A Message to Guy “Can’t Git-R-Done” Chapman

Guy “Crapman” Chapman is a SkeptiCoward©

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I’m NOT “Astroturfwatch” you twit
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“Guy” blogged another one of “The Skeptics™” #Fails [1]

He has a blog full of essentially misinformation, disinformation, misdirection, and lies regarding Burzynski, but the gist of it is that so far he has demonstrated to the entire world that he is that “Guy”, that “Yellow-Back” Chap, man, who has NOT demonstrated that he has the “Grapefruits”, to answer for his actions [2-4]

He claims my blog is “full of essentially incoherent commentary,” yet he offers NO explanation as to why it is that since its inception 2/14/2013, the Didymus Judas Thomas’ Hipocritical Oath Blog has had 9,626 visitors

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Where’s your stats, Guy ?

Lets “review” his latest piece of propaganda and Dezinformatsiya, shall we ?
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“The FDA approved a phase 3 trial, therefore Burzynski’s antineoplastons definitely work”
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#fail [5]

“[T]he emphasis in Phase 2 is on EFFECTIVENESS”

“Phase 3 studies begin if EVIDENCE of EFFECTIVENESS is shown in Phase 2″
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“The Lancet rejected publication of the sole paper known to have been sumbitted from the one completed phase 2 trial, therefore there is a global conspiracy to suppress Burzynski”
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#Fail [6]

Bob Blaskiewicz postulated during the Google+ Hangout on Saturday, that this is a generic, usual, normal course-of-business rejection letter

NO such example is on Al Gore’s Internet

Whose got one ?

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Even in a Tweet, everybody must include all caveats and the full body of knowledge with footnotes, or stand convicted of lying
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#FaiL

Do NOT post deceptive Twits:

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#faIL

@SceptiGuy, on 5/25/2013, what did you NOT understand about her 5/23/2013 Cease and Desist Tweet ?

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A trial at a reputable cancer center once took several years to complete and publish, therefore failure to complete and publish a single trial in 40 years means nothing
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#FaiL

So, does this mean you wanted Burzynski to publish the phase 2 clinical trial final results before the trials were finished ?
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“Failure to participate on a partisan blog means you refuse to debate”
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#FAil [7]

Is this just another one of “The Skeptics™” Red Herring’s you like to use ?

The About page on my blog is crystal clear:

“The decision is that he is neither guilty nor innocent doesn’t mean he doesn’t need to do work within his practice, and the FDA obviously needs to pursue things as well”

As I said on the Saturday Google+ Hangout, I consider myself to be a Skeptic Skeptic [8]

In other words, if you are going to be a true Skeptic, at least police yourself and “fact-check” before you insert foot-in-mouth and spread misinformation, disinformation, misdirection, and / or lies all over social media

Making lame excuses for NOT debating on my blog is like an atheist stating that they would NOT debate on Earth because creationists claim it was created by God
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“Failure to complete and publish trials is the single biggest reputational issue Burzynski has and it cannot be waved away or covered with a fig leaf of a single rejected paper”

“If you can’t understand why this is a problem, then we’re all wasting our time even talking to you”
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#FaIL [9]

YOUR failure to provide any citation(s), reference(s), and / or link(s) from the Declaration of Helsinki, United States Food and Drug Administration, National Cancer Institute (NCI) at the National Institutes of Health (NIH), or any other source to support your claim as to when you think Burzynski is required to publish, says it all
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“The average time from commencement of a trial to completion is 3-5 years”

“If a trial is going to be completed and published, very few take longer than 8 years to final publication”
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3/29/1996, then United States Food and Drug Administration Commissioner, David Kessler told the American people [10]:

2. The … FDA’s initiatives … will allow …the agency … to rely on smaller trials … fewer patients … if there is evidence … of partial response in clinical trials

A. What is the FDA’s definition of “smaller trials”?

B. What is the FDA’s definition of “fewer patients”?

Burzynski’s 2006 publication lists 1652 adults and 335 children (1,799 Total) [11]

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“A quick sample says that the first 60 of Burzynski’s phase 2 trials were all registered on the same day”

“1 November 1999, presumably following the consent decree which forbade him from administering antineoplastons outside of a registered clinical trial”
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fAil [11]

If you’re correct; which is rare, 3/29/1996, why did then US FDA Commissioner, David Kessler tell the American people [10]:

6. The uhh agency has … MANY … trials … has has approved trials … for patients … with antineoplastons ?

Why does Burzynski’s 11/25/1997 SEC Form 10-SB filing list 72 phase 2 clinical trials ? [12]

Could it be because you are wrong ?
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“The trial that completed, was finished in February 2005”
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Are you certain ? [13]

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“The single phase 3 trial is withdrawn”
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Guy, did you contact the National Cancer Institute (NCI) at the National Institutes of Health (NIH) like I did, where they advised me: “Not every cancer clinical trial taking place in the United States is listed on our NCI Clinical Trials Database” ? [14]
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“I do not choose to debate on DJT’s blog”
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Guy, can you see the yellow stripe down your back ?

(I won’t say “spine,” because you haven’t shown that you have one)
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“He has a long history of misrepresenting differences of opinion as evidence of deceit (e.g. his claim that 0/61 is evidence that I can’t count, rather than what tit is, brevity during a rapid exchange of suggested questions during a Google hangout, where the person to whom the suggestion is made, is fully aware of the full context of 0/1/61 published/complete/registered”
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Guy, why don’t you just PROVE IT ?

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#fAiL

Guy, hasn’t ONE been completed ?

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You wanted him to publish before the clinical trials were finished ?
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“So that kind of stuff is not the actions of an honest broker”
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Guy, what do you call all of your above FAILS?
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“I wouldn’t expect DJT to debate here, nor would I be interested in giving him a platform; am happy to debate in an open forum where there are comprehensible questions and some sort of moderation to prevent tactics such as the Gish gallop”
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Talk about “Gish galloping”

First you post: I wouldn’t expect DJT to debate here … “

and then you posted: ” … nor would I be interested in giving him a platform …”

which just shows that you were NOT sincere when you posted your 1st comment

What you are basically saying when you posted: ” … I am happy to debate in an open forum where there are comprehensible questions and some sort of moderation to prevent tactics such as the Gish gallop, is that you are NOT competent enough to call “Gish gallop” and prove it during any debate

You want “Mommy” to protect you from someone who is more intelligent than you are ?

That’s what I hear you saying
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“Sorry, your blog is not an “open forum” and the majority of what’s written there is gibberish”
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I understand you

My blog is meant for intelligent people who can grasp ideas, dry wit, and other concepts humans use to communicate with each other

Unfortunately, I take it you are NOT like the other 9,600* people who have visited my blog
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“I recommend you stop trying to satirise someone else’s style and instead write in your own words”
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Why would I take any advice from you ?

You’re one FAIL after another

I’ll satirize (and spell it correctly) that Ph.D. FAIL “Orac” all I want
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“And read them back, if necessary to a friend, so that you get the general air of “what the hell does that even mean?””

“knocked out of it”
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It’s readily apparent who needs to check them self

Because you act as if you’ve been “knocked out of it” for quite some time

Maybe you should wear a helmet
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“Twitter is about rapid-fire debate”
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What the problem is ?

“The Skeptics™” think Twitter is a “debate forum”, but you do NOT have the cranial capacity to “debate”

What “The Skeptics™” do is called “mental bastardization”
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“Don’t pretend that any statement is ever intended to be a nuanced and scientifically rigorous statement of the prevailing consensus view, because it isn’t, and it’s not pretending to be”
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As far as I’m concerned, the vast majority of your twits are “pretending”
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“It’s fair to ask for a source or a clarification, it’s grossly misleading to cherry-pick individual tweets and misrepresent a lack of detail as deliberate malfeasance”
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The FACT is, a plethora of your twittering has as its source, your posterior
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“That’s the kind of tactic that gets you ignored and dismissed as a mendacious time-sink; if that’s the image you’re striving for then fine but I don’t think it is”
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Everyone already knows what you are

Guy “Crapman”
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“There you go”
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I could NOT have said it better myself
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“And now, if you don’t mind, I will get on with other things”
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LIKE THIS ?

EXPLAIN THIS [15]

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Prove I spammed 🙂

Are you a man ?

Or are you a

SkeptiCoward© ?

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REFERENCES:
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[1] – 10/2013 – A Message to DJT
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http://t.co/Rd9CVSaKcq
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http://www.chapmancentral.co.uk/blahg/2013/10/a-message-to-a-djt/
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[2] – 3/24/2013 – Critiquing “Burzynski: Another fact-blind troll, who predicted that?”:
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https://stanislawrajmundburzynski.wordpress.com/2013/03/24/critiquing-burzynski-another-fact-blind-troll-who-predicted-that/
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[3] – 4/12/2013 – The dishonesty of Guy Chapman, “The Skeptics” shill:
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https://stanislawrajmundburzynski.wordpress.com/2013/04/12/the-dishonesty-of-guy-chapman-the-skeptics-shill/
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[4] – 5/5/2013 – guychapman (Guy Chapman) Critiquing “The Skeptic” Burzynski Critics: A Film Producer, A Cancer Doctor, And Their Critics (page 9):
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https://stanislawrajmundburzynski.wordpress.com/2013/05/05/guychapman-guy-chapman-critiquing-the-skeptic-burzynski-critics-a-film-producer-a-cancer-doctor-and-their-critics-page-9/
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[5] – 4/25/2013 – Burzynski: The FDA’s Drug Review Process: Ensuring Drugs Are Safe and Effective:
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https://stanislawrajmundburzynski.wordpress.com/2013/04/25/burzynski-the-fdas-drug-review-process-ensuring-drugs-are-safe-and-effective/
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[6] – 9/30/2013 – Bob Burzynski Skeptic Sez Multiforme Manuscript Meme Message Memorable:
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https://stanislawrajmundburzynski.wordpress.com/2013/09/30/bob-burzynski-skeptic-sez-multiforme-manuscript-meme-message-memorable/
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[7] – About | Didymus Judas Thomas’ Hipocritical Oath Blog
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https://stanislawrajmundburzynski.wordpress.com/about/
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[8] – 10/3/2013 – “The Skeptics™” Definition of “Debate”:
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https://stanislawrajmundburzynski.wordpress.com/2013/10/03/the-skeptics-definition-of-debate/
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[9] – 4/25/2013 – Burzynski: Declaration of Helsinki:
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https://stanislawrajmundburzynski.wordpress.com/2013/04/25/burzynski-declaration-of-helsinki/
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[10] – 6/8/2013 – WHAT IS MISDIRECTION? Critiquing “Antineoplastons: Has the FDA kept its promise to the American people ?”:
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https://stanislawrajmundburzynski.wordpress.com/2013/06/08/what-is-misdirection-critiquing-antineoplastons-has-the-fda-kept-its-promise-to-the-american-people/
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[11] – Treatments for Astrocytic Tumors in Children: Current and Emerging Strategies. Pediatric Drugs 2006;8:167-178. (Pediatr Drugs 2006; 8 (3)), 2.3. Targeted Therapy, pg. 174
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8/21/2013 – Critiquing David H. Gorski, MD, PhD, FACS http://www.sciencebasedmedicine.org/editorial-staff/david-h-gorski-md-phd-managing-editor/
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https://stanislawrajmundburzynski.wordpress.com/2013/08/21/critiquing-david-h-gorski-md-phd-facs-www-sciencebasedmedicine-orgeditorial-staffdavid-h-gorski-md-phd-managing-editor/
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[12] – 7/9/2013 – Burzynski: The Original 72 Phase II Clinical Trials:
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https://stanislawrajmundburzynski.wordpress.com/2013/07/09/burzynski-the-original-72-phase-ii-clinical-trials/
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[13] – 6/26/2013 – Burzynski: The Clinical Trials:
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https://stanislawrajmundburzynski.wordpress.com/2013/06/26/burzynski-the-clinical-trials/
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http://clinicaltrials.gov/archive/NCT00003509/2009_05_26/changes
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[14] – 4/26/2013 – Burzynski: Not Every Cancer Clinical Trial Taking Place In The United States Is Listed On Our NCI Clinical Trials Database:
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https://stanislawrajmundburzynski.wordpress.com/2013/04/26/burzynski-not-every-cancer-clinical-trial-taking-place-in-the-united-states-is-listed-on-our-nci-clinical-trials-database/
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[15]
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http://www.ncbi.nlm.nih.gov/pubmed/23408699/
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Critiquing David H. “Orac” Gorski, MD PhD and his Personalized MUD-Targeted Skeptic Therapy

I’ve made no secret of my opinion of a certain cancer “research” doctor named David H. Gorski, MD, PhD, of Wayne State University School of Medicine and Barbara Ann Karmanos Cancer Center / Institute, Detroit, Michigan fame

Gorski, as you may recall was responsible for this 6/3/2013 “Orac” posting:
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In which the latest movie about Stanislaw Burzynski’s “cancer cure” is reviewed…with Insolence
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http://scienceblogs.com/insolence/2013/06/03/in-which-the-latest-movie-about-stanislaw-burzynskis-cancer-cure-is-reviewed-with-insolence/
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Critiquing: In which the latest movie about Stanislaw Burzynski “cancer cure” is reviewed…with Insolence:
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https://stanislawrajmundburzynski.wordpress.com/2013/07/18/critiquing-in-which-the-latest-movie-about-stanislaw-burzynski-cancer-cure-is-reviewed-with-insolence-2/
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When last we left Gorski, his propaganda, which I characterize as pure propaganda so incompetently made that it would make blush blush

After a couple of winks I changed my characterization to say that it would have made Penn and Teller vomit in revulsion at its sheer incompetence

Be that as it may, I view Gorski as highly unethical and pseudononsense, an incompetent purveyor of “personalized MUD-targeted medicine for dummies,” and someone who might at one time have been on to something but, like all hacks, just couldn’t let go when it became clear that his personalized MUD-targeted Skeptic therapy was far more toxic than advertised and way less efficacious, if it’s even efficacious at all, which is highly doubtful.

Gorski claimed:

“[I]f I had screwed up, I would have admitted it”

Data talks

BS walks

And there’s no doubt that Gorski, too, is pure BS

In fact, I think I’m being too kind

I have yet to see his admission that he lied when he posted:

“how Burzynski never explains which genes are targeted by antineoplastons … “
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Critiquing: Dr. David H. “Orac” Gorski, M.D., Ph.D, L.I.A.R.:
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https://stanislawrajmundburzynski.wordpress.com/2013/08/07/critiquing-dr-david-h-orac-gorski-m-d-ph-d-l-i-a-r/
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8/12/2013 Gorski blogged:
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A study of antineoplastons fails to be published. Stanislaw Burzynski’s propagandist Eric Merola whines about it. News at 11.
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http://scienceblogs.com/insolence/2013/08/12/antineoplaston-fails-publication/ ======================================
In regards to antineoplastons, Gorski states:

“antineoplastons are chemotherapy”

“They even have significant toxicity!”

What science based medicine publication(s) does Gorski cite in support of his “theory”?

NONE !!!

