃
——————————————————————
(14:25)
——————————————————————
Gorski then states that out of 61 trials on clinicaltrials . gov, “most” are “closed or unknown”
——————————————————————
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
——————————————————————
(15:20)
——————————————————————
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”
——————————————————————
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
——————————————————————
CAN-1 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN

PATIENTS WITH REFRACTORY MALIGNANCIES

133 patients
——————————————————————
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
——————————————————————
Gorski continues his trend of #FAILURES when he mentions the additional types of treatments that Burzynski was offering, but he #FAILED to mention [12] 😂
——————————————————————
” … 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”
——————————————————————
(18:20)
——————————————————————
Gorski addresses the case of Tori Moreno
——————————————————————
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]
——————————————————————
(19:45)
——————————————————————
Gorski goes on to mention Burzynski patients going to Texas Children’s Hospital with hypernatremia issues
——————————————————————
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
——————————————————————
(20:00)
——————————————————————
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]
——————————————————————
(20:40)
——————————————————————
Gorski states that antineoplastons are chemotherapy
——————————————————————
No, Gorski, antineoplaston are:

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

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

“Boom, there you go”
——————————————————————
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”
——————————————————————
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 😷
——————————————————————
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:
——————————————————————
(18:45)
——————————————————————
” … and light as many fires under his butt as we can
——————————————————————
Mentions Rick Jaffe’s book Galileo’s Lawyer

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

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

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

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

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

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

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

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

“What she said”
——————————————————————
(35:20)
——————————————————————
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
——————————————————————
Gorski chirps:

“Yes”
——————————————————————
Bob yacks:

“as being controlled by evil skeptics
——————————————————————
Gorski ejaculates:

“No, seriously”
——————————————————————
Bob bleats:

“No”

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

“Wahahaha” 👿
——————————————————————
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]
——————————————————————
Enlightening ?

Inspiring ?

Amazing ?

Hypocrites

Apparatchiks [20]
======================================
REFERENCES:
======================================
[1]David Gorski – Why We Fight (Part I): Stanislaw Burzynski Versus Science-Based Medicine – TAM 2013 11/8/2013 (22:44)
——————————————————————

======================================
[2]Robert Blaskiewicz – Why We Fight (Part II): It’s All About The Patients – TAM 2013 11/8/2013 (22:36)
——————————————————————

======================================
[3] – Medical Cranks And Quacks
TAM 2013 JREF
11/8/2013 (42:42)
——————————————————————

======================================
[4]“Galileo’s Lawyer” Richard A. Jaffe, Esq.
——————————————————————
http://www.richardjaffe.com
======================================
[5] – 11/9/2013 – Pete Cohen chats with Dr. Stanislaw Burzynski:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/11/09/pete-cohen-chats-with-dr-stanislaw-burzynski/
======================================
[6] – 6/2012 – Journal of Cancer Therapy, 2012, 3, 192-200 doi:10.4236/jct.2012.33028 Published Online June 2012, Pg. 192
——————————————————————
http://www.burzynskiclinic.com/images/stories/Publications/9219.pdf
======================================
[7]Burzynski: Oh, RATS!!!:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/07/26/the-lancet-oncology-peer-review-team-d-12-01519-fail-2/
======================================
[8] – Critiquing: How Stanislaw Burzynski became Burzynski the Brave Maverick Doctor, part 1:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/07/22/critiquing-how-stanislaw-burzynski-became-burzynski-the-brave-maverick-doctor-part-1/
======================================
[9] – 9/19/2013 – Critiquing: National Cancer Institute (NCI) at the National Institutes of Health (NIH) CancerNet “fact sheet”:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/09/19/critiquing-national-cancer-institute-nci-at-the-national-institutes-of-health-nih-cancernet/
======================================
[10] – 9/25/2013 – Critiquing: National Council Against Health Fraud, Inc. – NCAHF News: JURY NULLIFICATION THWARTS BURZYNSKI CONVICTION:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/09/25/critiquing-national-council-against-health-fraud-inc-ncahf-news-jury-nullification-thwarts-burzynski-conviction/
======================================
[11] – 7/9/2013 – Burzynski: The Original 72 Phase II Clinical Trials:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/07/09/burzynski-the-original-72-phase-ii-clinical-trials/
======================================
[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:
——————————————————————
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/
======================================
[13] – Tori Moreno
——————————————————————
http://www.cancerinform.org/aburzinterview2.html
======================================
[14] – 9/1999 – Pediatrics. 1999 Sep;104(3 Pt 1):435-9
——————————————————————
http://www.ncbi.nlm.nih.gov/m/pubmed/10469766/
======================================
[15] – 11/2/2013 – Critiquing: Dr. Stanislaw Burzynski’s cancer “success” stories:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/11/02/critiquing-dr-stanislaw-burzynskis-cancer-success-stories/
——————————————————————
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
——————————————————————
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/
======================================
[16] – NOT ORDINARY CHEMOTHERAPY
——————————————————————
https://bulk.resource.org/courts.gov/c/F3/27/27.F3d.153.93-2071.html
======================================
[17] – 9/4/2013 – University of Michigan, where is alum Dr. David H. “Orac” Gorski’s Grapefruits ?:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/09/04/university-of-michigan-where-is-alum-dr-david-h-orac-gorskis-grapefruits/
======================================
[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:
——————————————————————
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/
======================================
[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
——————————————————————
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/
======================================
[20] – 11/9/2013 – Wikipedia Articles:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/09/11/burzynski-timeline/
======================================

Critiquing: Dr. David H. “Orac” Gorski and The Skeptics™ http://www.scienceblogs.com/Insolence

6/4/2013 Gorski made a remarkable admission:
======================================
http://scienceblogs.com/insolence/2013/06/04/stanislaw-burzynski-versus-the-bbc/
======================================
“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” ?
======================================
Gorski has claimed:
======================================
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/
======================================
6/5/2013 “ … I do know cancer science”
——————————————————————
http://scienceblogs.com/insolence/2013/06/05/odds-and-ends-about-burzynski-clinic/
======================================
11/2/2012 “Personally, having pored over Burzynski’s publications … “
——————————————————————
http://scienceblogs.com/insolence/2012/11/02/stanislaw-burzynski-fails-to-save-another-patient/
======================================
5/8/2013 “I’ve searched Burzynski’s publications … “
——————————————————————
http://scienceblogs.com/insolence/2013/05/08/eric-merola-and-stanislaw-burzynskis-secret-weapon-against-the-skeptics-fabio-lanzoni-part-2/
======================================
☆AnthonyJeselnik☆
🚫GorskonOrac🚫
You tweeted 12:44pm-3/30/13📄

——————————————————————
David Gorski (@gorskon) tweeted at 12:44pm – 30 Mar 13:

——————————————————————
Defend your tweet😅
#Burzynski—
(@FauxSkeptic) May 23, 2013

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

——————————————————————
@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
——————————————————————
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”)
======================================
7/22/2013 I published the below article on my blog:
======================================
Critiquing: In which Orac does Stanislaw Burzynski propagandist Eric Merola a favor…:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/07/22/critiquing-in-which-orac-does-stanislaw-burzynski-propagandist-eric-merola-a-favor/
======================================
“… 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:
——————————————————————
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
——————————————————————
Gorski, here’s:
——————————————————————
“the scientific rationale … to expect that (antineoplastons) might have antitumor activity”
� � � � � � � � � � � � � � � �
[1] 7/1971 Phenylacetic acid as potential therapeutic agent for treatment of HUMAN CANCER
� � � � � � � � � � � � � � � �
[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
——————————————————————
active peptides produce up to 97% inhibition of DNA synthesis and mitosis in neoplastic cells in tissue culture

� � � � � � � � � � � � � � � �
[3] 1990 AS2-1 (AS)
� � � � � � � � � � � � � � � �
2 / 14.5% – Complete Remission
——————————————————————
3 / 21%- Partial Remission
——————————————————————
7 / 50%- Stabilization of disease with objective improvement
——————————————————————
2 / 14.5% – Progression
——————————————————————
1st patient enrolled in Complete Remission 17 months and off treatment 16 months
� � � � � � � � � � � � � � � � �
[4] 4/1/1992 PHENYLACETATE-novel nontoxic inducer of TUMOR CELL differentiation
——————————————————————
Sodium PHENYLACETATE found to affect growth and differentiation of TUMOR CELLS in vitro at concentrations achieved in humans with no significant adverse effects
——————————————————————
Treatment of promyelocytic leukemia III.-60 cells resulted in rapid decline of myc oncogene expression followed by growth arrest and granulocyte differentiation
——————————————————————
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
——————————————————————
Conclusions:
——————————————————————
Sodium PHENYLACETATE is investigational new drug approved for human use by U.S. Food and Drug Administration
——————————————————————
drug already established as safe and effective in treatment of hyperammonemia (2-4); we propose use may be extended to CANCER preventation and therapy
� � � � � � � � � � � � � � � �
[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
——————————————————————
NaPA, which has an unpleasant odor, can be substituted by its pro-drug, sodium PHENYLBUTYRATE (NaPB), for oral administration
——————————————————————
Upon ingestion by humans, PHENYLBUTYRATE undergoes @-oxidation to PHENYLACETATE
——————————————————————
Both NaPA and NaPB already proved safe for the treatment of infants and adults
——————————————————————
It seems important therefore to further evaluate the clinical relevance of our experimental data
� � � � � � � � � � � � � � � �
[6] 5/1993 nontoxic differentiation inducer, sodium PHENYLACETATE (NaPA)
——————————————————————
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
� � � � � � � � � � � � � � � �
[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
——————————————————————
Systemic treatment of rats bearing intracranial GLIOMAS resulted in SIGNIFICANT TUMOR SUPPRESSION with no apparent toxicity to host
——————————————————————
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
� � � � � � � � � � � � � � � �
[8] 4/1/1994 Phenylacetate has recently been shown to suppress TUMOR growth and promote differentiation in experimental models
——————————————————————
phase I trial of PHENYLACETATE conducted in 17 patients with advanced solid TUMORS
——————————————————————
99% of PHENYLACETATE elimination was accounted for by conversion to PHENYLACETYLGLUTAMINE, which was excreted in the urine
——————————————————————
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
——————————————————————
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
� � � � � � � � � � � � � � � �
[9] 6/1/1994 PHENYLACETATE is naturally occurring plasma component that suppresses growth of TUMOR CELLS and induces differentiation in vitro
——————————————————————
Treatment with PHENYLACETATE extended survival … without associated adverse effects
——————————————————————
PHENYLACETATE, used at clinically achievable concentrations, prolongs survival of rats with MALIGNANT BRAIN TUMORS through induction of TUMOR differentiation
——————————————————————
role in treatment of BRAIN TUMORS and other CANCERS should be explored further
� � � � � � � � � � � � � � � �
[10] 9/1994 increasing incidence of melanoma and poor responsiveness of disseminated disease to conventional treatments call for development of new therapeutic approaches
——————————————————————
PHENYLACETATE, nontoxic differentiation inducer, can suppress growth of other NEUROECTODERMAL TUMORS, i.e., GLIOMAS, in laboratory models and HUMANS
——————————————————————
finding led us to explore efficacy of PHENYLACETATE and related aromatic fatty acids in MELANOMA
——————————————————————
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
——————————————————————
in vitro ANTITUMOR activity observed with nontoxic, pharmacologic concentrations of PHENYLACETATE and PHENYLBUTYRATE, suggesting potential clinical use of drugs in treatment of MELANOMAS
� � � � � � � � � � � � � � � �
[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
——————————————————————
Using the LA-N-5 cell line, we have determined that NaPA can stimulate the differentiation of neuroblastoma cells …
——————————————————————
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
� � � � � � � � � � � � � � � �
[12] 4/1995 (3/8/2013) PHENYLACETATE, an inducer of tumor cytostasis and differentiation, shows promise as relatively nontoxic antineoplastic agent
——————————————————————
PHENYLBUTYRATE, an odorless compound that also has activity in TUMOR models
� � � � � � � � � � � � � � � �
[13] 5/1995 Antineoplaston (Ap), new ANTITUMOR agent, clinically tested for effects on MALIGNANT BRAIN TUMORS
——————————————————————
1 – medulloblastoma
1 – pontine glioma
2 – anaplastic astrocytoma
2 – metastatic brain tumor
3 – glioblastoma (G,B)