What do the science based medicine publications indicate?
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[1] 4/1/1992 PHENYLACETATE-novel NONTOXIC inducer of tumor cell differentiation
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Sodium PHENYLACETATE found to affect growth and differentiation of tumor cells in vitro at concentrations achieved in humans WITH NO SIGNIFICANT ADVERSE EFFECTS
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PHENYLACETATE is effective in inducing tumor cell maturation and FREE OF CYTOTOXIC AND CARCINOGENIC EFFECTS, a combination that warrants attention to potential use in cancer intervention
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Sodium PHENYLACETATE is investigational new drug approved for human use by U.S. Food and Drug Administration
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DRUG ALREADY ESTABLISHED AS SAFE AND EFFECTIVE … we propose use may be extended to cancer preventation and therapy
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[2] 8/20/1992 Difficulties may be overcome through exploitation of recent discovery of sodium PHENYLACETATE as NONTOXIC inducer of differentiation …
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(pro-drug) Sodium 4-PHENYLBUTYRATE can be given in oral doses of 0.3 to 0.6 g per kilogram of body weight per day with NO ADVERSE REACTIONS
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Drug rapidly metabolized to PHENYLACETATE and PHENYLACETYLGLUTAMINE
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PHENYLACETATE (but not PHENYLACETYLGLUTAMINE) … CAN POTENTIATE EFFICACY OF OTHER DIFFERENTIATING AGENTS, such as cytotoxic drugs …
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[3] 9/15/1992 we explored efficacy of PHENYLACETATE, an amino acid derivative with LOW TOXICITY INDEX WHEN ADMINISTERED TO HUMANS
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PHENYLACETATE, used alone or in combination with other drugs, might offer safe and effective new approach to treatment
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[4] 5/1993 NONTOXIC differentiation inducer, sodium PHENYLACETATE (NaPA)
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In vitro antineoplastic activity was observed with drug concentrations that have been achieved in humans with NO SIGNIFICANT TOXICITIES, suggesting PA, used alone or in combination with other antitumor agents, warrants evaluation in treatment of advanced prostatic cancer
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[5] 10/1/1993 Sodium PHENYLACETATE (NaPA) and its precursor, sodium 4-PHENYLBUTYRATE (NaPB), can enhance HbF production in cultured erythroid progenitor derived from normal donors and patients with SS anemia or beta-thal, when used at pharmacologic concentrations
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NaPA and NaPB, BOTH ALREADY PROVEN SAFE AND EFFECTIVE IN TREATMENT OF CHILDREN
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[6] 2/15/1994 sodium PHENYLACETATE can induce cytostasis and reversal of malignant properties of cultured human glioblastoma cells, when used at pharmacological concentrations that are WELL TOLERATED BY CHILDREN AND ADULTS
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Systemic treatment of rats bearing intracranial gliomas resulted in significant tumor suppression with NO APPARENT TOXICITY to host
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[7] 4/1/1994 Pg. 1690
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protocol underwent several modifications over 6-month period
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Interest in PHENYLACETATE as anticancer agent generated by reports that ANTINEOPLASTON AS2-1, a preparation which by weight is 80% PHENYLACETATE, displayed clinical antitumor activity (13)
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17 patients (16 men / 1 woman) (36-75) median age 57
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Pg. 1693
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Clinical Toxicities. NO TOXICITY associated with bolus administration of drug
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Drug-related TOXICITY clearly related to serum
PHENYLACETATE
concentration
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3 episodes of Central Nervous System (CNS)
TOXICITY
, limited to CONFUSION
and LETHARGY and often preceded by emesis, occurred in patients treated at dose levels 3 and 4
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Symptoms resolved within 18 h of terminating drug infusion in all instances
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Pg. 1694
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PHENYLACETATE serum concentrations … were typically associated with CNS toxicity
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While ability to cross blood-brain barrier may underlie clinical improvement seen in patient with glioblastoma, could also explain dose-limiting side-effects of drug, i.e., nausea, vomiting, sedation, and confusion
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Limited experience with 150-mg/kg i.v. boluses suggests serum PHENYLACETATE concentrations occurring transiently
above 500 ug/ml are well tolerated
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Intermittent drug infusion should permit some drug washout to occur, thereby minimizing drug accumulation
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Predicts wide range of peak drug concentrations will be observed
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Possible these would be sufficiently transient so as not to produce CNS toxicity and troughs not prolonged as to abrogate antitumor activity of drug
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Dosing alternatives should be explored, our study indicates PHENYLACETATE can be safely administered by CIVI and result in clinical improvement in some patients with hormone-refractory
prostatic carcinoma and glioblastoma multiforme who failed conventional therapies
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[8] 6/1/1994 PHENYLACETATE is naturally occurring plasma component that suppresses growth of tumor cells and induces differentiation in vitro
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Treatment with PHENYLACETATE extended survival … WITHOUT ASSOCIATED ADVERSE EFFECTS
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[9] 9/1994 PHENYLACETATE, NONTOXIC differentiation inducer, can suppress growth of other neuroectodermal tumors, i.e., gliomas, in laboratory models and humans
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[10] 4/1995 PHENYLACETATE, an inducer of tumor cytostasis and differentiation, shows promise as RELATIVELY NONTOXIC antineoplastic agent in models and humans
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[11] 6/15/1995 Growth-inhibiting and differentiating effects of sodium PHENYLACETATE against hematopoietic and solid tumor cell lines has aroused clinical interest in use as anticancer drug
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In Phase I trial of PHENYLACETATE … commonly resulted in drug accumulation and REVERSIBLE DOSE-LIMITING NEUROLOGIC TOXICITY
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18 patients
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DOSE-LIMITING TOXICITY, consisting of REVERSIBLE CENTRAL NERVOUS SYSTEM DEPRESSION, observed for 3 patients at 2nd dose level
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[12] 10/12/1995 aromatic fatty acid PHENYLACETATE, a common metabolite of phenylalanine, shows promise as a RELATIVELY NON-TOXIC drug for cancer treatment
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[13] 10/1995 investigated effects of a NONTOXIC differentiation inducer, PHENYLACETATE (PA), on neuroectodermal tumor-derived cell lines
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[14] 1995 Antineoplastons, firstly described by Burzynski, are naturally occurring peptides and amino acid derivatives which control neoplastic growth
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toxicological study of Antineoplastons A-10 and AS2-1 in combination with other anticancer agents or radiation in 42 patients
46 tumors with terminal stage cancer
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Antineoplaston A-10 oral formulation
14 – patients
A-10 injectable formulation
25 – patients

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

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Major adverse effects that may have been related to agents used in combination with other conventional chemotherapeutic agents or radiation:
liver dysfunction
myelosuppression
general weakness
THESE EFFECTS WEREN’T SEEN WHEN EITHER ANTINEOPLASTON WAS ADMINISTERED ALONE

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MINOR ADVERSE EFFECTS OBSERVED IN SINGLE USE OF EITHER ANTINEOPLASTON A-10 OR AS2-1:
reduced albumin
increased alkaline phosphatase
increased amylase
reduced cholesterol
peripheral edema
eosinophilia
fingers rigidity
excess gas
headache
hypertension
maculopapullar rash
palpitation
adverse effects didn’t limit to continuation of either agent

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Antineoplaston A-10 and AS2-1 LESS TOXIC THAN CONVENTIONAL CHEMOTHERAPIES and useful in maintenance therapy for cancer patients
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[15] 1996 Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which control neoplastic growth
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reported cytostatic inhibitory effect of A10 on human hepatocellular carcinoma cells and differentiation inducing effect of AS2-1 on various tumor cells suggest potential benefit for treatment of human hepatocellular carcinoma since tumor recurs frequently despite initial successful treatment
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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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[16] 5/1996
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In pursuit of alternative treatments for chemoresistant tumor cells, tested response of multidrug-resistant (MDR) tumor cell lines to aromatic fatty acids phenylacetate (PA) and phenylbutyrate (PB), 2 differentiation inducers currently in clinical trials
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Both compounds induced cytostasis and maturation of multidrug-resistant breast, ovarian, and colon carcinoma cells with no significant effect on cell viability
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MDR cells generally more sensitive to growth arrest by PA and PB than their parental counterparts
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PA and PB potentiated cytotoxic activity of doxorubicin against MDR cells
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Taken together, in vitro data indicate PA and PB, differentiation inducers of aromatic fatty acid class, may provide alternative approach to treatment of MDR tumors
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[17] 12/1996 PHENYLACETATE (PA) and related aromatic fatty acids constitute novel class of RELATIVELY NONTOXIC antineoplastic agents
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[18] 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
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[19] 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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[20] 10/1997 Sodium PHENYLACETATE (PA) and sodium PHENYLBUTYRATE (PB) are aromatic fatty acids that can effect differentiation in a variety of cell lines at doses that may be clinically attainable
——————————————————————
Pg. 1760
——————————————————————
PB has been successfully administered to patients with urea acid cycle disorders and sickle cell anemia for extended periods of time, and NO HEMATOLOGICAL TOXICITY has been reported
——————————————————————
Significant HEMATOLOGICAL TOXICITY was not reported in a Phase I trial of PA in patients with malignancy
——————————————————————
Pg. 1761
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Because of its ATTRACTIVE CLINICAL TOXICITY PROFILE, PB represents an excellent candidate for clinical trials in this group of disorders
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[21] 11..12/1997 Antineoplaston AS2-1 exhibits cytostatic growth inhibition of human hepatocellular carcinoma cells in vitro and SHOWED MINIMUM ADVERSE EFFECTS in phase I clinical trial
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[22] 6/1999 Burkitt’s lymphoma (BL) is readily treated malignancy, recurrences, as well as disease arising in immunosuppressed patients, are notoriously resistant to conventional therapeutic approaches
——————————————————————
Using in vitro models of EBV-transformed lymphoblastoid as well as BL cell lines, we demonstrate increased expression of genes coding for HLA class I and EBV latent proteins by differentiation inducer PHENYLBUTYRATE (PB)
——————————————————————
Aromatic fatty acid also caused cytostasis associated with sustained declines in c-myc expression, a direct antitumor effect that was independent of EBV status
——————————————————————
Findings may have clinical relevance because in vitro activity has been observed with PB concentrations that are
WELL TOLERATED
and nonimmunosuppressive in humans, a desirable feature for different patient populations afflicted with this disease
======================================
[23] 8/2001 PHENYLBUTYRATE (PB) is aromatic fatty acid with multiple mechanisms of action including histone deacetylase inhibition
——————————————————————
Overall DRUG WELL TOLERATED with most common TOXICITIES being grade 1-2 DYSPEPSIA and FATIGUE
——————————————————————
Nonoverlapping dose-limiting TOXICITIES of NAUSEA/VOMITING and HYPOCALCEMIA were seen at 36 g/day
——————————————————————
PB (p.o.) IS WELL TOLERATED and achieves concentration in vivo shown to have biological activity in vitro
======================================
[24] 10/2001 Sodium PHENYLBUTYRATE (PB) demonstrates potent differentiating capacity in multiple hematopoietic and solid tumor cell lines
——————————————————————
Pharmacokinetics performed during and after first infusion period using validated high-performance liquid chromatographic assay and single compartmental pharmacokinetic model for PB and principal metabolite, PHENYLACETATE
——————————————————————
24 patients with hormone refractory prostate cancer being predominant tumor type
——————————————————————
All evaluable for TOXICITY and response
——————————————————————
Dose escalated 150 to 515 mg/kg/day
——————————————————————
One patient at 515 mg/kg/day and one at 345 mg/kg/day experienced this DLT
——————————————————————
Maximum tolerated dose 410 mg/kg/day for 5 days
——————————————————————
Recommended Phase II dose 410 mg/kg/day for 120 h
——————————————————————
Dose-limiting TOXICITY (DLT) was neuro-cortical, exemplified by EXCESSIVE SOMNOLENCE and CONFUSION and accompanied by clinically significant HYPOKALEMIA, HYPONATREMIA, and HYPERURICEMIA
——————————————————————
Other TOXICITIES mild, including FATIGUE and NAUSEA
——————————————————————
DLT in Phase I study for infusional PB
given for 5 days every 21 days is neuro-cortical in nature
——————————————————————
TOXICITY resolved < or =12 h of discontinuing infusion
======================================
[25] 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
——————————————————————
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
======================================
[26] 4/2005 Determined maximum tolerated dose (MTD), TOXICITY profile of … oral sodium PHENYLBUTYRATE (PB) in patients with recurrent malignant gliomas
——————————————————————
All PB doses of 9, 18, and 27 g/day WELL TOLERATED
——————————————————————
At 36 g/day, 2 of 4 patients developed dose-limiting grade 3 FATIGUE and SOMNOLENCE
——————————————————————
At MTD of 27 g/day, one of 7 patients developed reversible grade 3 SOMNOLENCE
======================================
[27] 4/2007 PHENYLBUTYRATE (PBA), and its metabolite PHENYLACETATE (PAA), induce growth inhibition and cellular differentiation in multiple tumor models
——————————————————————
Conversion of PBA to PAA and PHENYLACETYLGLUTAMINE (PAG) documented without catabolic saturation
——————————————————————
THERAPY WELL TOLERATED OVERALL
——————————————————————
Common ADVERSE EFFECTS included grade 1 NAUSEA/VOMITING, FATIGUE, and LIGHTHEADEDNESS
——————————————————————
Dose limiting TOXICITIES were SHORT-TERM MEMORY LOSS, SEDATION, CONFUSION, NAUSEA, and VOMITING
——————————————————————
Administration of PBA twice-daily infusion schedule is SAFE
======================================
None of the above publications indicate that antineoplastons are toxic as Gorski would have people believe

12/12/2011 Gorski published his attempt at trying to explain why antineoplastons are supposedly toxic
======================================
What Dr. Stanislaw Burzynski doesn’t want you to know about antineoplastons
——————————————————————
http://scienceblogs.com/insolence/2011/12/12/what-dr-stanislaw-burzynski-doesnt-want/
======================================
Gorski posited:

“He’s also prescribing huge doses of antineoplastons (up to 25 g/kg/d for A10 and 80 mg/kg/d for AS-2.1, as we have seen). both of these are so far above the maximal tolerated dose of 300 mg/kg/d determined in the phase I trial I cited above as to be terrifying”

In support of his “theory”, Gorski provided a link to the National Cancer Institute (NCI) at the National Institutes of Health (NIH):
——————————————————————
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/Table1
——————————————————————
However, as is the case with a lot of Gorski’s lame research, he makes you search for what he is referring to:

[14]Ba Primitive neuroectodermal tumor (13)

A10/AS2-1

Max dose: A10: 25 g/kg/d; AS2-1: 0.6 g/kg/d

Does this support Gorski’s “toxic theory”?
======================================
[28] 2005
——————————————————————
5 years 7 months (1-11) median age
——————————————————————
13 / 100% – children with recurrent disease or high risk
——————————————————————
5 / 38% – weren’t treated earlier with radiation therapy or chemotherapy
——————————————————————
3 / 23% – Complete Response
1 / 8% – Partial Response
4 / 31% – Stable Disease
5 / 38% – Progressive Disease

——————————————————————
6 / 46% – Survived 5+ years from initiation of ANP
——————————————————————
Serious side effects:
1 – anemia
1 – fever
1 – granulocytopenia

——————————————————————
average dosage of A10 was 10.3 g/kg/d and of AS2-1 was 0.38 g/kg/d
——————————————————————
REDUCED TOXICITY MAKES ANP PROMISING for very young children, patients at high risk of complication of standard therapy, and patients with recurrent tumors
======================================
The above sure does NOT support Gorski’s “toxic theory”

When science based medicine keeps saying the following:
======================================
[9] 9/1994 increasing incidence of melanoma and POOR RESPONSIVENESS OF DISSEMINATED DISEASE TO CONVENTIONAL TREATMENT CALL FOR DEVELOPMENT OF NEW THERAPEUTIC APPROACHES
======================================
[29] 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)
——————————————————————
Interestingly, IN CONTRAST TO THEIR RELATIVE RESISTANCE TO RADIATION and doxorubicin, ras-transformed cells were significantly more sensitive to PA than their parental cells
======================================
[30] 5/1996 CYOTOXIC 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
======================================
[15] 1996 Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which control neoplastic growth
——————————————————————
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
======================================
[31] 7/1997 Children with malignant GLIOMAS THAT PROGRESSED AFTER CONVENTIONAL THERAPY
——————————————————————
0 / 0% – EXHIBITED CLEAR-CUT TUMOR regression
======================================
[32] 2000 treatment combination PRODUCED NO SIGNIFICANT CHANGE in overall POOR prognosis of patients
——————————————————————
Most tumors responded initially to treatment but RECCURED as study progressed
——————————————————————
Based on POOR RESULTS, recommend ALTERNATIVE TREATMENTS be tested in patients with this type of tumor
======================================
[33] At time of approval, NO RESULTS were available from randomized controlled trials in refractory ANAPLASTIC ASTROCYTOMA that show clinical benefit such as improvement in disease-related symptoms or prolonged survival
======================================
[34] 12/2000 NO CLEAR PROOF OF EFFICACY
——————————————————————
NO BETTER THAN SURVIVAL BEFORE THE INTRODUCTION OF temozolomide
======================================
[35] 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
======================================
[36] 2004 outcome for patients with either type of tumor is POOR when STANDARD multimodality THERAPY IS USED
——————————————————————
children are ideal candidates for INNOVATIVE TREATMENT approaches
——————————————————————
33 / 100% – DIED OF DISEASE PROGRESSION
——————————————————————
administration of temozolomide after RT DIDN’T ALTER POOR PROGNOSIS associated with newly diagnosed diffuse BRAINSTEM GLIOMA in children
======================================
[37] 2/2008 addition of vincristine and oral VP-16 to standard external beam radiation causes moderate toxicity and DOESN’T IMPROVE SURVIVAL OF CHILDREN WITH DIFFUSE INTRINSIC BRAIN STEM GLIOMA
======================================
[38] 5/6/2009 Currently, NO DATA available from randomized controlled trials demonstrating improvement in disease-related symptoms or increased survival with Avastin in GLIOBLASTOMA
======================================
[39] 10/12/2011 Afinitor (ubependymal giant cell ASTROCYTOMA (SEGA) brain tumor)
——————————————————————
none of their tumors went away completely
======================================
[18] 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 CLINICALTOXICITY PROFILE makes them promising candidates for COMBINATION WITH CONVENTIONAL THERAPIES
======================================
So what does Gorski think is going to fill the void?