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

——————————————————————
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

——————————————————————
Effects of Ap on malignant brain tumors considered due to synergy, since administered with other drugs and acceleration of tumor cellular differentiation
——————————————————————
Ap useful as approach to remission maintenance therapy for brain tumors
� � � � � � � � � � � � � � � �
[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
——————————————————————
1 – refractory malignant glioma had partial response
——————————————————————
1 – hormone-independent prostate cancer achieved 50% decline in prostate specific antigen level, maintained 1 month
——————————————————————
High grade GLIOMAS and advanced prostate cancer are reasonable targets for Phase II clinical trials
� � � � � � � � � � � � � � � �
[15] 7/1995 aromatic fatty acids phenylacetate (PA) and phenylbutyrate (PB) induce tumour cell differentiation in experimental models and currently in clinical trials
——————————————————————
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
——————————————————————
Accumulating evidence has linked elevated ras expression with disease progression and FAILURE of TUMORS to RESPOND to CONVENTIONAL THERAPIES, including radiotherapy and certain chemotherapies
——————————————————————
observations led us to investigate response of ras-transformed cells to differentiation-inducer PHENYLACETATE (PA)
——————————————————————
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
——————————————————————
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
——————————————————————
ANTI-TUMOR ACTIVITY of PA was observed in cases involving either Ha- or Ki-ras and was independent of mode of oncogene activation
——————————————————————
Interestingly, in contrast to their relative resistance to radiation and doxorubicin, ras-transformed cells were significantly more sensitive to PA than their parental cells
——————————————————————
profound changes in TUMOR CELL and molecular biology were associated with reduced isoprenylation of ras-encoded p21
——————————————————————
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
————————————————————
PHENYLACETATE decreased transforming growth factor (TGF)-beta 2 production by medulloblastoma Daoy cells
————————————————————
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
————————————————————
slowly metabolized fatty acid alters tumor cell lipid metabolism causing … inhibition of protein prenylation critical to MALIGNANT growth
————————————————————
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
——————————————————————
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
——————————————————————
Antineoplaston A-10 oral formulation
14 – patients
A-10 injectable formulation
25 – patients

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

——————————————————————
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

——————————————————————
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

——————————————————————
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%
——————————————————————
No increase in size of tumor for more than 3 months:
8 / 17.4%

——————————————————————
Mean survival time of patients SIGNIFICANTLY LONGER than patients with tumors showing progressive increasing
——————————————————————
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

————————————————————
used at pharmacologically attainable concentrations … compounds induced profound cytostasis and LOSS of MALIGNANT PROPERTIES
————————————————————
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
————————————————————
PA’s GROWTH-INHIBITORY effects on a variety of cell lines
————————————————————
PA MARKEDLY DECREASED rat PROSTATIC GROWTH and ductal morphogenesis at concentrations that have previously been well tolerated in patients
————————————————————
Synthesis of DNA also significantly decreased per organ with PA
————————————————————
In common with earlier studies, we found PA INHIBITS PROSTATIC GROWTH
————————————————————
studies indicate there may be role for PA in treating BPH or elucidating mechanisms
� � � � � � � � � � � � � � � �
[22] 1996
Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which CONTROL NEOPLASTIC GROWTH

——————————————————————
These metabolites are water soluble and have ANTITUMOR EFFECT, they are further degraded to PHENYLACETIC acid
——————————————————————
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
——————————————————————
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
——————————————————————
We report effects of Antineoplaston A10 and AS2-1 on cell proliferation, cell morphology, cell cycle, and DNA in human hepatocellular carcinoma cell lines
——————————————————————
BOTH AGENTS INHIBITED CELL PROLIFERATION and increased number of cells in G0 and G1 phases and Antineoplaston AS2-1 induced APOPTOSIS
——————————————————————
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
————————————————————
studies using HUMAN PROSTATIC CARCINOMA, MELANOMA, and GLIOBLASTOMA cell lines showed a tight correlation between drug-induced cytostasis …
————————————————————
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
————————————————————
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
————————————————————
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 …
————————————————————
induction of p21WAF1/CIP1 mRNA by PA independent of cellular p53 status
————————————————————
PA effectively induced p21WAF1/CIP1 mRNA and growth inhibition of wild-type mouse embryonal fibroblasts
————————————————————
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
————————————————————
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
————————————————————
Both compounds induced cytostasis and maturation of multidrug-resistant BREAST, OVARIAN, and COLON CARCINOMA CELLS with no significant effect on cell viability
————————————————————
MDR cells generally more sensitive to GROWTH ARREST by PA and PB than parental counterparts
————————————————————
PA and PB potentiated the cytotoxic activity of doxorubicin against MDR cells
————————————————————
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
� � � � � � � � � � � � � � � �
[27] 8/1997 aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB) are novel ANTITUMOR AGENTS currently under clinical evaluation
————————————————————
ability to induce TUMOR differentiation in laboratory models and low clinical toxicity profile makes them promising candidates for COMBINATION with CONVENTIONAL THERAPIES
————————————————————
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
————————————————————
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
————————————————————
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
——————————————————————
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)
——————————————————————
2 patients have continued to be in good condition for more than 2 years without limitation of normal activities
——————————————————————
Antineoplaston AS2-1 may be effective and useful as maintenance agent after TAE and MCN in patients with liver cancer
� � � � � � � � � � � � � � � �
[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
————————————————————
Based on findings, NaPA and NaPB entered clinical trials at NATIONAL CANCER INSTITUTE
————————————————————
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
——————————————————————
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
——————————————————————
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
——————————————————————
Possible use of this combination for induction therapy in advanced cancer
� � � � � � � � � � � � � � � �
[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
——————————————————————
2 cases of advanced HCC treated with antineoplaston A10 I
——————————————————————
Both cases showed interesting responses to antineoplaston A10 I
——————————————————————
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
——————————————————————
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 …
————————————————————
Adult patients
————————————————————
43 – enrolled 12/1994-12/ 1996
40 – assessable
————————————————————
Reversible symptoms
————————————————————
fatigue
somnolence
were primary toxicities
————————————————————
only mild hematologic toxicity
————————————————————
30 / 75% – failed treatment within 2 months
————————————————————
7 / 17.5% – stable disease
————————————————————
3 – 7.5% – response defined as more than 50% reduction in tumor
————————————————————
Median time to treatment failure
————————————————————
2 months
————————————————————
35 – died
————————————————————
median survival
————————————————————
8 months
————————————————————
PHENYLACETATE HAS LITTLE ACTIVITY at this dose schedule in PATIENTS with RECURRENT MALIGNANT GLIOMA
————————————————————
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
——————————————————————
data suggest strong inverse association of urinary antineoplaston A-10 level with breast cancer
————————————————————
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
—————————————————————
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
—————————————————————
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
—————————————————————
“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
————————————————————
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
——————————————————————
Mutant p53 gene or malfunctioning p53 protein found in more than 50% of cancer cells impedes DNA repair or apoptosis induction
——————————————————————
May be why some cancers gain resistance to chemotherapy and radiation and become more resistant after frequent cancer treatments
——————————————————————
non-toxic p53 gene activator would induce cancer cell apoptosis and help damaged cancer cells to recover
——————————————————————
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
——————————————————————
Strategy would be most efficient for remission induction and maintenance CANCER therapy
——————————————————————
Antineoplastons are naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH
——————————————————————
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
——————————————————————
Agents thought to be good candidates for clinically easily applicable non-toxic p53 gene activators
——————————————————————
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
——————————————————————
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
——————————————————————
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
——————————————————————
2 patients in stage I showed LONGER RECURRENCE-FREE INTERVALS than those in more advanced stages
——————————————————————
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
——————————————————————
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
——————————————————————
Antineoplaston A10 given intravenously, followed by oral antineoplaston AS2-1
——————————————————————
Computed tomography scans done 1 and 4 years after initial diagnosis showed recurrent tumors
——————————————————————
Patient underwent 2nd and 3rd microwave ablation of recurrent tumors, and has survived for nearly 8 years WITHOUT SUFFERING ANY SERIOUS ADVERSE EFFECTS
——————————————————————
Currently FREE FROM CANCER
——————————————————————
Demonstrates potential effectiveness of NONTOXIC ANTITUMOR AGENT, antineoplastons, for controlling liver metastases from colon cancer
� � � � � � � � � � � � � � � �
======================================
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
——————————————————————
Pg. 92
——————————————————————
Antineoplaston A10 and AS2-1 are synthetic derivatives of phenylacetate (PN) acid, glutamine and isoglutamine
——————————————————————
A10 is sterile solution of sodium phenylacetylisoglutiminate (isoPG) in 4 : 1 ratio
——————————————————————
Antineoplaston AS2-1 is sterile solution of sodium phenylacetate (PN) and phenylacetylglutaminate (PG) in 4 : 1 ratio
——————————————————————
Pg. 93
======================================
combination of antineoplaston A10 and AS2-1 used instead of single drugs
——————————————————————
Based on previous observations, combination treatment has provided better results than single drugs
——————————————————————
Pg. 97
——————————————————————
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
——————————————————————
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
——————————————————————
[22-25]
——————————————————————
Initial clinical studies with antineoplaston therapy included testing of separate ingredients phenylacetate (PN) (antineoplaston AS5) and phenylacetylglutaminate (PG) (antineoplaston AS2-5)
——————————————————————
[26-28]
——————————————————————
studies failed to show marked anticancer activity of phenylacetate (PN) in malignant glioma, confirmed by phase II study by North
——————————————————————
Pg. 99
——————————————————————
American Brain Tumor Consortium
——————————————————————
[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
——————————————————————
[31]
——————————————————————