His clinical trial drug ?

The potentially profitable drug Gorski is in the process of conducting a clinical trial for is the ALS drug Riluzole, made by Sanofi-Aventis and marketed as Rilutek

Apparently, David Gorski has had his eye on that drug for a long time, but as a possible treatment for breast cancer

As suggested by a 2008-2009 webpage of a breast cancer website:

“Three years ago in another cancer (melanoma), Dr. Gorski’s collaborators found that glutamate might have a role in promoting the transformation of the pigmented cells in the skin (melanocytes) into the deadly skin cancer melanoma”

“More importantly for therapy, it was found that this protein can be blocked with drugs, and, specifically, in melanoma cell lines and tumor models of melanoma using a drug originally designed to treat ALS and already FDA-approved for that indication (Riluzole) can inhibit the growth of melanoma.”
————————————————————
http://www.ageofautism.com/2010/06/david-gorskis-financial-pharma-ties-what-he-didnt-tell-you.html
————————————————————
Better luck next time with your personal MUD-targeted Skeptic therapy Gorski

� � � � � � � � � � � � � � � � �
References:
————————————————————
Dvorit D. Samid learned about antineoplastons from Burzynski
� � � � � � � � � � � � � � � � �
[1] 4/1/1992
� � � � � � � � � � � � � � � � �
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
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Cancer Res. 1992 Apr 1;52(7):1988-92
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Cancer Res 52:1988,1992
http://m.cancerres.aacrjournals.org/content/52/7/1988.full.pdf#page=1
SAMID D, Shack S, Ti-Sherman L
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
PHENYLACETATE-A novel nontoxic inducer of TUMOR CELL differentiation
↵1 Supported by Elan Pharmaceutical Corporation Grant G174ED
Reference: 12 (SAMID, D.)
� � � � � � � � � � � � � � � � �
[2] .8/20/1992
� � � � � � � � � � � � � � � � �
Dover GJ, Brusilow S, SAMID D. Increased fetal hemoglobin in patients receiving sodium 4-PHENYLBUTYRATE. N Engl J Med. 1992 Aug 20;327(8):569–570
http://www.ncbi.nlm.nih.gov/pubmed/1378939/
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http://www.ncbi.nlm.nih.gov/m/pubmed/1378939/
August 20, 1992
N Engl J Med 1992; 327:569-570
http://www.nejm.org/doi/full/10.1056/NEJM199208203270818
N Engl J Med 327569, 1992
Dvorit Samid, Ph.D
National Cancer Institute
, Bethesda, MD
� � � � � � � � � � � � � � � � �
[3] 9/15/1992
� � � � � � � � � � � � � � � � �
SAMID D, Yeh A, Prasanna P. Induction of erythroid differentiation and fetal hemoglobin production in human leukemic cells treated with phenylacetate. Blood. 1992 Sep 15;80(6):1576–1581
http://www.ncbi.nlm.nih.gov/pubmed/1381630/
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http://www.ncbi.nlm.nih.gov/m/pubmed/1381630/
Blood September 15, 1992 vol. 80 no. 6 1576-1581
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.full.pd
Blood 80:1576, 1992
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.abstract
Blood 80(6):1576–1581
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.full.pdf
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD
SAMID D References: 15, 20-21 and 34
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[4] 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/
J Clin Invest. 1993 May; 91(5): 2288–2295
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC288233/
Published in Volume 91, Issue 5 (May 1993)
http://m.jci.org/articles/view/116457
J Clin Invest. 1993;91(5):2288–2295
1993, The American Society for Clinical Investigation
http://m.jci.org/articles/view/116457/pdf.mobile
J Clin Invest 91:2288, 1993
PMCID: PMC288233
doi:10.1172/JCI116457
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
SAMID D References: 9, 13-14, 17 and 33
� � � � � � � � � � � � � � � � �
[5] .10/1/1993
� � � � � � � � � � � � � � � � �
Enhanced fetal
hemoglobin production by PHENYLACETATE and 4-PHENYLBUTYRATE in erythroid precursors derived from normal blood donors and patients with sickle cell anemia and P-thalassemia
http://www.ncbi.nlm.nih.gov/pubmed/7691251/
Blood. 1993 Oct 1;82(7):2203-9
http://www.ncbi.nlm.nih.gov/m/pubmed/7691251/
Blood 822203, 1993
http://m.bloodjournal.hematologylibrary.org/content/82/7/2203.full.pd
Blood October 1, 1993 vol. 82 no. 7 2203-2209
http://m.bloodjournal.hematologylibrary.org/content/82/7/2203.abstract
1993 82: 2203-2209
http://m.bloodjournal.hematologylibrary.org/content/82/7/2203.full.pdf
Blood 82(7):2203–2209
Department of Hematology, Hadassah University Hospital, Jerusalem, Israel
Fibach E, Prasanna P, Rodgers GP, SAMID D
SAMID D References: 15, 19-21 and 32
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[6] 2/15/1994
� � � � � � � � � � � � � � � � �
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/
Cancer Res February 15, 1994 54; 891
http://cancerres.aacrjournals.org/content/54/4/891/
Cancer Res 1994;54:891-895
Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
Work supported by funds from Elan Pharmaceutical Research Corporation through Cooperative Research and Development Agreement (CACR-0139)
� � � � � � � � � � � � � � � � �
[7] 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. 1994 Apr 1;54(7):1690-4
http://www.ncbi.nlm.nih.gov/m/pubmed/8137283
Cancer Res 54(7):1690-4 (1994), PMID.8137283
http://m.cancerres.aacrjournals.org/content/54/7/1690.abstract
Clinical Pharmacology Branch, National Cancer Institute, NIH, Bethesda, Maryland
http://m.cancerres.aacrjournals.org/content/54/7/1690.full.pdf
Thibault A, Cooper MR, Figg WD, Venzon DJ, Sartor AO, Tompkins AC, Weinberger MS, Headlee DJ, McCall NA, SAMID D, et al.
http://cancerres.aacrjournals.org/content/54/7/1690
Study supported in part by grant from Elan Pharmaceutical Research Co
SAMID D
References: 8-12
BURZYNSKI
Reference: 13
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[8] 6/1/1994
� � � � � � � � � � � � � � � � �
Growth inhibition, tumor maturation, and extended survival in experimental brain tumors in rats treated with PHENYLACETATE.
http://www.ncbi.nlm.nih.gov/pubmed/8187079/
Cancer Res 54:2934-2927, 1994
http://www.ncbi.nlm.nih.gov/m/pubmed/8187079/
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http://m.cancerres.aacrjournals.org/content/54/11/2934.abstract?ijkey=03bc67e581ef77536842806b949046916458d548&keytype2=tf_ipsecsha
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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
Ram Z, SAMID D, Walbridge S, et al:
http://cancerres.aacrjournals.org/content/54/11/2923
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[9] 1994
� � � � � � � � � � � � � � � � �
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
� � � � � � � � � � � � � � � � �
[10] 4/1995
� � � � � � � � � � � � � � � � �
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://onlinelibrary.wiley.com/doi/10.1002/j.1552-4604.1995.tb04075.x/abstract;jsessionid=43600D49608A093971D675F3DB5FF13D.d01t03
Piscitelli SC, Thibault A, Figg WD, et al: (SAMID D)
http://jcp.sagepub.com/content/35/4/368
Pharmacy Department, National Institutes of Health, Bethesda, Maryland, USA
DOI: 10.1002/j.1552-4604.1995.tb04075.x
http://m.jcp.sagepub.com/content/35/4/368.abstract?ijkey=74bff0d86ce76b404728762fe2a1bfde1641fa41&keytype2=tf_ipsecsha
� � � � � � � � � � � � � � � �
[11] 6/15/1995
� � � � � � � � � � � � � � � �
Phase I study of PHENYLACETATE administered twice daily to patients with cancer
http://www.ncbi.nlm.nih.gov/pubmed/7773944/
Cancer. 1995 Jun 15;75(12):2932-8
http://www.ncbi.nlm.nih.gov/m/pubmed/7773944/
Cancer 75(12):2932–2938
Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
Thibault A, SAMID D, Cooper MR, Figg WD, Tompkins AC, Patronas N, et al
� � � � � � � � � � � � � � � � �
[12] 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
� � � � � � � � � � � � � � � � �
[13] 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&amp;
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[14] 1995
� � � � � � � � � � � � � � � � �
Toxicological study on antineoplastons A-10 and AS2-1 in cancer patients
http://www.ncbi.nlm.nih.gov/pubmed/8667595
Kurume Med J. 1995;42(4):241-9
http://www.ncbi.nlm.nih.gov/m/pubmed/8667595
The Kurume Medical Journal
Vol. 42 (1995) No. 4 P 241-249
https://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_article
JST.Journalarchive/kurumemedj1954/42.241
https://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_pdf
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://dx.doi.org/10.2739/kurumemedj.42.241
Tsuda H, Hara H, Eriguchi N, Nishida H, Yoshida H, Kumabe T, Sugita Y
https://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_article/references
Burzynski References: 1 – 3 and 5
Nishida et al. (Japan) A-10 Reference: 4 and 7
Muldoon et al. A-10 Reference: 6
� � � � � � � � � � � � � � � � �
[15] 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
� � � � � � � � � � � � � � � �
[16] 5/1996
� � � � � � � � � � � � � � � �
Vulnerability of multidrug-resistant tumor cells to the aromatic fatty acids phenylacetate and PHENYLBUTYRATE
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/
Clin Cancer Res 2(5):865–872
http://m.clincancerres.aacrjournals.org/content/2/5/865.abstract
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland, USA
http://m.clincancerres.aacrjournals.org/content/2/5/865.full.pdf
Shack S, Miller A, Liu L, Prasanna P, Thibault A, SAMID D
http://clincancerres.aacrjournals.org/content/2/5/865
� � � � � � � � � � � � � � � � �
[17] 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/
Cell Growth Differ 7(12):1609–1615
http://cgd.aacrjournals.org/cgi/reprint/7/12/1609.pdf
Laboratory of Cellular and Molecular Biology, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, Maryland, USA
� � � � � � � � � � � � � � � � �
[18] 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
� � � � � � � � � � � � � � � � �
[19] 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
� � � � � � � � � � � � � � � �
[20] 10/1997
� � � � � � � � � � � � � � � �
Impact of the putative differentiating agents sodium PHENYLBUTYRATE and sodium PHENYLACETATE on proliferation, differentiation, and apoptosis of primary neoplastic myeloid cells
http://www.ncbi.nlm.nih.gov/pubmed/9815560/
Clin Cancer Res. 1997 Oct;3(10):1755-62
http://www.ncbi.nlm.nih.gov/m/pubmed/9815560/
Clin Cancer Res October 1997 3; 1755
http://m.clincancerres.aacrjournals.org/content/3/10/1755.full.pd
Clin Cancer Res. 1997a;3:1755–1762
http://m.clincancerres.aacrjournals.org/content/3/10/1755.abstract
The Johns Hopkins Oncology Center, Baltimore, Maryland, USA
http://m.clincancerres.aacrjournals.org/content/3/10/1755.full.pdf
Gore SD, SAMID D, Weng LJ
� � � � � � � � � � � � � � � � �
[21] 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
� � � � � � � � � � � � � � � �
[22] 6/1999
� � � � � � � � � � � � � � � �
PHENYLBUTYRATE induces cell differentiation and modulates Epstein-Barr virus gene expression in Burkitt’s lymphoma cells
http://www.ncbi.nlm.nih.gov/pubmed/10389940/
Clin Cancer Res. 1999 Jun;5(6):1509-16
http://www.ncbi.nlm.nih.gov/m/pubmed/10389940/
Clin Cancer Res 5(6):1509–1516
http://m.clincancerres.aacrjournals.org/content/5/6/1509.abstract
Clin Cancer Res June 1999 5; 1509
http://m.clincancerres.aacrjournals.org/content/5/6/1509.long
Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA
http://clincancerres.aacrjournals.org/content/5/6/1509
Bar-Ner M, Thibault A, Tsokos M, Magrath IT, SAMID D
Supported in part by funds from Elan Pharmaceutical Research Corporation
� � � � � � � � � � � � � � � � �
[23] 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. 2001 Aug;7(8):2292-.300
http://www.ncbi.nlm.nih.gov/m/pubmed/11489804
Clin Cancer Res 7(8):2292-.300 (2001), PMID.11489804
http://m.clincancerres.aacrjournals.org/content/7/8/2292.long
Division of Medical Oncology, Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, USA
J Gilbert, S D Baker, … M A Carducci
SAMID D References: 2-3, 5-6, 15 and 20
� � � � � � � � � � � � � � � � �
[24] 10/2001
� � � � � � � � � � � � � � � � �
A Phase I clinical and pharmacological evaluation of sodium PHENYLBUTYRATE on an 120-h infusion schedule
http://www.ncbi.nlm.nih.gov/pubmed/11595694
Clin Cancer Res. 2001 Oct;7(10):3047-55
http://www.ncbi.nlm.nih.gov/m/pubmed/11595694
Clin Cancer Res 7(10):3047-55 (2001), PMID.11595694
http://m.clincancerres.aacrjournals.org/content/7/10/3047.long
Division of Medical Oncology, The Johns Hopkins Oncology Center, Bunting-Blaustein Cancer Research Building, Baltimore, MD, USA
M A Carducci, J Gilbert, … R C Donehower
SAMID D References: 10-11, 13-14, 17-18, 23-24, 27, 33, 40-41 and 47
� � � � � � � � � � � � � � � � �
[25] 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 Antineoplastonsfor Colon Cancer with Unresectable Multiple Liver Metastases:
Report of a Case
A10 and AS2-1 – Phase II Clinical Trial
Hideaki Tsuda
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
� � � � � � � � � � � � � � � �
[26] 4/2005
� � � � � � � � � � � � � � � �
Oral sodium PHENYLBUTYRATE in patients with recurrent malignant gliomas:

A dose escalation and pharmacologic study
http://www.ncbi.nlm.nih.gov/pubmed/15831235/
Neuro Oncol. 2005 Apr;7(2):177-82
http://www.ncbi.nlm.nih.gov/m/pubmed/15831235/
Neuro-oncol. 2005 April; 7(2): 177–182 PMCID: PMC1871887
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1871887/pdf/neu0702p177.pdf
The New Approaches to Brain Tumor Therapy CNS Consortium, Winship Cancer Institute, Emory University, Atlanta, GA, USA
Buckner Reference: 3
SAMID D References: 12, 17 and 19-21
� � � � � � � � � � � � � � � � �
[27] 4/2007
� � � � � � � � � � � � � � � � �
Phase I dose escalation clinical trial of PHENYLBUTYRATE sodium administered twice daily to patients with advanced solid tumors
http://www.ncbi.nlm.nih.gov/pubmed/17053987
Invest New Drugs. 2007 Apr;25(2):131-8. Epub 2006 Oct 20
http://www.ncbi.nlm.nih.gov/m/pubmed/17053987
Investigational New Drugs
April 2007, Volume 25, Issue 2, pp 131-138
http://link.springer.com/article/10.1007%2Fs10637-006-9017-4
Invest New Drugs 25(2):131-8 (2007), PMID.17053987
Department of Medicine, Memorial Sloan-Kettering Cancer Center, Joan and Sanford I. Weill Medical College of Cornell Medical Center, New York, New York, USA
Luis H LH Camacho, Jon J Olson, … Mark G MG Malkin
SAMID D References: 4-5, 7, 20, 24, 30 and 32-38
� � � � � � � � � � � � � � � � �
[28] 2005
� � � � � � � � � � � � � � � � �
14. Burzynski SR, Weaver RA, Janicki T, et al.: Long-term survival of high-risk pediatric patients with primitive neuroectodermal tumors treated with antineoplastons A10 and AS2-1. Integr Cancer Ther 4 (2): 168-77, 2005
http://www.ncbi.nlm.nih.gov/pubmed/15911929/
Integr Cancer Ther. 2005 Jun;4(2):168-77
http://www.ncbi.nlm.nih.gov/m/pubmed/15911929/
� � � � � � � � � � � � � � � � �
[29] 9/27/1995
� � � � � � � � � � � � � � � � �
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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[30] 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
� � � � � � � � � � � � � � � � �
[31] 7/1997
� � � � � � � � � � � � � � � � �
A phase I study of high-dose tamoxifen for the treatment of refractory malignant gliomas of childhood
http://www.ncbi.nlm.nih.gov/pubmed/9815790/
Clin Cancer Res. 1997 Jul;3(7):1109-15
http://www.ncbi.nlm.nih.gov/m/pubmed/9815790/
Clin Cancer Res July 1997 3; 1109
http://m.clincancerres.aacrjournals.org/content/3/7/1109.full.pd
Department of Neurosurgery, Children’s Hospital of Pittsburgh, Pittsburgh, Pennsylvania, USA
http://clincancerres.aacrjournals.org/content/3/7/1109
� � � � � � � � � � � � � � � � �
[32] 2000
� � � � � � � � � � � � � � � � �
Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse BRAINSTEM GLIOMAS:

results of a Brazilian cooperative study
http://www.ncbi.nlm.nih.gov/pubmed/10715294/
Brainstem Glioma Cooperative Group
http://www.ncbi.nlm.nih.gov/m/pubmed/10715294/
J Clin Oncol 18, 1246-1253
http://m.jco.ascopubs.org/content/18/6/1246.long
� � � � � � � � � � � � � � � � �
[33]
� � � � � � � � � � � � � � � � �
http://clincancerres.aacrjournals.org/content/11/19/6767.full
� � � � � � � � � � � � � � � � �
[34] 12/2000
� � � � � � � � � � � � � � � � �
Temozolomide and ANAPLASTIC ASTROCYTOMA:

new indication
http://www.ncbi.nlm.nih.gov/pubmed/11475493/
Prescrire Int. 2000 Dec;9(50):170-1.
http://www.ncbi.nlm.nih.gov/m/pubmed/11475493/
� � � � � � � � � � � � � � � � �
[35] 2002
� � � � � � � � � � � � � � � � �
A novel strategy for remission induction and maintenance in cancer therapy
A10 and AS2-1
H Tsuda
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
� � � � � � � � � � � � � � � � �
[36] 2004
� � � � � � � � � � � � � � � � �
Supratentorial high-grade ASTROCYTOMA and DIFFUSE BRAINSTEM GLIOMA:

two challenges for the pediatric oncologist
http://www.ncbi.nlm.nih.gov/pubmed/15047924/
Oncologist. 2004;9(2):197-206.
http://www.ncbi.nlm.nih.gov/m/pubmed/15047924/
Oncologist 9, 197-206
http://m.theoncologist.alphamedpress.org/content/9/2/197.long
Division of Neuro-Oncology, Department of Hematology-Oncology, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA
1/1/2005 (11/24/2004) – Role of temozolomide after radiotherapy for newly diagnosed diffuse BRAINSTEM GLIOMA in children:

results of a multiinstitutional study (SJHG-98)
http://www.ncbi.nlm.nih.gov/pubmed/15565574
Cancer. 2005 Jan 1;103(1):133-9.
http://www.ncbi.nlm.nih.gov/m/pubmed/15565574
Cancer 103, 133-139
http://onlinelibrary.wiley.com/doi/10.1002/cncr.20741/abstract;jsessionid=6717837591CCC8FCBD8E46163808E221.d03t01
Cancer
Volume 103, Issue 1, pages 133–139, 1 January 2005
http://onlinelibrary.wiley.com/doi/10.1002/cncr.20741/full
Article first published online: 24 NOV 2004
References:
http://onlinelibrary.wiley.com/doi/10.1002/cncr.20741/references
Cited By:
http://onlinelibrary.wiley.com/doi/10.1002/cncr.20741/citedby
DOI: 10.1002/cncr.20741
Department of Hematology-Oncology, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA
——————————————————————
Cancer 103, 133-139
� � � � � � � � � � � � � � � � �
[37] 2/2008 (Article first published online: 2/2/2007)
� � � � � � � � � � � � � � � � �
Treatment of children with diffuse intrinsic BRAIN STEM GLIOMA with radiotherapy, vincristine and oral VP-16:

a Children’s Oncology Group phase II study
http://www.ncbi.nlm.nih.gov/pubmed/17278121
Pediatr Blood Cancer. 2008 Feb;50(2):227-30
http://www.ncbi.nlm.nih.gov/m/pubmed/17278121
University of Rochester Medical Center, Rochester, New York, USA
http://onlinelibrary.wiley.com/doi/10.1002/pbc.21154/abstract;jsessionid=DE7A67EFBAC1A184F6805F11CFC4F30B.d02t02
Article first published online: 2 FEB 2007
DOI: 10.1002/pbc.21154
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[38] 5/6/2009
� � � � � � � � � � � � � � � � �
U.S. Food and Drug Administration (FDA) granted accelerated approval of Avastin (bevacizumab) for people with GLIOBLASTOMA (brain cancer) with progressive disease following prior therapy
——————————————————————
effectiveness of Avastin in AGGRESSIVE form of BRAIN CANCER based on improvement in objective response rate
——————————————————————
http://www.drugs.com/newdrugs/fda-grants-accelerated-approval-avastin-combination-paclitaxel-chemotherapy-first-line-advanced-852.html
According to FDA analysis of study
——————————————————————
Study AVF3708g
——————————————————————
Study NCI 06-C-0064E
——————————————————————
Efficacy of Avastin in GLIOBLASTOMA that progressed following prior therapy supported by another study that used same response assessment criteria as AVF3708g
——————————————————————
http://www.cancer.gov/cancertopics/druginfo/fda-bevacizumab
——————————————————————
http://www.drugs.com/newdrugs/fda-grants-accelerated-approval-avastin-brain-cancer-glioblastoma-has-progressed-following-prior-1342.html
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[39] 10/12/2011 (Published online: 8/1/2011)
� � � � � � � � � � � � � � � � �
Everolimus tablets for patients with subependymal giant cell ASTROCYTOMA
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3389821/
Expert Opin Pharmacother. Author manuscript; available in PMC 2012 July 5.
Published in final edited form as:
Expert Opin Pharmacother. 2011 October; 12(14): 2265–2269.
Published online 2011 August 1. doi: 10.1517/14656566.2011.601742
PMCID: PMC3389821
NIHMSID: NIHMS385824
——————————————————————
http://www.fda.gov/AboutFDA/CentersOffices/OfficeofMedicalProductsandTobacco/CDER/ucm231967.htm
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Is Dr. David H. “Orac” Gorski Down and Out in Detroit and an Ethically Bankrupt Researcher ?

After Gorski’s “research” of Burzynski’s phase I (1) clinical trials:

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/
he asserts:

“For one thing, in 1976 Burzynski had no animal data to speak of”

“In fact, the question of animal studies is an interesting one”

“Both Elias and Jaffe recount a story in which ANPs didn’t work in animal tumors, and Burzynski has been quoted in multiple places as claiming that ANPs are species-specific and that ANPs derived from human blood and urine don’t work in animal tumor models”

“This is in contrast to what Null reports in his near-contemporaneous account, in which he stated that in tissue culture and animal models Burzynski’s ANPs worked “specifically against certain types of cancer,” all with “no toxic side effects”

“It makes one wonder whether the “species specificity” was an excuse developed later to explain the lack of animal data”
� � � � � � � � � � � � � � � � �
National Cancer Institute (NCI) at the National Institutes of Health (NIH)

Laboratory/Animal/Preclinical Studies:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page4
“Burzynski states that antineoplaston A is species-specific because it had no therapeutic effect when the human preparation was tested on animal tumor systems”

“Although this finding limits the usefulness of animal model testing, the developer has suggested that a “marked” therapeutic effect was produced in a xenograft bearing human tumor tissue.[1]”

“This claim is made only for antineoplaston A”

“Other formulations of antineoplastons have not been tested in animal models”

Gorski should REALLY read his own blog:
http://scienceblogs.com/insolence/2013/01/21/quoth-joe-mercola-i-love-me-some-burzynski-antineoplastons/
Comment #158 – Didymus Judas Thomas

At the Tu-Quack Center Educate Orac Oracle Phase I

February 4, 2013

.11/15/1982.- 2 Toronto physicians, Martin E. Blackstein, Head of the Division of Oncology at Mount Sinai Hospital & Daniel E. Bergsagel, Chief of Medicine at Princess Margaret Hospital, visited the Burzynski clinic & research institute
.
Both were powerful & respected physicians in the Canadian cancer establishment
.
They returned with a blistering, critical report
.
The essence of their critique was
.
(1) there was little evidence that antineoplastons had significant antitumor activity against human or animal cancers;
.
(2) SRB’s argument that antineoplastons were species-specific created a line of argument for avoiding standard animal & tissue culture screens & required testing in humans
.
SRB cooperated but was dubious
.
There were several test-tube & preventative models in which the drug had showed effectiveness, but the standard NCI pre-screen, P388 mouse leukemia, was not 1 of them. …
.
As he had predicted, these compounds were not effective against mouse leukemia
.
SRB reasonably suggested that NCI try the Antineoplastons in cell-culture assays that were similar to “human solid tumors, especially adenocarcinoma of the breast” …
.
SRB was hardly alone in voicing doubts about the P388 mouse model
.
1983 – Ironically, it was Dr. John Vendetti himself, chief of the NCI’s Drug Evaluation Branch, who coauthored an article in which he argued the limitations of this very mouse system
.
Scientists at NCI had found, for instance, that of 79 drugs which had previously been judged negative in the P388, 14 showed “significant activity” when retested in cell culture assays [1] [2]

Comment #163 – Didymus Judas Thomas

February 4, 2013

Orac’s blog hates links reformatting (www removed)
.
[1] http://www.commonweal.org/pubs/choices/21.html
[2] 9 Moss, The Cancer Ind., 14, 299-300
(Ralph Moss, The Cancer Industry)
�
27. Burzynski SR, Hendry LB, Mohabbat MO, et al. Purification of structure determination, synthesis and animal toxicity studies of antineoplaston A10. In: Proceedings of the 13th International Congress of Chemotherapy. Vienna, Austria; 1983:17, PS. 12.4 11-4.
�
34. Burzynski SR, Mohabbat MO, Burzynski B. Animal toxicology studies on oral formulation of antineoplaston A10. Drug Exptl Clin Res. 1984;10:113-118.
�
40. Ashraf AQ, Liau MC, Kampalath BN, et al. Pharmacokinetic study of radioactive antineoplaston A10 following oral administration in rats. Drugs Exptl Clin Res. 1987;13(suppl 1):45-50.
http://www.ncbi.nlm.nih.gov/pubmed/3569015/
�
http://www.ncbi.nlm.nih.gov/m/pubmed/3569015/
43. Ashraf AQ, Kampalath BN, Burzynski SR. Pharmacokinetic analysis of antineoplaston A10 injections following intravenous administration in rats. Adv Exptl Clin Chemother. 1988;6:33-39.

Burzynski: The Clinical Trials

(Being added to)

clinicaltrials . gov does NOT contain the same data as the National Cancer Institute (NCI) at the National Institutes of Health (NIH) cancer . gov web-site:
� � � � � � � � � � � � � � � � �
50 – Unknown
7 – Withdrawn
2 – Terminated
1 – Not yet recruiting
1 – Completed
61 – TOTAL
� � � � � � � � � � � � � � � � �
1 – Not Yet Recruiting (Open)(Phase 3)
1 – Completed
2 – Terminated (Withdrawn due to slow enrollment)
7 – Withdrawn (This study has been withdrawn prior to enrollment)
10 – Recruiting (Open)
11 – Open (1 Not Yet Recruiting / 10 Recruiting)
40 – Active, not recruiting (Closed)
61 – TOTAL
� � � � � � � � � � � � � � � � �
Below 1 st link: 10 Active (Open):
http://cancer.gov/clinicaltrials/search/results?protocolsearchid=11475951
� � � � � � � � � � � � � � � � �
Below 2nd link: 25 Closed-1st screen / 15 Closed-1 Completed-2nd screen:
http://cancer.gov/clinicaltrials/search/results?protocolsearchid=11476036
� � � � � � � � � � � � � � � � �
1 – Completed
2 – Terminated (Withdrawn due to slow enrollment)
7 – Withdrawn (This study has been withdrawn prior to enrollment)
9=WITHDRAWN
1 – Not Yet Recruiting (Open)
10 – Recruiting (Open)
11=OPEN (1 Not Yet Recruiting / 10 Recruiting)
40 – Active, not recruiting (Closed)
61 – TOTAL
� � � � � � � � � � � � � � � � �
1=COMPLETED
9=WITHDRAWN
11=OPEN
40=CLOSED
61-TOTAL
� � � � � � � � � � � � � � � � �
The “one” COMPLETED trial:

The below 2nd link: 25 Closed-1st screen / 15 Closed-1 COMPLETED-2nd screen:
http://cancer.gov/clinicaltrials/search/results?protocolsearchid=11476036
Antineoplaston Therapy in Treating Patients With Stage IV Melanoma
Phase: Phase II
Type: Treatment
Status: COMPLETED
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066552, BC-ME-2, NCT00003509
http://clinicaltrials.gov/ct2/results?term=&recr=Completed&rslt=&type=&cond=&intr=&titles=&outc=&spons=&lead=Burzynski+&id=&state1=&cntry1=&state2=&cntry2=&state3=&cntry3=&locn=&gndr=&phase=1&rcv_s=&rcv_e=&lup_s=&lup_e=
COMPLETED

Antineoplaston Therapy in Treating Patients With Stage IV Melanoma

Condition: Melanoma (Skin)

Interventions:

Drug: antineoplaston A10
Drug: antineoplaston AS2-1

1 study: Melanoma
1 study: Neoplasms, Germ Cell and Embryonal
1 study: Neoplasms, Nerve Tissue
1 study: Neuroectodermal Tumors
1 study: Neuroendocrine Tumors
1 study: Neuroepithelioma
1 study: Nevus
1 study: Nevus, Pigmented

1 study found, shown on map

Region Number of
Name Studies
World 1
North America 1
United States [map] 1 [studies]

Found 1 study with search of:

COMPLETED | Burzynski [Lead] | Phase 2

Recognized Terms and Synonyms:
burzynski: 61 studies
http://clinicaltrials.gov/ct2/show/NCT00003509?recr=Completed&lead=Burzynski&phase=1&rank=1
Trial record 1 of 1 for:

COMPLETED | Burzynski [Lead] | Phase 2

Antineoplaston Therapy in Treating Patients With Stage IV Melanoma

This study has been COMPLETED

Sponsor: Burzynski Research Institute

Information provided by:
National Cancer Institute (NCI)

ClinicalTrials.gov Identifier: NCT00003509

11/1/1999 – First received

5/23/2009 – Last updated

5/2009 – Last verified
http://clinicaltrials.gov/ct2/archive/NCT00003509
Securities and Exchange Commission (SEC) filings “one” COMPLETED trial:

Burzynski Clinical Trials (The SEC filings):
https://stanislawrajmundburzynski.wordpress.com/2013/04/11/burzynski-clinical-trials-2/
Certain prospective protocols which have reached a Milestone as of May 1, 2012

Antineoplaston Therapy in Treating Patients With Stage IV Melanomau
Melanoma (Skin)
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
COMPLETED
Age 18 and over
Protocol IDs
CDR0000066552
BC-ME-2, NCT00003509
http://cancer.gov/clinicaltrials/BC-ME-2
2009_05_26 Study Changes Recruitment status, Recruitment, Misc.
1 clinical_study study_id
2
is_fda_regulated Yes
is_section_801 Yes
delayed_posting No
resp_party name_title Stanislaw R. Burzynski
name_title organization Burzynski Clinic
organization resp_party

Fm: Active, not recruiting
To: COMPLETED

status date
Fm: 2008-04
To: 2009-05

date
Fm: 2008-01
To: 2005-02

last_release_date
Fm: 2008-07-23
To: 2009-05-23
http://clinicaltrials.gov/archive/NCT00003509/2009_05_26/changes
So, we know the “COMPLETED” date is:

2009-05-23 (5/23/2009)

To put this in perspective, the below study done in 2006, was NOT published until about 7 years later, in 2013

2/13/2013 – The frequency, cost, and clinical outcomes of HYPERNATREMIA in patients hospitalized to a comprehensive CANCER center
http://www.ncbi.nlm.nih.gov/pubmed/23404230
Over 3 month period in 2006 re 3,446 patients, most of the HYPERNATREMIA (90 %) was acquired during hospital stay
http://www.ncbi.nlm.nih.gov/m/pubmed/23404230
Division of Internal Medicine, UT MD Anderson Cancer Center, Houston, TX, USA