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
——————————————————————
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
� � � � � � � � � � � � � � � �
[41] 8/2005 Antineoplastons such as A10 include naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH OF CELLS
——————————————————————
Findings indicate antineoplaston A10 ANTITUMOR EFFECT could be utilized as effective therapy for breast cancer patients
� � � � � � � � � � � � � � � �
[42] 2006 Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which CONTROL NEOPLASTIC GROWTH
——————————————————————
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
——————————————————————
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
� � � � � � � � � � � � � � � �
[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
——————————————————————
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
� � � � � � � � � � � � � � � �
[44] 10/1/2010 As degradation product of Antineoplaston A10 in vivo, PHENYLACETYL GLUTAMINE showed ANTITUMOR ACTIVITIES
——————————————————————
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%
——————————————————————
results revealed it might become potential PET imaging agent for DETECTING TUMORS
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References:
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[1] 7/1971
� � � � � � � � � � � � � � � �
Neish, W. J. P. Phenylacetic acid as a potential therapeutic agent for the treatment of HUMAN CANCER. Experientia (Basel), 27: 860-861, 1971
http://www.ncbi.nlm.nih.gov/pubmed/5139518/
Experientia. 1971 Jul;27(7):860-1
http://www.ncbi.nlm.nih.gov/m/pubmed/5139518/
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[2] 1976
� � � � � � � � � � � � � � � �
Biological active peptides in human urine: III. Inhibitors of the growth of human leukemia, osteosarcoma, and HeLa cells
http://www.ncbi.nlm.nih.gov/m/pubmed/1066715
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
http://www.ncbi.nlm.nih.gov/pubmed/2152694/
Drugs Exp Clin Res. 1990;16(7):361-9
http://www.ncbi.nlm.nih.gov/m/pubmed/2152694/
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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
http://www.ncbi.nlm.nih.gov/m/pubmed/1372534/
Cancer Res 1992;52:1988-1992
http://m.cancerres.aacrjournals.org/content/52/7/1988.abstract
Cancer Res April 1, 1992 52; 1988v I
http://cancerres.aacrjournals.org/content/52/7/1988
Cancer Res. 1992 Apr 1;52(7):1988-92
http://m.cancerres.aacrjournals.org/content/52/7/1988.full.pdf
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
http://m.cancerres.aacrjournals.org/content/52/7/1988.full.pdf#page=1
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
� � � � � � � � � � � � � � � �
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
� � � � � � � � � � � � � � � �
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
� � � � � � � � � � � � � � � �
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
� � � � � � � � � � � � � � � �
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
� � � � � � � � � � � � � � � �
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
http://www.ncbi.nlm.nih.gov/m/pubmed/7488244/
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
http://www.ncbi.nlm.nih.gov/pubmed/8667595
Tsuda H
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://www.ncbi.nlm.nih.gov/m/pubmed/8667595
Burzynski References: 1 – 3 and 5
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_article
Nishida et al. (Japan) A-10 Reference: 4 and 7
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_article/references
Muldoon et al. A-10 Reference: 6
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_pdf
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[20] 2/1996
� � � � � � � � � � � � � � � �
Lipid metabolism as a target for BRAIN CANCER therapy:
Synergistic activity of lovastatin and sodium PHENYLACETATE against human glioma cells
http://www.ncbi.nlm.nih.gov/pubmed/8592143/
J Neurochem 66:710-716, 1996
http://www.ncbi.nlm.nih.gov/m/pubmed/8592143/
J Neurochem. 1996 Feb;66(2):710-6.
http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.1996.66020710.x/abstract
DOI: 10.1046/j.1471-4159.1996.66020710.x
http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.1996.66020710.x/abstract;jsessionid=913EBF64F1FA2FD0D08BD94FDDE391D5.d03t01
Article first published online: 23 NOV 2002
http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.1996.66020710.x/abstract;jsessionid=E929EA030144CC973FECF4DAA1D9D50C.d01t04
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland, USA
Prasanna P, Thibault A, Liu L, et al: (SAMID D)
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[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
http://www.ncbi.nlm.nih.gov/m/pubmed/8627880/
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
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[22] 1996
� � � � � � � � � � � � � � � �
Inhibitory effect of antineoplaston A10 and AS2-1 on human hepatocellular carcinoma
Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/pubmed/8755117
Kurume Med J. 1996;43(2):137-47
http://www.ncbi.nlm.nih.gov/m/pubmed/8755117
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article
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
http://www.ncbi.nlm.nih.gov/m/pubmed/8759039/
Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD, USA
http://www.sciencedirect.com/science/article/pii/0006295296003401
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[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
http://www.ncbi.nlm.nih.gov/m/pubmed/8827086/
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
http://www.ncbi.nlm.nih.gov/m/pubmed/8959328/
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
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[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
http://www.ncbi.nlm.nih.gov/pubmed/9816242/
Clin Cancer Res. 1996 May;2(5):865-72
http://www.ncbi.nlm.nih.gov/m/pubmed/9816242/
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
http://www.ncbi.nlm.nih.gov/pubmed/9269314/
Int J Radiat Biol. 1997 Aug;72(2):211-8
http://www.ncbi.nlm.nih.gov/m/pubmed/9269314/
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
http://www.ncbi.nlm.nih.gov/pubmed/21590224
Oncol Rep. 1997; 4:1213- 1216
http://www.ncbi.nlm.nih.gov/m/pubmed/21590224
Oncol Rep. 1997 Nov-Dec;4(6):1213-6
http://www.spandidos-publications.com/or/4/6/1213
Oncol Rep 4 (6):1213-6 (1997)
Oncology Reports
4 (6):1213-6
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
http://www.ncbi.nlm.nih.gov/pubmed/9547596
Adv Exp Med Biol (1997), PMID.9547596
http://www.ncbi.nlm.nih.gov/m/pubmed/9547596
Adv Exp Med Biol. 1997;400A:501-5
http://link.springer.com/chapter/10.1007%2F978-1-4615-5325-0_67
DOI
10.1007/978-1-4615-5325-0_67
http://link.springer.com/content/pdf/10.1007%2F978-1-4615-5325-0_67.pdf
Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury 2
Advances in Experimental Medicine and Biology Volume 400, 1997, pp 501-505
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD USA
D D SAMID, W R WR Hudgins, … C E CE Myers
� � � � � � � � � � � � � � � �
[30] 5 – 6/1998
� � � � � � � � � � � � � � � �
Quick response of advanced cancer to chemoradiation therapy with antineoplastons
H Tsuda A10 and AS2-1 – I
http://www.ncbi.nlm.nih.gov/pubmed/9538158
Oncol. Rep. 1998;5:597–600
http://www.ncbi.nlm.nih.gov/m/pubmed/9538158
Oncol Rep. 1998 May-Jun;5 (3):597-600
http://www.spandidos-publications.com/or/5/3/597
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
http://www.ncbi.nlm.nih.gov/pubmed/9769368
Oncol Rep. 1998;5:1363-1367
http://www.ncbi.nlm.nih.gov/m/pubmed/9769368
Oncol Rep. 1998 Nov-Dec;5 (6):1363-7
http://www.spandidos-publications.com/or/5/6/1363
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:
a North American Brain Tumor Consortium report
http://www.ncbi.nlm.nih.gov/pubmed/10071293/
J Clin Oncol. 1999 Mar;17(3):984-90
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J Clin Oncol 17(3):984-90 (1999), PMID.10071293
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S M Chang, J G Kuhn, … M D Prados
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[33] 7/3/2000
� � � � � � � � � � � � � � � �
(A10) – Potential utility of antineoplaston A-10 levels in breast cancer
http://www.ncbi.nlm.nih.gov/pubmed/10814881
Cancer Lett 155:67-70, 2000
http://www.ncbi.nlm.nih.gov/m/pubmed/10814881
Cancer Lett 155(1):67-70 (2000)
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Cancer Lett. 2000 Jul.3;155(1):67-70
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DOI: 10.1016/S0304-3835(00)00408-0
http://www.sciencedirect.com/science/article/pii/S0304383500004080
Cancer Letters, Elsevier Science
Department of Pharmacognosy, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