Department of General Internal Medicine, University of Texas MD Anderson Cancer Center

Division of Endocrinology, Mayo Clinic

Support Care Cancer. 2013 Feb 13. [Epub ahead of print]

Supportive Care in Cancer
February 2013

DOI
10.1007/s00520-013-1734-6
http://link.springer.com/article/10.1007%2Fs00520-013-1734-6
� � � � � � � � � � � � � � � � �
Let’s look at “FACTS” which are supported by citation(s), reference(s), and / or link(s)
� � � � � � � � � � � � � � � � �
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
� � � � � � � � � � � � � � � � �
1 – Not Yet Recruiting + 10 – Recruiting –
(11=OPEN)
2 – WITHDRAWN
(Withdrawn due to slow enrollment)
7 – WITHDRAWN
(This study has been withdrawn prior to enrollment)
(9=WITHDRAWN)
40 – Active, not recruiting –
(40=CLOSED)
(1=COMPLETED)
61=TOTAL
� � � � � � � � � � � � � � � � �
1 – Not Yet Recruiting –
(1=OPEN)
10 Active –
(10=OPEN)
(9=WITHDRAWN)
25 CLOSED +15 CLOSED –
(40=CLOSED)
(1= COMPLETED)
61=TOTAL
� � � � � � � � � � � � � � � � �
10 – Recruiting
(OPEN)
1 Not Yet Recruiting / 10 Recruiting –
(11=OPEN)
(9=WITHDRAWN)
40 – Active, not recruiting
(40=CLOSED)
(1= COMPLETED)
61=TOTAL
� � � � � � � � � � � � � � � � �
11=1 Not Yet Recruiting / 10 Recruiting –
(11=OPEN)
(9=WITHDRAWN)
(40=CLOSED)
(1= COMPLETED)
61=TOTAL
� � � � � � � � � � � � � � � � �
11 – OPEN (ACTIVE)
2 – WITHDRAWN
(Withdrawn due to slow enrollment)
7 – WITHDRAWN
(This study has been withdrawn prior to enrollment)
= 9 WITHDRAWN
� � � � � � � � � � � � � � � � �
1 – Not Yet Recruiting
(1=OPEN)(Phase 3)
10 – Recruiting
(10=OPEN)
11=TOTAL
� � � � � � � � � � � � � � � � �
1 – Not Yet Recruiting + 10 – Recruiting –
(11=OPEN)
11=TOTAL
� � � � � � � � � � � � � � � � �
1 – Not Yet Recruiting –
(1=OPEN)
10 Active –
(10=OPEN)
11=TOTAL
� � � � � � � � � � � � � � � � �
10 – Recruiting
(OPEN)
1 Not Yet Recruiting / 10 Recruiting –
(11=OPEN)
11=TOTAL
� � � � � � � � � � � � � � � � �
11=1 Not Yet Recruiting / 10 Recruiting –
(11=OPEN)
11=TOTAL
� � � � � � � � � � � � � � � � �
The below 1st link: 10 Active (Open):
http://cancer.gov/clinicaltrials/search/results?protocolsearchid=11475951
� � � � � � � � � � � � � � � � �
1. Antineoplaston Therapy in Treating Patients With Stage IV ADRENAL GLAND Cancer
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months and over
Sponsor: Other
Protocol IDs: CDR0000066485, BC-AD-2, NCT00003453

2. Antineoplaston Therapy in Treating PATIENTS WITH BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066489, BC-BT-9, NCT00003457

3. Antineoplaston Therapy in Treating CHILDREN WITH BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066490, BC-BT-10, NCT00003458

4. Antineoplaston Therapy in Treating CHILDREN WITH LOW-GRADE ASTROCYTOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066504, BC-BT-13, NCT00003468

5. Antineoplaston Therapy in Treating PATIENTS WITH ANAPLASTIC ASTROCYTOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066507, BC-BT-15, NCT00003470

6. Antineoplaston Therapy in Treating Patients With Recurrent or Refractory MIXED GLIOMAs
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066510, BC-BT-18, NCT00003473

7. Antineoplaston Therapy in Treating PATIENTS WITH PRIMARY MALIGNANT BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066512, BC-BT-21, NCT00003475

8. Antineoplaston Therapy in Treating CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066513, BC-BT-22, NCT00003476

9. Antineoplaston Therapy in Treating CHILDREN WITH VISUAL PATHWAY GLIOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066514, BC-BT-23, NCT00003477

10. Antineoplaston Therapy in Treating Patients With Residual or Recurrent ANAPLASTIC ASTROCYTOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066585, BC-BT-8, NCT00003537
� � � � � � � � � � � � � � � � �
Securities and Exchange Commission (SEC) filings 10 “ACTIVE” (OPEN) trials:

Burzynski Clinical Trials (The SEC filings):
https://stanislawrajmundburzynski.wordpress.com/2013/04/11/burzynski-clinical-trials-2/
11/25/1997 – FORM 10-SB
http://pdf.secdatabase.com/2573/0000950110-97-001598.pdf
11/25/1997 – Company sponsoring 72 Phase II clinical trials conducted pursuant to INDs filed with FDA which are currently ongoing
� � � � � � � � � � � � � � � � �
1. AD-2 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN PATIENTS WITH CARCINOMA OF THE ADRENAL GLAND
7/20/96 – Revised
9/28/96 – Revised
4/14/97 – Revised

2. BT-9 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN PATIENTS WITH BRAIN TUMORS
11 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised

3. BT-10 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH BRAIN TUMORS
5 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised

4. BT-13 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH LOW GRADE ASTROCYTOMA
7 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
9/5/97 – Revised

5. BT-15 PHASE II STUDY OF ANTINEOPLASTON A10 AND AS2-1 IN ADULT PATIENTS WITH ANAPLASTIC ASTROCYTOMA
7/26/96 – Revised
10/4/96 – Revised
4/14/97 – Revised
9/5/97 – Revised

6. BT-18 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN ADULT PATIENTS WITH MIXED GLIOMA
12 40
7/26/96 – Revised
10/4/96 – Revised
12/9/96 – Revised
4/14/97 – Revised

7. BT-21 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN ADULT PATIENTS WITH PRIMARY MALIGNANT BRAIN TUMORS
19 40
9/5/95 – Partially Amended, pg.
9/10/96 – Revised
4/14/97 – Revised
8/25/97 – Revised

8. BT-22 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
4 40
11/5/97 – Partially Amended, pg.
4/14/97 – Revised
9/10/97 – Revised

9. BT-23 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 INFUSIONS IN CHILDREN WITH VISUAL PATHWAY GLIOMA
2 40
5/22/96 –
11/18/96 – Revised
4/14/97 – Revised

10. BT-8 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN PATIENTS WITH ANAPLASTIC ASTROCYTOMA
9 40
4/14/97 – Revised
9/15/97 – Revised
� � � � � � � � � � � � � � � � �
1. – 10. (2) CONSOLIDATED:
� � � � � � � � � � � � � � � � �
1. AD-2 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN PATIENTS WITH CARCINOMA OF THE ADRENAL GLAND
7/20/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
1. Antineoplaston Therapy in Treating Patients With Stage IV ADRENAL GLAND Cancer
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months and over
Sponsor: Other
Protocol IDs: CDR0000066485, BC-AD-2, NCT00003453

2. BT-9 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN PATIENTS WITH BRAIN TUMORS
11 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
2. Antineoplaston Therapy in Treating PATIENTS WITH BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066489, BC-BT-9, NCT00003457

3. BT-10 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH BRAIN TUMORS
5 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
3. Antineoplaston Therapy in Treating CHILDREN WITH BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066490, BC-BT-10, NCT00003458

4. BT-13 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH LOW GRADE ASTROCYTOMA
7 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
9/5/97 – Revised
4. Antineoplaston Therapy in Treating CHILDREN WITH LOW-GRADE ASTROCYTOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066504, BC-BT-13, NCT00003468

5. BT-15 PHASE II STUDY OF ANTINEOPLASTON A10 AND AS2-1 IN ADULT PATIENTS WITH ANAPLASTIC ASTROCYTOMA
7/26/96 – Revised
10/4/96 – Revised
4/14/97 – Revised
9/5/97 – Revised
5. Antineoplaston Therapy in Treating PATIENTS WITH ANAPLASTIC ASTROCYTOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066507, BC-BT-15, NCT00003470

6. BT-18 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN ADULT PATIENTS WITH
MIXED GLIOMA

12 40
7/26/96 – Revised
10/4/96 – Revised
12/9/96 – Revised
4/14/97 – Revised
6. Antineoplaston Therapy in Treating Patients With Recurrent or Refractory MIXED GLIOMAs
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066510, BC-BT-18, NCT00003473

7. BT-21 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN ADULT PATIENTS WITH PRIMARY MALIGNANT BRAIN TUMORS
19 40
9/5/95 – Partially Amended, pg.
9/10/96 – Revised
4/14/97 – Revised
8/25/97 – Revised
7. Antineoplaston Therapy in Treating PATIENTS WITH PRIMARY MALIGNANT BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066512, BC-BT-21, NCT00003475

8. BT-22 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
4 40
11/5/97 – Partially Amended, pg.
4/14/97 – Revised
9/10/97 – Revised
8. Antineoplaston Therapy in Treating CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066513, BC-BT-22, NCT00003476

9. BT-23 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 INFUSIONS IN CHILDREN WITH VISUAL PATHWAY GLIOMA
2 40
5/22/96 –
11/18/96 – Revised
4/14/97 – Revised
9. Antineoplaston Therapy in Treating CHILDREN WITH VISUAL PATHWAY GLIOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066514, BC-BT-23, NCT00003477

10. BT-8 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN PATIENTS WITH ANAPLASTIC ASTROCYTOMA
9 40
4/14/97 – Revised
9/15/97 – Revised
10. Antineoplaston Therapy in Treating Patients With Residual or Recurrent ANAPLASTIC ASTROCYTOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066585, BC-BT-8, NCT00003537
� � � � � � � � � � � � � � � � �
Burzynski Clinical Trials (The SEC filings):
https://stanislawrajmundburzynski.wordpress.com/2013/04/11/burzynski-clinical-trials-2/
Certain prospective protocols which have reached a Milestone as of May 1, 2012

The results of Protocols

10. BT-08
2. BT-09
3. BT-10
4. BT-13
5. BT-15
6. BT-18
7. BT-21
8. BT-22
9. BT-23

5/1/2012 – set forth below

1. Antineoplaston Therapy in Treating Patients With Stage IV ADRENAL GLAND Cancer
Adrenocortical Carcinoma
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months and over
Protocol IDs
CDR0000066485
BC-AD-2, NCT00003453
http://cancer.gov/clinicaltrials/BC-AD-2
2. Antineoplaston Therapy in Treating PATIENTS WITH BRAIN TUMORS
Brain and Central Nervous System Tumors
Drug: antineoplaston
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 18 and over
Protocol IDs
CDR0000066489
BC-BT-9, NCT00003457
http://cancer.gov/clinicaltrials/BC-BT-9
· Protocol BT-09, involving the study of Antineoplastons A10 and AS2-1 in PATIENTS WITH BRAIN TUMORS
BT-09 – Protocol #
40 – Patients Accrued
28 – Evaluable Patients
4 / 14.3% – # and % of Patients Showing Complete Response
5 / 17.9% – # and % of Patients Showing Partial Response
13 / 46.4% – # and % of Patients Showing Stable Disease
6 / 21.4% – # and % of Patients Showing Progressive Disease

3. Antineoplaston Therapy in Treating CHILDREN WITH BRAIN TUMORS
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months to 17 years
Protocol IDs
CDR0000066490
BC-BT-10, NCT00003458
http://cancer.gov/clinicaltrials/BC-BT-10
· Protocol BT-10, involving the study of Antineoplastons A10 and AS2-1 in CHILDREN WITH BRAIN TUMORS
BT-10 – Protocol #
30 – Patients Accrued
22 – Evaluable Patients
3 / 13.6% – # and % of Patients Showing Complete Response
1 / 4.5% – # and % of Patients Showing Partial Response
7 / 31.8% – # and % of Patients Showing Stable Disease
11 / 50.0% – # and % of Patients Showing Progressive Disease

4. Antineoplaston Therapy in Treating CHILDREN WITH LOW-GRADE ASTROCYTOMA
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months to 17 years
Protocol IDs
CDR0000066504
BC-BT-13, NCT00003468
http://cancer.gov/clinicaltrials/BC-BT-13
· Protocol BT-13, involving the study of Antineoplastons A10 and AS2-1 in CHILDREN WITH LOW GRADE ASTROCYTOMA, a type of PMBT
BT-13 – Protocol #
17 – Patients Accrued
14 – Evaluable Patients
6 / 42.9% – # and % of Patients Showing Complete Response
1 / 7.1% – # and % of Patients Showing Partial Response
5 / 35.7% – # and % of Patients Showing Stable Disease
2 / 14.3% – # and % of Patients Showing Progressive Disease

5. Antineoplaston Therapy in Treating PATIENTS WITH ANAPLASTIC ASTROCYTOMA
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 18 and over
Protocol IDs
CDR0000066507
BC-BT-15, NCT00003470
http://cancer.gov/clinicaltrials/BC-BT-15
· Protocol BT-15, involving the study of Antineoplastons A10 and AS2-1 in adult PATIENTS WITH ANAPLASTIC ASTROCYTOMA, a type of PMBT
BT-15 – Protocol #
27 – Patients Accrued
20 – Evaluable Patients
3 / 15.0% – # and % of Patients Showing Complete Response
2 / 10.0% – # and % of Patients Showing Partial Response
9 / 45.0% – # and % of Patients Showing Stable Disease
6 / 30.0% – # and % of Patients Showing Progressive Disease

6. Antineoplaston Therapy in Treating Patients With Recurrent or Refractory MIXED GLIOMAs
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 18 and over
Protocol IDs
CDR0000066510
BC-BT-18, NCT00003473
http://cancer.gov/clinicaltrials/BC-BT-18
Protocol BT-18, involving a study of Antineoplastons A10 and AS2-1 in the treatment of “MIXED GLIOMA,” a type of PMBT
BT-18 – Protocol #
20 – Patients Accrued
13 – Evaluable Patients
3 / 23.1% – # and % of Patients Showing Complete Response
1 / 7.7% – # and % of Patients Showing Partial Response
3 / 23.1% – # and % of Patients Showing Stable Disease
6 / 46.2% – # and % of Patients Showing Progressive Disease

7. Antineoplaston Therapy in Treating Patients With PRIMARY MALIGNANT BRAIN TUMORS
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 18 and over
Protocol IDs
CDR0000066512
BC-BT-21, NCT00003475
http://cancer.gov/clinicaltrials/BC-BT-21
· Protocol BT-21, involving the study of Antineoplastons A10 and AS2-1 in adults with PRIMARY MALIGNANT BRAIN TUMORS
BT-21 – Protocol #
40 – Patients Accrued
23 – Evaluable Patients
2 / 8.7% – # and % of Patients Showing Complete Response
2 / 8.7% – # and % of Patients Showing Partial Response
9 / 39.1% – # and % of Patients Showing Stable Disease
10 / 43.5% – # and % of Patients Showing Progressive Disease

8. Antineoplaston Therapy in Treating CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months to 17 years
Protocol IDs
CDR0000066513
BC-BT-22, NCT00003476
http://cancer.gov/clinicaltrials/BC-BT-22
· Protocol BT-22, involving a study of Antineoplastons A10 and AS2-1 in CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
BT-22 – Protocol #
40 – Patients Accrued
24 – Evaluable Patients
1 / 4.2% – # and % of Patients Showing Complete Response
3 / 12.5% – # and % of Patients Showing Partial Response
9 / 37.5% – # and % of Patients Showing Stable Disease
11 / 45.8% – # and % of Patients Showing Progressive Disease

9. Antineoplaston Therapy in Treating CHILDREN WITH VISUAL PATHWAY GLIOMA
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months to 17 years
Protocol IDs
CDR0000066514
BC-BT-23, NCT00003477
http://cancer.gov/clinicaltrials/BC-BT-23
(· Protocol BT-23, involving a study of Antineoplastons A10 and AS2-1 in CHILDREN WITH VISUAL PATHWAY GLIOMA)
BT-23- Protocol #
16 – Patients Accrued
12 – Evaluable Patients
3 / 25% – # and % of Patients Showing Complete Response
2 / 16.7% – # and % of Patients Showing Partial Response
6 / 50.0% – # and % of Patients Showing Stable Disease
1 / 8.3% – # and % of Patients Showing Progressive Disease

10. Antineoplaston Therapy in Treating Patients With Residual or Recurrent ANAPLASTIC ASTROCYTOMA
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Recruiting
Phase II / Phase 2
ACTIVE
Age 18 and over
Protocol IDs
CDR0000066585
BC-BT-8, NCT00003537
http://cancer.gov/clinicaltrials/BC-BT-8
· Protocol BT-08, involving the study of Antineoplastons A10 and AS2-1 in patients with ANAPLASTIC ASTROCYTOMA
BT-08 – Protocol #
19 – Patients Accrued
14- Evaluable Patients
4 / 28.6% – # and % of Patients Showing Complete Response
0 / 0.0% – # and % of Patients Showing Partial Response
6 / 42.9% – # and % of Patients Showing Stable Disease
4 / 28.6% – # and % of Patients Showing Progressive Disease
� � � � � � � � � � � � � � � � �
1. – 10. (3) CONSOLIDATED:
� � � � � � � � � � � � � � � � �
1. AD-2 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN PATIENTS WITH CARCINOMA OF THE ADRENAL GLAND
7/20/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
1. Antineoplaston Therapy in Treating Patients With Stage IV ADRENAL GLAND Cancer
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months and over
Sponsor: Other
Protocol IDs: CDR0000066485, BC-AD-2, NCT00003453
1. Antineoplaston Therapy in Treating Patients With Stage IV ADRENAL GLAND Cancer
Adrenocortical Carcinoma
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months and over
Protocol IDs
CDR0000066485
BC-AD-2, NCT00003453
http://cancer.gov/clinicaltrials/BC-AD-2
2. BT-9 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN PATIENTS WITH BRAIN TUMORS
11 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
2. Antineoplaston Therapy in Treating PATIENTS WITH BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066489, BC-BT-9, NCT00003457
2. Antineoplaston Therapy in Treating PATIENTS WITH BRAIN TUMORS
Brain and Central Nervous System Tumors
Drug: antineoplaston
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 18 and over
Protocol IDs
CDR0000066489
BC-BT-9, NCT00003457
http://cancer.gov/clinicaltrials/BC-BT-9
· Protocol BT-09, involving the study of Antineoplastons A10 and AS2-1 in PATIENTS WITH BRAIN TUMORS
BT-09 – Protocol #
40 – Patients Accrued
28 – Evaluable Patients
4 / 14.3% – # and % of Patients Showing Complete Response
5 / 17.9% – # and % of Patients Showing Partial Response
13 / 46.4% – # and % of Patients Showing Stable Disease
6 / 21.4% – # and % of Patients Showing Progressive Disease

3. BT-10 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH BRAIN TUMORS
5 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
3. Antineoplaston Therapy in Treating CHILDREN WITH BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066490, BC-BT-10, NCT00003458
3. Antineoplaston Therapy in Treating CHILDREN WITH BRAIN TUMORS
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months to 17 years
Protocol IDs
CDR0000066490
BC-BT-10, NCT00003458
http://cancer.gov/clinicaltrials/BC-BT-10
· Protocol BT-10, involving the study of Antineoplastons A10 and AS2-1 in CHILDREN WITH BRAIN TUMORS
BT-10 – Protocol #
30 – Patients Accrued
22 – Evaluable Patients
3 / 13.6% – # and % of Patients Showing Complete Response
1 / 4.5% – # and % of Patients Showing Partial Response
7 / 31.8% – # and % of Patients Showing Stable Disease
11 / 50.0% – # and % of Patients Showing Progressive Disease

4. BT-13 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH LOW GRADE ASTROCYTOMA
7 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
9/5/97 – Revised
4. Antineoplaston Therapy in Treating CHILDREN WITH LOW-GRADE ASTROCYTOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066504, BC-BT-13, NCT00003468
4. Antineoplaston Therapy in Treating CHILDREN WITH LOW-GRADE ASTROCYTOMA
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months to 17 years
Protocol IDs
CDR0000066504
BC-BT-13, NCT00003468
http://cancer.gov/clinicaltrials/BC-BT-13
· Protocol BT-13, involving the study of Antineoplastons A10 and AS2-1 in CHILDREN WITH LOW GRADE ASTROCYTOMA, a type of PMBT
BT-13 – Protocol #
17 – Patients Accrued
14 – Evaluable Patients
6 / 42.9% – # and % of Patients Showing Complete Response
1 / 7.1% – # and % of Patients Showing Partial Response
5 / 35.7% – # and % of Patients Showing Stable Disease
2 / 14.3% – # and % of Patients Showing Progressive Disease

5. BT-15 PHASE II STUDY OF ANTINEOPLASTON A10 AND AS2-1 IN ADULT PATIENTS WITH ANAPLASTIC ASTROCYTOMA
7/26/96 – Revised
10/4/96 – Revised
4/14/97 – Revised
9/5/97 – Revised
5. Antineoplaston Therapy in Treating PATIENTS WITH ANAPLASTIC ASTROCYTOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066507, BC-BT-15, NCT00003470
5. Antineoplaston Therapy in Treating PATIENTS WITH ANAPLASTIC ASTROCYTOMA
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 18 and over
Protocol IDs
CDR0000066507
BC-BT-15, NCT00003470
http://cancer.gov/clinicaltrials/BC-BT-15
· Protocol BT-15, involving the study of Antineoplastons A10 and AS2-1 in adult PATIENTS WITH ANAPLASTIC ASTROCYTOMA, a type of PMBT
BT-15 – Protocol #
27 – Patients Accrued
20 – Evaluable Patients
3 / 15.0% – # and % of Patients Showing Complete Response
2 / 10.0% – # and % of Patients Showing Partial Response
9 / 45.0% – # and % of Patients Showing Stable Disease
6 / 30.0% – # and % of Patients Showing Progressive Disease

6. BT-18 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN ADULT PATIENTS WITH
MIXED GLIOMA

12 40
7/26/96 – Revised
10/4/96 – Revised
12/9/96 – Revised
4/14/97 – Revised
6. Antineoplaston Therapy in Treating Patients With Recurrent or Refractory MIXED GLIOMAs
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066510, BC-BT-18, NCT00003473
6. Antineoplaston Therapy in Treating Patients With Recurrent or Refractory MIXED GLIOMAs
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 18 and over
Protocol IDs
CDR0000066510
BC-BT-18, NCT00003473
http://cancer.gov/clinicaltrials/BC-BT-18
Protocol BT-18, involving a study of Antineoplastons A10 and AS2-1 in the treatment of “MIXED GLIOMA,” a type of PMBT
BT-18 – Protocol #
20 – Patients Accrued
13 – Evaluable Patients
3 / 23.1% – # and % of Patients Showing Complete Response
1 / 7.7% – # and % of Patients Showing Partial Response
3 / 23.1% – # and % of Patients Showing Stable Disease
6 / 46.2% – # and % of Patients Showing Progressive Disease

7. BT-21 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN ADULT PATIENTS WITH PRIMARY MALIGNANT BRAIN TUMORS
19 40
9/5/95 – Partially Amended, pg.
9/10/96 – Revised
4/14/97 – Revised
8/25/97 – Revised
7. Antineoplaston Therapy in Treating Patients With PRIMARY MALIGNANT BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066512, BC-BT-21, NCT00003475
7. Antineoplaston Therapy in Treating Patients With PRIMARY MALIGNANT BRAIN TUMORS
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 18 and over
Protocol IDs
CDR0000066512
BC-BT-21, NCT00003475
http://cancer.gov/clinicaltrials/BC-BT-21
· Protocol BT-21, involving the study of Antineoplastons A10 and AS2-1 in adults with PRIMARY MALIGNANT BRAIN TUMORS
BT-21 – Protocol #
40 – Patients Accrued
23 – Evaluable Patients
2 / 8.7% – # and % of Patients Showing Complete Response
2 / 8.7% – # and % of Patients Showing Partial Response
9 / 39.1% – # and % of Patients Showing Stable Disease
10 / 43.5% – # and % of Patients Showing Progressive Disease

8. BT-22 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
4 40
11/5/97 – Partially Amended, pg.
4/14/97 – Revised
9/10/97 – Revised
8. Antineoplaston Therapy in Treating CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066513, BC-BT-22, NCT00003476
8. Antineoplaston Therapy in Treating CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months to 17 years
Protocol IDs
CDR0000066513
BC-BT-22, NCT00003476
http://cancer.gov/clinicaltrials/BC-BT-22
· Protocol BT-22, involving a study of Antineoplastons A10 and AS2-1 in CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
BT-22 – Protocol #
40 – Patients Accrued
24 – Evaluable Patients
1 / 4.2% – # and % of Patients Showing Complete Response
3 / 12.5% – # and % of Patients Showing Partial Response
9 / 37.5% – # and % of Patients Showing Stable Disease
11 / 45.8% – # and % of Patients Showing Progressive Disease

9. BT-23 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 INFUSIONS IN CHILDREN WITH VISUAL PATHWAY GLIOMA
2 40
5/22/96 –
11/18/96 – Revised
4/14/97 – Revised
9. Antineoplaston Therapy in Treating CHILDREN WITH VISUAL PATHWAY GLIOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 6 months to 17 years
Sponsor: Other
Protocol IDs: CDR0000066514, BC-BT-23, NCT00003477
9. Antineoplaston Therapy in Treating CHILDREN WITH VISUAL PATHWAY GLIOMA
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months to 17 years
Protocol IDs
CDR0000066514
BC-BT-23, NCT00003477
http://cancer.gov/clinicaltrials/BC-BT-23
(· Protocol BT-23, involving a study of Antineoplastons A10 and AS2-1 in CHILDREN WITH VISUAL PATHWAY GLIOMA)
BT-23- Protocol #
16 – Patients Accrued
12 – Evaluable Patients
3 / 25% – # and % of Patients Showing Complete Response
2 / 16.7% – # and % of Patients Showing Partial Response
6 / 50.0% – # and % of Patients Showing Stable Disease
1 / 8.3% – # and % of Patients Showing Progressive Disease

10. BT-8 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN PATIENTS WITH ANAPLASTIC ASTROCYTOMA
9 40
4/14/97 – Revised
9/15/97 – Revised
10. Antineoplaston Therapy in Treating Patients With Residual or Recurrent ANAPLASTIC ASTROCYTOMA
Phase: Phase II
Type: Treatment
Status: Active
Age: 18 and over
Sponsor: Other
Protocol IDs: CDR0000066585, BC-BT-8, NCT00003537
10. Antineoplaston Therapy in Treating Patients With Residual or Recurrent ANAPLASTIC ASTROCYTOMA
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Recruiting
Phase II / Phase 2
ACTIVE
Age 18 and over
Protocol IDs
CDR0000066585
BC-BT-8, NCT00003537
http://cancer.gov/clinicaltrials/BC-BT-8
· Protocol BT-08, involving the study of Antineoplastons A10 and AS2-1 in patients with ANAPLASTIC ASTROCYTOMA
BT-08 – Protocol #
19 – Patients Accrued
14- Evaluable Patients
4 / 28.6% – # and % of Patients Showing Complete Response
0 / 0.0% – # and % of Patients Showing Partial Response
6 / 42.9% – # and % of Patients Showing Stable Disease
4 / 28.6% – # and % of Patients Showing Progressive Disease
� � � � � � � � � � � � � � � � �
http://www.burzynskiclinic.com/scientific-publications.html
Interim Reports on Clinial Trials:

16. 2003

DRUGS IN R&D
Drugs in R and D
(Drugs in Research and Development)

BT-11

BRAIN STEM GLIOMA

Phase II study of antineoplaston A10 and AS2-1 in patients with recurrent diffuse intrinsic BRAIN STEM GLIOMA:

a preliminary report.
http://www.ncbi.nlm.nih.gov/pubmed/12718563
Burzynski, S.R., Lewy, R.I., Weaver, R.A., Axler, M.L., Janicki, T.J., Jurida, G.F., Paszkowiak, J.K., Szymkowski, B.G., Khan, M.I., Bestak, M.
http://www.ncbi.nlm.nih.gov/m/pubmed/12718563
Drugs R D. 2003;4(2):91-101
Drugs in R&D 2003;4:91-101
http://www.burzynskiclinic.com/images/stories/Publications/960.pdf
6 months – median duration: treatment

12 patients:
2 years / 33.3% – Survival
2 / 17% – alive and tumour free for over 5 years since initial diagnosis

from start of treatment:
5 years – 1 alive for more than
4 years – 1 alive for more than

Only mild and moderate toxicities observed:
3 – skin allergy
2 – anaemia
2 – fever
2 – hypernatremia
1 – agranulocytosis
1 – hypoglycaemia
1 – numbness
1 – tiredness
1 – myalgia
1 – vomiting

2003 – Protocol – recurrent diffuse intrinsic BRAIN STEM GLIOMA
12 – Patients Accrued
10 – Evaluable Patients
2 / 20% – # and % of Patients Showing Complete Response
3 / 30% – # and % of Patients Showing Partial Response
3 / 30% – # and % of Patients Showing Stable Disease
2 / 20% – # and % of Patients Showing Progressive Disease
� � � � � � � � � � � � � � � � �
RECURRENT DIFFUSE INTRINSIC BRAIN STEM GLIOMA

11/25/1997 – FORM 10-SB
http://pdf.secdatabase.com/2573/0000950110-97-001598.pdf
10/1997 – clinical trials reached Milestone

Clinical Trial BT-11

trial of Clinical Trial BT-11 involves patients with BRAIN STEM GLIOMA

5/1996 – trial approved by FDA

10/1997 – Protocol – BRAIN STEM GLIOMA
12 – Patients Accrued
12 – Evaluable Patients
1 / 20% – # and % of Patients Showing Complete Response
3 / 30% – # and % of Patients Showing Partial Response
8 / 50% – # and % of Patients Showing Stable Disease or Progressive Disease

BT-11 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN PATIENTS WITH BRAIN STEM GLIOMA
15 40
5/15/96 – Revised
7/11/96 – Revised
9/28/96 – Revised
5/10/97 – Revised
� � � � � � � � � � � � � � � � �
5/1/2012 – prospective protocols which have reached Milestone

results of Protocols:

BT-11

5/1/2012 – set forth below

Form 10-Q (For the fiscal year ended February 29, 2012)
(as of May 1, 2012) Protocol BT
http://www.sec.gov/Archives/edgar/data/724445/000110465912040430/a12-12972_110k.htm
RECURRENT DIFFUSE INTRINSIC BRAIN STEM GLIOMA

Antineoplaston Therapy in Treating Patients With BRAIN STEM GLIOMA
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
CLOSED
Age 6 months and over
Protocol IDs
CDR0000066491
BC-BT-11, NCT00003459
http://cancer.gov/clinicaltrials/BC-BT-11
· Protocol BT-11, involving the study of Antineoplastons A10 and AS2-1 in patients with BRAINSTEM GLIOMA

BT-11 – Protocol #
40 – Patients Accrued
28 – Evaluable Patients
5 / 17.9% – # and % of Patients Showing Complete Response
4 / 14.3% – # and % of Patients Showing Partial Response
12 / 42.9% – # and % of Patients Showing Stable Disease
7 / 25.0% – # and % of Patients Showing Progressive Disease
� � � � � � � � � � � � � � � � �
BT-11 (RECURRENT DIFFUSE INTRINSIC) BRAIN STEM GLIOMA (3) CONSOLIDATED:
http://clinicaltrials.gov/show/NCT00003459
8/1998 – Study Start Date
� � � � � � � � � � � � � � � � �
BT-11 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN PATIENTS WITH BRAIN STEM GLIOMA
15 40
5/15/96 – Revised
7/11/96 – Revised
9/28/96 – Revised
5/10/97 – Revised

10/1997 – Protocol BT-11 – BRAIN STEM GLIOMA
12 – Patients Accrued
12 – Evaluable Patients
1 / 20% – # and % of Patients Showing Complete Response
3 / 30% – # and % of Patients Showing Partial Response
8 / 50% – # and % of Patients Showing Stable Disease or Progressive Disease

2003 – Protocol – recurrent diffuse intrinsic BRAIN STEM GLIOMA
12 – Patients Accrued
10 – Evaluable Patients
2 / 20% – # and % of Patients Showing Complete Response
3 / 30% – # and % of Patients Showing Partial Response
3 / 30% – # and % of Patients Showing Stable Disease
2 / 20% – # and % of Patients Showing Progressive Disease

5/1/2012 – Protocol BT-11
Antineoplaston Therapy in Treating Patients With BRAIN STEM GLIOMA
Brain and Central Nervous System Tumors
http://cancer.gov/clinicaltrials/BC-BT-11
· Protocol BT-11 patients with BRAINSTEM GLIOMA
BT-11 – Protocol #
40 – Patients Accrued
28 – Evaluable Patients
5 / 17.9% – # and % of Patients Showing Complete Response
4 / 14.3% – # and % of Patients Showing Partial Response
12 / 42.9% – # and % of Patients Showing Stable Disease
7 / 25.0% – # and % of Patients Showing Progressive Disease
http://clinicaltrials.gov/archive/NCT00003459/2007_10_17/changes
10/17/2007 – Updated
1 clinical_study status
2
Fm: No longer recruiting
To: Active, not recruiting
� � � � � � � � � � � � � � � � �

Scientific Publications
(former web-site screenshots)
http://www.circare.org/info/bri/burzynski_fdauntitled_promo_2012.pdf

http://www.burzynskiclinic.com/scientific-publications.html
Interim Reports on Clinial Trials:

2003 – NEURO-ONCOLOGY

2003 – Phase II study of Antineoplastons A10 and AS2-1 (ANP) in children with recurrent and progressive multicentric glioma

A preliminary report
http://www.burzynskiclinic.com/images/stories/Publications/970.pdf
Neuro-Oncology. 2003; 5: 358

2004 – NEURO-ONCOLOGY

Weaver, R.A., Burzynski, S.R., Bestak, M., Lewy, R.I., Janicki, T.J., Szymkowski, B., Jurida, G., Khan, M.I., Dolgopolov, V.