� � � � � � � � � � � � � � � �
[34] 8/31/2000
� � � � � � � � � � � � � � � �
Immune modulatory potentials of antineoplaston A-10 in breast cancer patients
http://www.ncbi.nlm.nih.gov/pubmed/10893443
Cancer Lett 157: 2000
http://www.ncbi.nlm.nih.gov/m/pubmed/10893443
Cancer Lett 157 (1):57-63 (2000)
http://www.cancerletters.info/article/S0304-3835(00)00472-9/abstract
Cancer Lett. 2000 Aug.31;157(1):57-63
http://www.sciencedirect.com/science/article/pii/S0304383500004729
(Cancer Lett., 2000, 157, 57)
http://dr-labouzeid.webs.com/A10-Cancer%20Letters%20157.pdf
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
http://www.ncbi.nlm.nih.gov/pubmed/11199474
333 (12):431-4 (2000)
http://www.ncbi.nlm.nih.gov/m/pubmed/11199474
DOI: 10.1002/1521-4184(200012)333:123.0.CO;2-M
http://onlinelibrary.wiley.com/doi/10.1002/1521-4184(200012)333:12%3C431::AID-ARDP431%3E3.0.CO;2-M/abstract
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
http://www.ncbi.nlm.nih.gov/pubmed/11489804
Clin Cancer Res 7(8):2292-300 (2001), PMID.11489804
http://www.ncbi.nlm.nih.gov/pubmed/11489804
Clin Cancer Res. 2001 Aug;7(8):2292-300
http://m.clincancerres.aacrjournals.org/content/7/8/2292.long
J Gilbert, S D Baker, … M A Carducci
SAMID References: 2-3, 5-6, 15 and 22
� � � � � � � � � � � � � � � �
[37] 2002
� � � � � � � � � � � � � � � �
A novel strategy for remission induction and maintenance in cancer therapy
H Tsuda A10 and AS2-1
http://www.ncbi.nlm.nih.gov/pubmed/11748457
Oncol Rep 2002;9:65–8
http://www.ncbi.nlm.nih.gov/m/pubmed/11748457
Oncol. Rep. 2002;9:65-68
http://www.spandidos-publications.com/or/9/1/65
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
http://www.ncbi.nlm.nih.gov/pubmed/12579278
Oncol Rep. 2003 Mar-Apr;10(2):391-7
http://www.ncbi.nlm.nih.gov/m/pubmed/12579278
Oncol Rep. 2003;10:391-397
http://www.spandidos-publications.com/or/10/2/391
Spandidos Publications
http://www.burzynskiclinic.com/images/stories/Publications/964.pdf
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
http://www.ncbi.nlm.nih.gov/pubmed/12768372
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
http://www.springerlink.com/content/b48ch3ha165nbrqp
Surg Today. 2003;33(6):448-53
http://link.springer.com/article/10.1007%2Fs10595-002-2503-2
Surg Today 2003; 33:448–53
http://link.springer.com/content/pdf/10.1007%2Fs10595-002-2503-2
Surg Today. 2003; 33:448-453
http://link.springer.com/article/10.1007%2Fs10595-002-2503-2?LI=true
33 (6):448-53
http://link.springer.com/content/pdf/10.1007%2Fs10595-002-2503-2
Surgery Today, Springer
http://sciencelinks.jp/j-east/article/200313/000020031303A0389449.php
Surg Today 2003
http://sciencelinks.jp/j-east/article/200313/000020031303A0389449.php
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
� � � � � � � � � � � � � � � �
[40] 2003
� � � � � � � � � � � � � � � �
http://www.ncbi.nlm.nih.gov/pubmed/12718563
——————————————————————
Drugs in R and D
——————————————————————
http://www.ncbi.nlm.nih.gov/m/pubmed/12718563
——————————————————————
(Drugs in Research and Development)
——————————————————————
http://www.burzynskiclinic.com/images/stories/Publications/960.pdf
——————————————————————
Drugs R D. 2003;4(2):91-101
Drugs in R&D 2003;4:91-101
——————————————————————
Pg. 100
======================================
[22] Tsuda H, Hara H, Eriguchi N, et al. Inhibitory effect of antineoplaston A10 on breast cancer transplanted to athymic mice and human hepatocellular carcinoma cell lines. Kurume Med J 1990; 37: 97-104
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[23] Wood J, Copland JA, Muldoon TG, et al. 3-phenylacetylamino-2, 6-piperidinedione inhibition of rat Nb2 lymphoma cell mitogenesis. Proc Soc Exp Biol Med 1991; 197: 404-8
——————————————————————
[24] Xu-W, Yu R, Gao C, et al. The preliminary antitumor assay of antineoplaston A10 against the s180 and the effects of cAMP levels in tumor and liver tissues of mice. Adv Exp Clin Chemother 1988; 2: 41-4
——————————————————————
[25] Hashimoto K, Kogo T, Shintomi Y, et al. The anticancer effect of antineoplaston A10 on human breast cancer serially transplanted to athymic mice. Nippon Gan Chiryo Gakkai Shi 1990; 25: 1-5
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[28] Burzynski SR. Potential of antineoplastons in diseases of old age. Drugs Aging 1995; 7: 157-67
======================================
[29] Chang SM, Kuhn JG, Robins HI, et al. Phase II study of phenylacetate in patients with recurrent malignant glioma: a North American Brain Tumor Consortium Report. J Clin Oncol 1999; 17: 984-90
======================================
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[31] Burzynski SR. Efficacy of antineoplastons A10 and AS2-1. Mayo Clin Proc 1999; 74: 641-2
� � � � � � � � � � � � � � � �
[41] 8/2005
� � � � � � � � � � � � � � � �
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
http://www.ncbi.nlm.nih.gov/m/pubmed/16012735
Antineoplaston induces G(1) arrest by PKCalpha and MAPK pathway in SKBR-3 breast cancer cells
http://www.spandidos-publications.com/or/14/2/489
Oncol Rep. 8/2005; 14(2):489-94
http://gyouseki.kurume-u.ac.jp/PDF/ichiran_2005.pdf
Oncol Rep 14(2):489-94 (2005)
http://research.kurume-u.ac.jp/K90RES.php?scode=49485632873864
Oncol Rep. 2005; 14:489–94
http://onlinelibrary.wiley.com/doi/10.1002/iub.574/abstract
Oncol. Rep. 14, 489–494
http://onlinelibrary.wiley.com/doi/10.1002/iub.574/full
Oncology Reports, 8/2005, Volume 14 Number 2
Pages: 489-494
http://onlinelibrary.wiley.com/store/10.1002/iub.574/asset/574_ftp.pdf?v=1&t=hbr9z60q&s=0b1c1e8655db9c54b45dbf72062e8b11cb7895ac
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
Tsuda H, et al
http://www.ncbi.nlm.nih.gov/pubmed/8755117
Kurume Med J. 1996;43(2):137-47
http://www.ncbi.nlm.nih.gov/m/pubmed/8755117
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article
Kurume Medical Journal
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_pdf
� � � � � � � � � � � � � � � �
[43] 1/2008
� � � � � � � � � � � � � � � �
Preclinical studies of molecular-targeting diagnostic and therapeutic strategies against breast cancer
http://www.ncbi.nlm.nih.gov/pubmed/18224398
antineoplaston
http://www.ncbi.nlm.nih.gov/m/pubmed/18224398
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
� � � � � � � � � � � � � � � �
[44] 10/2010
� � � � � � � � � � � � � � � �
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
� � � � � � � � � � � � � � � �

Burzynski – The Antineoplaston Randomized Japan Phase II Clinical Trial Study

Burzynski – The Antineoplaston Randomized Japan Phase II Clinical Trial Study

Randomized Phase II Study of Hepatic Arterial Infusion with or without Antineoplastons as Adjuvant Therapy after Hepatectomy for liver Metastases from Colorectal Cancer

Annals of Oncology 2010;21:viii221
http://www.burzynskiclinic.com/images/stories/Publications/8774.pdf

http://oncologypro.esmo.org/meeting-resources/meeting-abstracts/european-society-for-medical-oncology-esmo-2010/randomized-phase-ii-study-of-hepatic-ar-3558.aspx

http://abstracts.webges.com/viewing/view.php?congress=esmo2010&congress_id=296&publication_id=3558

11. Antineoplaston Therapy Doubles 5-Year Survival Rate Following Curative Resection of Hepatic Mets (May 27/09)
Positive results borne from PHASE II clinical study of ANTINEOPLASTON therapy (ANP therapy) in metastatic colon cancer following curative resection of liver mets

study performed in Japan

study consisted of 65 colon cancer patients who had undergone curative resection of liver mets and were randomized to one of following groups:

1. infusion of X

2. infusion of X plus IV ANP therapy

There was significant difference in overall survival between the 2 groups

5 year survival rate:
X plus ANP therapy arm – 63% vs.
X only arm – 32%

Recurrence rate differed for the 2 groups
34%
69%

Lead investigator claims ANP therapy may find application not only in treatment of brain tumors as reported previously, but also in more common colorectal cancer
http://finance.yahoo.com/news/Metastatic-Colon-Cancer-In-a-bw-15355368.html?.v=1

http://www.colorectal-cancer.ca/IMG/pdf/CCAC_Research_June_19_2009.pdf

ANTINEOPLASTON Therapy Doubles 5-Year Survival Rate Following Curative Resection of Hepatic Mets

Randomized Phase II Study of Hepatic Arterial Infusion with or without Antineoplastons as Adjuvant Therapy after Hepatectomy for Liver Metastases from Colorectal Cancer
http://oncologypro.esmo.org/meeting-resources/meeting-abstracts/european-society-for-medical-oncology-esmo-2010/randomized-phase-ii-study-of-hepatic-ar-3558.aspx

Publication date: May 17, 2010
Category: Colorectal cancer
Publisher: ESMO
Y. Ogata; K. Shirouzu; K. Matono; M. Ushijima; S. Uchida; H. Tsuda
http://abstracts.webges.com/viewing/view.php?congress=esmo2010&congress_id=296&publication_id=3558

Abstract: 3558
Congress: ESMO 2010
Type: Publication
Topic: Colorectal cancer
Authors: Y. Ogata, K. Shirouzu, K. Matono, M. Ushijima, S. Uchida, H. Tsuda; Kurume/JP
http://www.biomeddefine.com/sdx/t31/all/100/epithelial+neoplasm+glandular+piperidines+chemical+ingredient.html

http://www.biomeddefine.com/sdx/t31/all/100/ca+secondary+cancer+piperidines+chemical+ingredient.html

Antineoplaston Therapy Doubles Five-Year Survival Rate Following Curative Resection of Hepatic Mets

Metastatic Colon Cancer:

In a Randomized Phase II Clinical Study, Antineoplaston Therapy Doubled the 5-Year Survival Rate Following Curative Resection of Hepatic Metastases
http://www.drugs.com/clinical_trials/metastatic-colon-cancer-randomized-phase-ii-clinical-study-antineoplaston-therapy-doubled-5-year-7307.html

HOUSTON–(BUSINESS WIRE)–May 27, 2009 – The Burzynski Research Institute, Inc.

(BRI) is pleased to announce the results of a RANDOMIZED Phase II clinical study of ANTINEOPLASTON therapy (ANP therapy) in metastatic colon cancer following curative resection of hepatic metastases

study was performed at Kurume University School of Medicine (Japan) Department of Surgery

A report of the study results is currently in press
http://oncologypro.esmo.org/meeting-resources/meeting-abstracts/european-society-for-medical-oncology-esmo-2010/randomized-phase-ii-study-of-hepatic-ar-3558.aspx

http://abstracts.webges.com/viewing/view.php?congress=esmo2010&congress_id=296&publication_id=3558

3 – 4/2003 – ANTINEOPLASTON AS2-1 – Japan
http://www.ncbi.nlm.nih.gov/m/pubmed/12579278
The preventive effect of ANTINEOPLASTON AS2-1 on HCC recurrence

We designed a PHASE II clinical trail to clarify whether ANTINEOPLASTON AS2-1 … prolongs the recurrence-free interval of HCC patients who undergo frequent treatments for recurrence

10 patients enrolled in trial

2 in stage I
6 in stage II
1 in stage III
1 in stage IV-B

10 patients experienced 35 recurrence-free intervals

Recurrence-free intervals during ANTINEOPLASTON AS2-1 administration were significantly longer than those without ANTINEOPLASTON AS2-1 …

Patients who experienced recurrence-free intervals with and without ANTINEOPLASTON AS2-1 showed longer intervals during ANTINEOPLASTON AS2-1 administration than those before and after ANTINEOPLASTON AS2-1 administration …

2 patients in stage I showed longer recurrence-free intervals than those in more advanced stages

… ANTINEOPLASTON AS2-1 … prolonged the recurrence-free interval between regional treatments and improved survival rate of these patients

Tsuda H, Sata M, Kumabe T, Uchida M, Hara H

Department of Anesthesiology, Kurume Daiichi Social Insurance Hospital, Kushihara Kurumeshi, Fukuoka, Japan