Phase II study of Antineoplastons A10 and AS2-1 (ANP) in recurrent glioblastoma multiforme
http://www.burzynskiclinic.com/images/stories/Publications/1218.pdf
Neuro-Oncology. 2004; 6: 384

2004 – NEURO-ONCOLOGY

Burzynski, S.R., Weaver, R. Bestak. M., Lewy, R.I., Janicki, T., Jurida, G., Szymkowski, B., Khan, M., Dolgopolov, V.

Long-term survivals in phase II studies of Antineoplastons A10 and AS2-1 (ANP) in patients with diffuse intrinsic brain stem glioma
http://www.burzynskiclinic.com/images/stories/Publications/1219.pdf
Neuro-Oncology. 2004; 6: 386

2004 – NEURO-ONCOLOGY

Burzynski, S.R., Weaver, R. Bestak. M., Janicki, T., Jurida, G., Szymkowski, B., Khan, M., Dolgopolov, V.

Phase II studies of antineoplastons A10 and AS2-1 (ANP) in children with atypical teratoid/rhabdoid tumors (AT/RT) of the central nervous system

A preliminary report
http://www.burzynskiclinic.com/images/stories/Publications/1146.pdf
Neuro-Oncology. 2004; 6: 427

2004 – NEURO-ONCOLOGY

Burzynski, S.R., Weaver, R. Bestak. M., Janicki, T., Szymkowski, B., Jurida, G., Khan, M., Dolgopolov, V.

Treatment of primitive neuroectodermal tumors (PNET) with antineoplastons A10 and AS2-1 (ANP)

Preliminary results of phase II studies
http://www.burzynskiclinic.com/images/stories/Publications/1147.pdf
Neuro-Oncology. 2004; 6: 428

2004 – DRUGS IN R&D

Burzynski, S.R., Weaver, R., Lewy, R., Janicki, T. Jurida, G., Szymkowski, B., Khan, M., Bestak, M.

Phase II study of antineoplaston A10 and AS2-1 in children with recurrent and progressive multicentric glioma

A Preliminary Report
http://www.burzynskiclinic.com/images/stories/Publications/1194.pdf
Drugs R&D 2004;5(6):315-326

2004 – INTEGRATIVE CANCER THERAPIES

Review Articles on Clinical Trials:

Burzynski, S.R.

The Present State of Antineoplaston Research
http://www.burzynskiclinic.com/images/stories/Publications/994.pdf
Integrative Cancer Therapies 2004;3:47-58

2004 – INTEGRATIVE CANCER THERAPIES

Burzynski, S.R., Lewy, R.I., Weaver, R., Janicki, T., Jurida, G., Khan, M., Larisma, C.B., Paszkowiak, J., Szymkowski, B.

Long-term survival and complete response of a patient with recurrent diffuse intrinsic brain stem glioblastoma multiforme
http://www.burzynskiclinic.com/images/stories/Publications/1145.pdf
Integrative Cancer Therapies 2004;3:257-261

2004 – DRUGS IN R&D
Drugs in R and D (Drugs in Research and Development)

2004 – Phase II study of antineoplaston A10 and AS2-1 in children with recurrent and progressive multicentric glioma :

a preliminary report
http://www.ncbi.nlm.nih.gov/pubmed/15563234
Drugs R D. 2004;5(6):315-26
http://www.ncbi.nlm.nih.gov/m/pubmed/15563234
incurable recurrent and progressive multicentric glioma

antineoplaston A10 and AS2-1 (ANP)

9 – median age

6 – pilocytic astrocytoma

4 – low-grade astrocytoma
1 – astrocytoma grade 2

1 – visual pathway glioma: biopsy not performed due to dangerous location

16 months – average duration intravenous ANP therapy

19 months – average duration oral ANP

1 – non-evaluable due to only 4 weeks of ANP: lack of follow-up scans

1 – stable disease discontinued ANP against medical advice: died 4.5 years later

10 – alive and well from 2 to >14 years post-diagnosis

1 – serious toxicity of reversible tinnitus, 1 day’s duration

2004 – Protocol – incurable recurrent and progressive multicentric glioma
12 – Patients Accrued
33% – % of Patients Showing Complete Response
25% – % of Patients Showing Partial Response
33% – % of Patients Showing Stable Disease
0 / 0% – # and % of Patients Showing Progressive Disease

CHILDREN WITH INCURABLE RECURRENT AND PROGRESSIVE MULTICENTRIC GLIOMA
6 – pilocytic astrocytoma
4 – low-grade astrocytoma
1 – astrocytoma grade 2
1 – visual pathway glioma: biopsy not performed due to dangerous location
12 – TOTAL

11/25/1997 – FORM 10-SB
http://pdf.secdatabase.com/2573/0000950110-97-001598.pdf
BT-13 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH LOW GRADE ASTROCYTOMA
7 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
9/5/97 – Revised

BT-23 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 INFUSIONS IN CHILDREN WITH VISUAL PATHWAY
GLIOMA

2 40
5/22/96 –
11/18/96 – Revised
4/14/97 – Revised

5/1/2012 – prospective protocols which have reached Milestone

results of Protocols:

BT-13
BT-23

5/1/2012 – set forth below

Form 10-Q (For the fiscal year ended February 29, 2012)
(as of May 1, 2012) Protocol BT
http://www.sec.gov/Archives/edgar/data/724445/000110465912040430/a12-12972_110k.htm
CHILDREN WITH INCURABLE RECURRENT AND PROGRESSIVE MULTICENTRIC GLIOMA (3) CONSOLIDATED:
6 – pilocytic astrocytoma
4 – low-grade astrocytoma
1 – astrocytoma grade 2
1 – visual pathway glioma: biopsy not performed due to dangerous location
12 – TOTAL
http://clinicaltrials.gov/show/NCT00003468
5/1996 – Study Start Date

BT-13 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH LOW GRADE ASTROCYTOMA
7 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
9/5/97 – Revised
Antineoplaston Therapy in Treating Children With Low-Grade Astrocytoma
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months to 17 years
Protocol IDs
CDR0000066504
BC-BT-13, NCT00003468
http://cancer.gov/clinicaltrials/BC-BT-13
· Protocol BT-13, involving the study of Antineoplastons A10 and AS2-1 in children with low grade astrocytoma, a type of PMBT
BT-13 – Protocol #
17 – Patients Accrued
14 – Evaluable Patients
6 / 42.9% – # and % of Patients Showing Complete Response
1 / 7.1% – # and % of Patients Showing Partial Response
5 / 35.7% – # and % of Patients Showing Stable Disease
2 / 14.3% – # and % of Patients Showing Progressive Disease
http://clinicaltrials.gov/show/NCT00003468
12/2011 – Estimated Primary Completion Date (Final data collection date for primary outcome measure)
6/9/2009 – Updated
1 clinical_study date
2
Fm: 2008-12
To: 2009-06
3 date last_release_date
4
Fm: 2008-12-23
To: 2009-06-09
5 last_release_date clinical_study
http://clinicaltrials.gov/show/NCT00003477
6/1996 – Study Start Date

BT-23 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 INFUSIONS IN CHILDREN WITH VISUAL PATHWAY
GLIOMA

2 40
5/22/96 –
11/18/96 – Revised
4/14/97 – Revised
Antineoplaston Therapy in Treating Children With Visual Pathway Glioma
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
ACTIVE
Age 6 months to 17 years
Protocol IDs
CDR0000066514
BC-BT-23, NCT00003477
http://cancer.gov/clinicaltrials/BC-BT-23
(· Protocol BT-23, involving a study of Antineoplastons A10 and AS2-1 in children with visual pathway glioma)
BT-23- Protocol #
16 – Patients Accrued
12 – Evaluable Patients
3 / 25% – # and % of Patients Showing Complete Response
2 / 16.7% – # and % of Patients Showing Partial Response
6 / 50.0% – # and % of Patients Showing Stable Disease
1 / 8.3% – # and % of Patients Showing Progressive Disease
http://clinicaltrials.gov/show/NCT00003477
12/2011 – Estimated Primary Completion Date (Final data collection date for primary outcome measure)
http://clinicaltrials.gov/archive/NCT00003477/2009_06_09/changes
6/9/2009 – Updated
1 clinical_study date
2
Fm: 2008-12
To: 2009-06
3 date last_release_date
4
Fm: 2008-12-23
To: 2009-06-09
5 last_release_date clinical_study
� � � � � � � � � � � � � � � � �
2005 – INTEGRATIVE CANCER THERAPIES

Burzynski, S.R., Weaver, R.A., Janicki, T., Szymkowski, B., Jurida, G., Khan, M., Dolgopolov, V.

Long-term survival of high-risk pediatric patients with primitive neuroectodermal tumors treated with Antineoplastons A10 and AS2-1
http://www.burzynskiclinic.com/images/stories/Publications/1220.pdf
Integrative Cancer Therapies 2005;4(2):168-177

2005 – INTEGRATIVE CANCER THERAPIES

6/2005 – Long-term survival of high-risk pediatric patients with primitive neuroectodermal tumors treated with antineoplastons A10 and AS2-1
http://www.ncbi.nlm.nih.gov/pubmed/15911929
Integr Cancer Ther. 2005 Jun;4(2):168-77
http://www.ncbi.nlm.nih.gov/m/pubmed/15911929
Phase II / Phase 2 studies

Primitive neuroectodermal tumors (PNETs)
usually successfully treated with craniospinal radiation and chemotherapy

difficulties with standard treatment can be encountered in:

1. very young children
2. adult patients at high risk of complication from standard treatment
3. patients with recurrent tumors

13 children – recurrent disease or high risk

treated with antineoplastons (ANP)

5 years, 7 months (range, 1-11) – median age

8 – Medulloblastoma
3 – pineoblastoma
2 – other PNET

Previous treatments:

12 – surgery (1 had biopsy only, suboccipital craniotomy)
6 – chemotherapy
6 – radiation therapy
6 – had not received prior chemotherapy or radiation

treatment – intravenous infusions of 2 formulations of ANP, A10 and AS2-1

20 months – administered for average

6 (46%) survived more than 5 years from initiation of ANP

5 – not treated earlier with radiation therapy or chemotherapy

serious side effects:
1 – fever
1 – granulocytopenia
1 – anemia

study ongoing and accruing additional patients

percentage of response is lower than standard treatment of favorable PNET

long-term survival in poor-risk cases and reduced toxicity makes ANP promising for:
1. very young children
2. patients at high risk of complication of standard therapy
3. patients with recurrent tumors

2005 – Protocol – Long-term survival of high-risk pediatric patients with primitive neuroectodermal tumors
13 – Patients Accrued
23% – % of Patients Showing Complete Response
8% – % of Patients Showing Partial Response
31% – % of Patients Showing Stable Disease
38% – # and % of Patients Showing Progressive Disease

LONG-TERM SURVIVAL OF HIGH-RISK PEDIATRIC PATIENTS WITH PRIMITIVE NEUROECTODERMAL TUMORS:
8 – Medulloblastoma
3 – pineoblastoma
2 – other
PNET (Primitive neuroectodermal tumors)

13 – TOTAL

11/25/1997 – FORM 10-SB
http://pdf.secdatabase.com/2573/0000950110-97-001598.pdf
BT-12 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH PRIMITIVE NEUROECTODERMAL TUMORS; (PNET)

5 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised

5/1/2012 – prospective protocols which have reached Milestone

results of Protocols:

BT-12

5/1/2012 – set forth below

Form 10-Q (For the fiscal year ended February 29, 2012)
(as of May 1, 2012) Protocol BT
http://www.sec.gov/Archives/edgar/data/724445/000110465912040430/a12-12972_110k.htm
LONG-TERM SURVIVAL OF HIGH-RISK PEDIATRIC PATIENTS WITH PRIMITIVE NEUROECTODERMAL TUMORS:
8 – Medulloblastoma
3 – pineoblastoma
2 – other PNET (Primitive neuroectodermal tumors)
13 – TOTAL
http://clinicaltrials.gov/show/NCT00003460
9/1995 – Study Start Date

BT-12 PHASE II STUDY OF ANTINEOPLASTONS A10 AND AS2-1 IN CHILDREN WITH PRIMITIVE NEUROECTODERMAL TUMORS; (PNET)

5 40
7/11/96 – Revised
9/28/96 – Revised
4/14/97 – Revised
Antineoplaston Therapy in Treating Children With Primitive Neuroectodermal Tumors
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
CLOSED
Age 6 months to 17 years
Protocol IDs
CDR0000066492
BC-BT-12, NCT00003460
http://cancer.gov/clinicaltrials/BC-BT-12
· Protocol BT-12, involving the study of Antineoplastons A10 and AS2-1 in Children With Primitive Neuroectodermal Tumors
http://clinicaltrials.gov/show/NCT00003460
12/2011 – Estimated Primary Completion Date (Final data collection date for primary outcome measure)

7/14/2009 – Updated
1 clinical_study oversight_info
2 regulatory_authority
United States: Federal Government
3 oversight_info status
4
Fm: Recruiting
To: Active, not recruiting
5 status last_release_date
6
Fm: 2009-06-09
To: 2009-07-14
7 last_release_date
8 init_disposition_release_date
9 init_results_release_date clinical_study

Antineoplaston Therapy in Treating Children With Primitive Neuroectodermal Tumors
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
CLOSED
Age 6 months to 17 years
Protocol IDs
CDR0000066492
BC-BT-12, NCT00003460
http://cancer.gov/clinicaltrials/BC-BT-12
· Protocol BT-12, involving the study of Antineoplastons A10 and AS2-1 in children with primitive neuroectodermal tumors (PNET)

BT-12 – Protocol #
13 – Patients Accrued
11 – Evaluable Patients
3 / 27.3% – # and % of Patients Showing Complete Response
1 / 9.1% – # and % of Patients Showing Partial Response
3 / 27.3% – # and % of Patients Showing Stable Disease
4 / 36.4% – # and % of Patients Showing Progressive Disease

5/1/2012 – prospective protocols which have reached Milestone

results of Protocols:

BT-12

5/1/2012 – set forth below

Form 10-Q (For the fiscal year ended February 29, 2012)
(as of May 1, 2012) Protocol BT
http://www.sec.gov/Archives/edgar/data/724445/000110465912040430/a12-12972_110k.htm
Antineoplaston Therapy in Treating Children With Primitive Neuroectodermal Tumors
Brain and Central Nervous System Tumors
Drug: antineoplaston A10
Drug: antineoplaston AS2-1
Phase II / Phase 2
CLOSED
Age 6 months to 17 years
Protocol IDs
CDR0000066492
BC-BT-12, NCT00003460
http://cancer.gov/clinicaltrials/BC-BT-12
BT-12 – Protocol #
13 – Patients Accrued
11 – Evaluable Patients
3 / 27.3% – # and % of Patients Showing Complete Response
1 / 9.1% – # and % of Patients Showing Partial Response
3 / 27.3% – # and % of Patients Showing Stable Disease
4 / 36.4% – # and % of Patients Showing Progressive Disease
� � � � � � � � � � � � � � � � �
Interim Reports on Clinial Trials:

Iwaaaa.pdf
Neuro-Oncology. 2006; 8:466

2006 – INTEGRATIVE CANCER THERAPIES

Burzynski, S.R., Janicki, T.J., Weaver, R.A., Burzynski, B.

Targeted therapy with Antineoplastons A10 and AS2-1 of high grade, recurrent, and progressive brainstem glioma
http://www.burzynskiclinic.com/images/stories/Publications/5825.pdf
Integrative Cancer Therapies 2006;5(1):40-47

2006 – PEDIATRIC DRUGS

Burzynski, S.R.

Treatments for Astrocytic Tumors in Children: Current and Emerging Strategies
http://www.burzynskiclinic.com/images/stories/Publications/1252.pdf
Pediatric Drugs 2006;8:167-178

2006 – NEURO-ONCOLOGY

Burzynski, S.R., Weaver, R.A., Szymkowski, B., Janicki, T.J., Khan, M.I., Dolgopolov, V.

Complete response of a diffuse intrinsic brainstem tumor and von Hippel Lindau (VHL) disease to antineoplastons A10 and AS2-1 (ANP):

a case report
http://www.burzynskiclinic.com/images/stories/Publications/2104.pdf
Neuro-Oncology. 2006; 8:439

3/2006 – INTEGRATIVE CANCER THERAPIES

3/2006 – Targeted therapy with antineoplastons A10 and AS2-1 of high-grade, recurrent, and progressive brainstem glioma
http://www.ncbi.nlm.nih.gov/pubmed/16484713
Integr Cancer Ther. 2006 Mar;5(1):40-7
http://www.ncbi.nlm.nih.gov/m/pubmed/16484713
Brainstem glioma carries worst prognosis of all malignancies of the brain

Most patients with brainstem glioma fail standard radiation therapy and chemotherapy and do not survive longer than 2 years

Treatment even more challenging when inoperable tumor of high-grade pathology (HBSG)

patients with inoperable tumor of high-grade pathology (HBSG) treated with antineoplastons in 4 phase 2 trials

39% – overall survival at 2 years
22% – overall survival at 5 years

17+ years maximum survival – patient with anaplastic astrocytoma

5+ years – patient with glioblastoma

39% – Progression-free survival at 6 months

5+ year survival in recurrent diffuse intrinsic glioblastomas and anaplastic astrocytomas of brainstem in small group of patients

18 – evaluable
4 – glioblastomas
14 – anaplastic HBSG

14 – diffuse intrinsic tumors
12 – recurrence
6 – did not have radiation therapy or chemotherapy

Antineoplastons A10 (A10I) and AS2-1 injections

5 months – median duration

Responses assessed by gadolinium-enhanced magnetic resonance imaging and positron emission tomography

Antineoplastons tolerated very well:
1 case – grade 4 toxicity (reversible anemia)

2006 – Protocol – high-grade pathology (HBSG)
18 – Evaluable Patients
11% – % of Patients Showing Complete Response
11% – % of Patients Showing Partial Response
39% – % of Patients Showing Stable Disease
39% – % of Patients Showing Progressive Disease

INOPERABLE TUMOR OF HIGH-GRADE PATHOLOGY (HBSG), RECURRENT, AND PROGRESSIVE BRAINSTEM GLIOMA:
4 – glioblastomas (patient with glioblastoma)
14 – anaplastic HBSG (patient with anaplastic astrocytoma)
18 – TOTAL ; evaluable)
14 – diffuse intrinsic tumors
12 – recurrence
(recurrent diffuse intrinsic glioblastomas and anaplastic astrocytomas of brainstem)
6 – did not have radiation therapy or chemotherapy
18 – TOTAL

11/25/1997 – FORM 10-SB
http://pdf.secdatabase.com/2573/0000950110-97-001598.pdf
patients with inoperable tumor of high-grade pathology (HBSG) treated with antineoplastons in 4 PHASE 2 TRIALS:

INOPERABLE TUMOR OF HIGH-GRADE PATHOLOGY (HBSG), RECURRENT, AND PROGRESSIVE BRAINSTEM GLIOMA:
4 – glioblastomas (patient with glioblastoma)
14 – anaplastic HBSG (patient with anaplastic astrocytoma)
18 – TOTAL ; evaluable)
14 – diffuse intrinsic tumors
12 – recurrence
(recurrent diffuse intrinsic glioblastomas and anaplastic astrocytomas of brainstem)
6 – did not have radiation therapy or chemotherapy
18 – TOTAL

Wikipedia, your Burzynski BIAS is showing

As I have proven previously, Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia is BIASED, when it comes to the Burzynski Clinic Wikipedia article:
http://en.m.wikipedia.org/wiki/Burzynski_Clinic
WikipediA or WikipediAin’t ?:
https://stanislawrajmundburzynski.wordpress.com/2013/05/16/wikipedia-or-wikipediaint/
Wikipedia, what’s your motivation?:
https://stanislawrajmundburzynski.wordpress.com/2013/05/02/wikipedia-whats-your-motivation/
I show JzG what a “FACT” is: Burzynski: FAQ (Frequently Asked Questions): Clinical Trial Results:
https://stanislawrajmundburzynski.wordpress.com/2013/05/14/i-show-jzg-what-a-fact-is-burzynski-faq-frequently-asked-questions-clinical-trial-results/
guychapman (Guy Chapman) Critiquing “The Skeptic” Burzynski Critics: A Film Producer, A Cancer Doctor, And Their Critics (page 9):
https://stanislawrajmundburzynski.wordpress.com/2013/05/05/guychapman-guy-chapman-critiquing-the-skeptic-burzynski-critics-a-film-producer-a-cancer-doctor-and-their-critics-page-9/
12/26/2012 I requested that Wikipedia add the below Houston’s KPRC News article re Lola A. Quinlan, to the Burzynski Clinic Wikipedia article, considering that they had previously posted there:
http://en.wikipedia.org/wiki/Burzynski_Clinic
Lawsuits

“In January 2012, Lola Quinlan, an elderly, stage IV cancer patient, sued Dr Burzynski…”

“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.”

http://m.click2houston.com/news/Houston-cancer-doctor-draws-new-complaints-from-patients/-/16714936/8581480/-/hmrbjk/-/index.html

http://www.jag-lawfirm.com/burzynski-suit-kprc-02012012.html
Thank you very much.” Didymus Judas Thomas 15:03, 26 December 2012
http://en.wikipedia.org/w/index.php?title=Talk:Burzynski_Clinic&diff=prev&oldid=529836971
So, what was Wikipedia’s NON-BIASED rational wiki reasoning for NOT including this Houston, Texas, news article reference?

Dear Didymus Judas Thomas,

The Wikipedia page Talk:Burzynski Clinic has been changed on
December 26, 2012 by Arthur Rubin

See
http://en.wikipedia.org/w/index.php?title=Talk:Burzynski_Clinic&diff=next&oldid=529836971
to view this change.

Editor’s summary: /* Law Suits */ So?

Contact the editor:
mail: http://en.wikipedia.org/wiki/Special:EmailUser/Arthur_Rubin
wiki: http://en.wikipedia.org/wiki/User:Arthur_Rubin
Arthur Rubin advised:

“: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.” — Arthur Rubin 15:24, 26 December 2012

I had the impression that Arthur Rubin had not even bothered to read the article in question, and replied:

“::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, 27 December 2012 Didymus Judas Thomas 12/27/2012

Arthur Rubin’s, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ response?

SILENCE

Well, you know the saying:

Silence IS Golden

(Wikipedia: Neutral Point of View)

WP:NPOV clearly indicates:
“Editing from a neutral point of view (NPOV) means representing FAIRLY, PROPORTIONATELY, and as far as possible WITHOUT BIAS, ALL significant views that have been published by reliable sources.”

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

“ALL Wikipedia articles and other encyclopedic content MUST be written from a neutral point of view.”

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

“NPOV is a fundamental principle of Wikipedia and of other Wikimedia projects.”

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

“This policy is NONNEGOTIABLE and ALL editors and articles MUST follow it.”

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

“The principles upon which this policy is based CANNOT be superseded by OTHER POLICIES or GUIDELINES, or by editors’ consensus.”

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

(Words CAPITALIZED for emphasis only.).

“1 Explanation of the neutral point of view.”

“This page in a nutshell:”

“Articles mustn’t take sides, but should explain the sides, fairly and without bias.”

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

“This applies to both what you say and how you say it.”

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

“Editors, while naturally having their own points of view, should strive in good faith to provide complete information, and not to promote one particular point of view over another.”

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

“As such, the neutral point of view does not mean exclusion of certain points of view, but including all notable and verifiable points of view.”.

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

[[WP:NPOV]] “History of NPOV:” (Content # 6). “The relative prominence of each viewpoint among Wikipedia editors or the general public is not relevant and should not be considered.”

(Wikipedia: Simplified Ruleset)

[[WP:SR]] “Wikipedia does not have its own views, or determine what is “correct.”

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

“Instead, editors try to summarize what good sources have said about ideas and information.”

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

“Differing views are presented objectively and without bias as they are reported in reliable sources—sources that have a reputation for being accurate.”

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

“Good sources are the base of the encyclopedia, and anyone must be able to realistically check whether contributions can be backed up by one.”.

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

[[WP:NPOVFAQ]]

(Wikipedia: Neutral Point of View Frequently Asked Questions)

Wikipedia:Neutral point of view/FAQ
http://en.m.wikipedia.org/wiki/Wikipedia:Neutral_point_of_view/FAQ
[[WP:NPOVFAQ]]

See also Wikipedia:WikiProject Countering systemic bias.
http://en.m.wikipedia.org/wiki/Wikipedia:WikiProject_Countering_systemic_bias
[[WP:CSB]]

Did Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’ do this?

Is Wikipedia’s Burzynski BIAS showing?

YOU decide, because in my opinion it IS, since this piece of “Yellow Journalism” is referenced in the Burzynski Clinic Wikipedia article:

2010 film, Burzynski – Cancer is Serious Business

Prior to the debut of “Burzynski”, Houston Press correspondent Craig Malisow mocked the film’s lack of objectivity, characterizing it as “a puff-piece paean that cherrypicks facts and ignores any criticism”, and criticized the project for presenting only Burzynski’s side of the story.” [60]
60^ Malisow, Craig (2010-06-02). “Stanlislaw Burzynski: New Movie Proves He’s A Cancer-Fighting Giant – Houston News – Hair Balls”. Blogs.houstonpress.com. Retrieved 2011-11-25.

Jun 2, 2010 – Houston’s Stanislaw Burzynski, who sells a so-called cancer …

(Hair Balls hasn’t seen the movie, but nowhere in the … )

So, in a nutshell, Wikipedia will reference “Yellow Journalism” by a “Hack” who posts an article about a movie he has NOT even seen, but will NOT reference a news article which is posted on Lola A. Quinlan’s attorney’s web-site, which contains comments from her attorney, as well as Dr. Stanislaw R. Burzynski’s attorney

Wikipedia, your BIAS is showing

“The U.S. v. Article’~ court stated that the FDA’s responsibility was to protect the ultimate consumer, which included protection of “the ignorant, the unthinking and the credulous.”‘

“the ignorant

the unthinking and

the credulous.”‘

Arthur Rubin, and Jimmy (call me “Jimbo”) Donal Wales’ Wikipedia whiners’, which are you?

Critiquing “All truth comes from public debate”: A corollary to crank magnetism

http://t.co/vh3cgAR6hW

onforb.es/11pwse9

http://t.co/vh3cgAR6hW

http://www.forbes.com/sites/peterlipson/2013/04/19/a-film-producer-a-cancer-doctor-and-their-critics
The difference between Randy Hinton and I:

RH: Forbes (#Forbes) and Facebook
bloodsucker’s
child killer’s
COG’s
crap
GOBLIN’S
maggot’s
medical mafia
medical mafia internet propaganda minister’s
oral sex
pharmawhores
propaganda
smear
undermind

Me: Forbes
Dr.
Mr.

“Orac:”-“One also can’t help but note a similarity here between DJT and Mr. Hinton, but what that means I will leave to each individual reader to decide for him or herself”

Me:-Any questions?

The differences between Dr. David H. Gorski (also known as: Orac, @oracknows, @gorskon, @ScienceBasedMed, #sciencebasedmedicine,
http://www.scienceblogs.com/Insolence, http://www.sciencebasedmedicine.org) and I:
DHG:
anthropogenic global warming
anthropogenic global warming denialism
anti-GMO hysteria
antivaccine propagandist
antivaccinationism
antivaccinationist
antivaccinationists
ban hammers
banning
crank
cranks
crankery
crank magnetism
crank playbook
creationism
creationists
criticize
criticism
cynically
delusion
Gish gallop
HIV-AIDS denialist
Holocaust denial denialists go birther
“human shields”
kook
kooks
propagandist
pseudoscience
purveyors of “alternative medicine”
quackery
quacking
ramblings
stalked off
troll
troll’s
trolling
obnoxious troll
9/11 Truthers

Me:
I do NOT have 3 Twitter accounts like Dr. Gorski; who sometimes uses them to twit the same jargon, which is then sometimes retwitted by lemming “sheeple”

Any questions ?

“Orac:”-“… challenging my blog bud Peter Lipson (a.k.a. PalMD, who wrote a very good post about how Eric Merola …”

THIS “very good post” ?

Critiquing “The Skeptic” Burzynski Critics: A Film Producer, A Cancer Doctor, And Their Critics (page 1)
https://stanislawrajmundburzynski.wordpress.com/2013/04/27/critiquing-the-skeptic-burzynski-critics-a-film-producer-a-cancer-doctor-and-their-critics-page-1/
Any questions ?

“Orac:“-Didymus did it in a mere month or two

Me:-1st post: #59 – Didymus Judas Thomas – The United States of America – November 28, 2012
http://scienceblogs.com/insolence/2012/11/26/significance-of-the-tmb-dismissal-case-against-burzynski/
Last post: #197 – Didymus Judas Thomas – At the Tu-Quack Center Selective Memory MazeFebruary 12, 2013
http://scienceblogs.com/insolence/2013/02/08/will-the-fda-finally-slap-down-stanislaw-burzynski-for-good/
I confess, in the past I have accused “Orac” of being “fact-challenged”

“Orac:”--“cowardice.”

IMPORTANT: The live “debate”-A Film Producer, A Cancer Doctor, And Their Critics | Didymus Judas Thomas’ Hipocritical Oath Blog
https://stanislawrajmundburzynski.wordpress.com/2013/04/27/important-the-live-debate-a-film-producer-a-cancer-doctor-and-their-critics/
#73 – Didymus Judas Thomas – At the Tu-Quack Center Oracles of Deny to Respond tree – January 30, 2013
http://scienceblogs.com/insolence/2013/01/28/an-excellent-explanation-of-how-dubious-stanislaw-burzynskis-activities-are
Me:-Any questions ?

“Orac”-“In any case, DJT quickly stalked off to WordPress to form his own blog, where he continued his ramblings in much the same way that he did in the comments of this blog…”

I confess, my “ramblings” consist of direct “quotes” and “facts” from the United States Supreme Court, Department of Health and Human Services (HHS), U.S. Food and Drug Administration (FDA), National Cancer Institute (NCI) at the National Institutes of Health (NIH), etc., and I understand that “Orac” considers that kind of information to be “ramblings,” and has difficulty comprehending them because of:

Orac:”-“…my fragile eggshell mind…”

Me:-Any questions ?
http://scienceblogs.com/insolence/2013/04/26/all-truth-comes-from-public-debate-a-corollary-to-crank-magnetism/
“Orac’s” blogsplat:-PRICELESS

Me:-Any questions ?

4/19/2013 @ 9:43PM
Peter Lipson: “Speech is best countered by more speech”

Burzynski: What happens when a clinical trial is over?

National Cancer Institute (NCI) at the National Institutes of Health (NIH), Cancer Clinical Trials, 15. What happens when a clinical trial is over?,” advises:
“The results of clinical trials are OFTEN published in peer-reviewed scientific journals”
” … WHETHER OR NOT the results are published in a peer-reviewed scientific journal … ”
http://m.cancer.gov/topics/factsheets/clinical-trials
This makes it clear that clinical trial results “are OFTEN” published, but sometimes they are “NOT” published “in a peer-reviewed scientific journal”