Oncol Rep. 2003 Mar-Apr;10(2):391-7
http://www.spandidos-publications.com/or/10/2/391

http://www.burzynskiclinic.com/images/stories/Publications/964.pdf
References:

3. 1976 – BURZYNSKI – ANTINEOPLASTONS
BURZYNSKI SR
ANTINEOPLASTONS;
Biochemical defense against cancer
Physiol Chem Phys 8: 275-279, 1976

4. 1996 – ANTINEOPLASTON A10 and AS2-1 – Japan
Tsuda H, Hara H, Eriguchi N, et al
Toxicology study on ANTINEOPLASTON A10 and AS2-1 in cancer patients
Kurume Med J 42: 241-246, 1996

12. 1987 – BURZYNSKI – ANTINEOPLASTON A10
Hendry LB, Muldoon TG, BURZYNSKI SR, et al
Stereochemical modelling studies of the interaction of ANTINEOPLASTON A10 with DNA
Drugs Exp Clin Res 1: 77-81, 1987

14. 1992 – SAMID (learned from BURZYNSKI)
Samid D, Shack S, and Sherman LT
Phenylacetate:
A novel nontoxic inducer of tumor cell differentiation
Cancer Res 52: 1988-1992, 1992

15. 1989 – BURZYNSKI

16. 1992 – ANTINEOPLASTON A10 – Japan

17. 1996 – ANTINEOPLASTON A10 and AS2-1 – Japan
Tsuda H, Iemura A, Sata M, et al
Inhibitory effect of ANTINEOPLASTON A10 and AS2-1 on human hepatocellular carcinoma cells
Kurume Med J 43: 137-47, 1996

19. 1998 – ANTINEOPLASTONS – Japan

20. 2002 – Japan

PUBLICATIONS BY S.R. BURZYNSKI AND ASSOCIATES (NOT INCLUDING PUBLICATIONS BEFORE 2002)
http://www.burzynskiclinic.com/scientific-publications.html

1996 – ANTINEOPLASTON A10 and AS2-1 – Japan
http://www.ncbi.nlm.nih.gov/m/PubMed/8755117
Inhibitory effect of ANTINEOPLASTON A10 and AS2-1 on human hepatocellular carcinoma cells

ANTINEOPLASTONS, first described by Burzynski …

ANTINEOPLASTON A10 is the first chemically identified ANTINEOPLASTONS

These metabolites are water soluble and have ANTITUMOR effect …

The mixture of phenylacetylglutamine and phenylacetic acid in the ratio of 1 to 4 was also shown to have ANTITUMOR effect in tissue culture study, then formulated as ANTINEOPLASTON AS2-1

The 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 the treatment of human hepatocellular carcinoma since this tumor recurs frequently despite initial successful treatment

Tsuda H, Iemura A, Sata M, Uchida M, Yamana K, Hara H.

Kurume University School of Medicine, Japan

1) Departments of Anesthesiology
2) Departments of Pathology
3) Departments of Medicine
4) Departments of Radiology
5) Departments of Surgery

Released 2009/08/11

Kurume Med J. 1996;43(2):137-47

The Kurume Medical Journal
https://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article
PDF:
https://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_pdf
References:
https://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article/references
1. 1976 – BURZYNSKI – ANTINEOPLASTON
BURZYNSKI SR
ANTINEOPLASTON;
Biochemical defense against cancer
Physiol Chem Phys 1976; 8:275-279

2. 1985 – BURZYNSKI – ANTINEOPLASTON A10
BURZYNSKI SR, and Hai TT
ANTINEOPLASTON A10
Drugs of the Future 1985; 10:103-105

3. 1986 – BURZYNSKI – ANTINEOPLASTON AS2-1 and AS2-5
BURZYNSKI SR, Mohabbat MO, and Lee SS
Preclinical studies of ANTINEOPLASTON AS2-1 and ANTINEOPLASTON AS2-5
Drugs Exp Clin Res 1986 (Suppl); 1:25-28

4. 1988 – JAPAN – ANTINEOPLASTON A10
Eriguchi N, Hara H, Yoshida H, Nishida H, Nakayama T et al.
Chemopreventive effect of ANTINEOPLASTON A10 on Urethane-induced pulmonary neoplasia in mice
J Jpn Soc Cancer Ther 1988; 23 (7):1560-1565

5. 1987 – BURZYNSKI – ANTINEOPLASTON A10
Hendry LB, Muldoon TG, BURZYNSKI SR, Copland JA, and Lerner AF
Stereochemical modelling studies of the interaction of ANTINEOPLASTON A10 with DNA
Drugs Exp Clin Res 1987 (Suppl); 1:77-81

7. 1986 – BURZYNSKI
Liau MC, and BURZYNSKI SR
Altered methylation complex isozymes as selective targets for cancer chemotherapy
Drugs Exp Clin Res 1986 (Suppl); 1:77-86

8. 1988 – see 5. – ANTINEOPLASTON A10
Muldoon TG, Copland JA, and Hendry LB
Actions of ANTINEOPLASTON A10 on the genesis and maintenance of specific subpopulations of rodent mammary tumor cells
Advances in Experimental and Clinical Chemotherapy 1988; 1:15-18

10. 1991 – JAPAN – ANTINEOPLASTON A10
Nishida H, Yoshida H, Eriguchi N, Hoshino K, Kubota H et al.
Inhibitory effect of orally administered ANTINEOPLASTON A10 on the growth curve of human breast cancer transplanted to athymic mice
J Jpn Soc Cancer Ther 1991; 26:596-601

12. 1991 – SAMID (learned from BURZYNSKI)
Samid D, Yeh T-J and Shack S
Interferon in combination with antitumorigenic phenylderivatives; potentiation of INF alpha activity in vitro
Br J Haematol 1991; 79 (Suppl) 1:81-83

13. 1992 – SAMID (learned from BURZYNSKI)
Samid D, Shack S, and Sherman LT
Phenylacetate:
A novel nontoxic inducer of tumor cell differentiation
Cancer Research 1992; 52:1988-1992
http://europepmc.org/abstract/MED/8755117/reload=0;jsessionid=MhBwMcen2a7a9AibBaLc.2