United States Food and Drug Administration (FDA): September 28, 2013 “The Skeptics™” Burzynski discussion: By Bob Blaskiewicz – 2:19:51

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[1] – September 28, 2013 “The Skeptics™” Burzynski discussion: By Bob Blaskiewicz – 2:19:51
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BB – Bob Blaskiewicz
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DJT – Didymus Judas Thomas
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0:47:00
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BB“Ummm, o-kay”

“Uh, I want to turn this over to the people who are watching”

“Um, I want to give them a a chance to address you as well”

“Uhmmm, hi everyone”
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0:48:00
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0:53:00
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BB“A every time that I and and and and, and David (James @StortSkeptic the Skeptic Canary) points this out, that um, you you know you’re not going to speculate about the the FDA but then at every turn you’re invoking the FDA as being obstructionist
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0:54:02
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BB“I, I just find that to be contradictory and and self-defeating
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DJT – Bob, exactly where did I invoke “the FDA as being obstructionist” ?
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1:02:00
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BB“Um, it’s it’s it’s not the FDA’s, but you understand it’s not the FDA’s job to tell someone that their drug doesn’t work
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1:03:00
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BB“it’s it’s it’s up to Burzynski

“It’s up to Burzynski to show that his drug does work”

“And it’s always been his burden of proof

“He’s the one that’s been claiming this miracle cancer cure, forever”
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DJT – Bob, Burzynski showed and proved what he needed to prove to the FDA in order to do phase 2 clinical trials, 9/3/2004 – FDA granted “orphan drug designation” (“ODD”) for Antineoplastons (A10 & AS2-1 Antineoplaston) for treatment of patients with brain stem glioma, .10/30/2008 – FDA granted “orphan drug designation” (“ODD”) for Antineoplastons (A10 and AS2-1 Antineoplaston) for treatment of gliomas, and FDA approved phase 3 [1-2]

Oh, and Bob, exactly when did Burzynski 1st claim “this miracle cancer cure” ?
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1:04:02
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BB“Um, that we’d love to see, however we can’t see, however we can’t see it because of proti protri proprietary uh protections that the FDA is giving to Burzynski, right ?”

They’re not sharing his trial designs because they are his trial designs, right ?”

“That the makeup of his drug that he’s distributing are his, uh design, and his intellectual property

“So the FDA is protecting him, uh from outside scrutiny
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DJT – Bob, you make it sound like it’s part of some grand “conspiracy” between Burzynski and the FDA to keep information from “The Skeptics™” [3]
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21CFR601

Subpart F–Confidentiality of Information

Sec. 601.50

Confidentiality of data and information in an investigational new drug notice for a biological product

(a) The existence of an IND notice for a biological product will not be disclosed by the Food and Drug Administration unless it has previously been publicly disclosed or acknowledged
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BB“While you may imagine that that, that that the FDA is is somehow antagonistic toward him

“They’ve given him every opportunity, over 60 opportunities to prove himself worth uh their confidence and hasn’t
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DJT – Bob, that certainly explains the 9/3/2004 and .10/30/2008 ODD’s and phase 3 clinical trial approvals by the FDA – NOT [1-2]
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1:05:00
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1:42:00
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BB“I don’t, the thing is though that, that that’s a inver, shifting the burden of proof off of Burzynski”

“Burzynski has to prove them wrong, has to prove him right”

“The FDA is not there to say this doesn’t work”
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DJT – Bob, who initiated and put into place the clinical trial hold ?

Burzynski ?

FDA ?

Both ?
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1:43:30
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BB“So, I mean, honestly, um, saying “Well, when the F, FDA tells you that it doesn’t work, the FDA’s never gonna say that because that’s not their job
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1:44:00
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BB“That’s not an option, because they’re never gonna do it

“They relinquish, a lot of authority, over to Burzynski, and his Institutional Review Board, which, I would mention, has failed 3 reviews in a row”
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Bob, where are the “final reports” for those “3 reviews” ?
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BB“Right ?”

“It is Burzynski’s job to be convincing”

“It is not our uh, uh, it it it he hasn’t produced in decades

“In decades”

“In hundreds and hundreds of patients, who’ve payed to be on this”

“Hell, we’d we’d we’d like a prelim, well when you’re talking about something that is so difficult as brainstem glioma, that type of thing gets, really does in the publishing stream get fast-tracked there”
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DJT – Bob, Burzynski has provided numerous phase 2 clinical trial preliminary reports, which our #fave oncologist has chosen to ignore [4]
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BB“they test it”

“Yeah, and they they they want uh, that was evidence of fast-tracking is what, that rejection was uh e was very quickly
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DJT – Bob, have you checked The Lancet Oncology [5] to see what was so much more important than Burzynski’s “phase 2 clinical trial Progression-Free Survival (PFS) and Overall Survival (OS) re patients 8 – 16 years after diagnosis, results” [6] and the Japanese antineoplaston study ? [7]
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BB“So, how long will it be before Burzynski doesn’t publish, that you decide that uh perhaps he’s he‘s, doesn’t have the goods ?

“Um, so, uh, uh again, the FDA is not the arbiter of this

“It’s ultimately Burzynski”

“You’ve been speculating about what the FDA’s motivation are like crazy”

“Why not speculate about Burzynski a little bit”
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DJT – Well, how have I been speculating ?
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1:46:00
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BB“Well actually I’m not even asking you to speculate about Burzynski, I’m only asking you to tell me, how long would it take, uh how, for him to go unpublished like this, um, for this long, before you would doubt it ?”
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DJT – Note how, above, without proving it, Bob claimed “at every turn you’re invoking the FDA as being obstructionist”, and now, directly above, again, without proving it, Bob claims “You’ve been speculating about what the FDA’s motivation are like crazy”
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DJT – what the journals keep saying, in response
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BB“What ?”
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DJT – You know, are they going to give The Lancet response, like they did in 2 hours and such, saying, “Well, we think your message would be best heard elsewhere,” or they gonna gonna give The Lancet response of, “Well, we don’t have room in our publication this time, well, because we’re full up, so, try and pick another place” ?
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BB“But these but but but that doesn’t have any bearing on

“That doesn’t”

“Oh I’m not asking you how long, how long, would it take you for you to start doubting whether or not he has the goods ?

“How long would it take ?”

“It’s a it’s a it’s a question that should be answered by a number uh uh months ?

“Years ?”

“How long ?”

“It’s been 15 years already”
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DJT – Well, you like to jump up and down with the “15 year” quote, but then again I always get back to, Hey, it’s when, when the report, when the clinical trial is done
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1:47:06
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DJT – Not that he’s been practicing medicine medicine for 36 years, or whatever, it’s when the clin, clinical trial was done
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BB – “I could push it back to 36 years”

“He hasn’t shown that it works for 36 years”

“I can do that”

“I was being nice”
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DJT – Note how Bob acts like he’s been hit with “The Stupid Stick”

If he wants to go back “36 years”, I can refer back to 1991 (11/15/1991) – Michael J. Hawkins, M.D., Chief, Investigational Drug Branch, Department of Health &Human Services (HHS), Public Health Service, National Institutes of Health (NIH), National Cancer Institute (NCI), sent a 1 page Memorandum Re:
Antineoplaston
to Decision Network, which advised, in part:

It was the opinion of the site visit team that antitumor activity was documented in this best case series and that the conduct of Phase II trials was indicated to determine the response rate” [8]
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DJT – The FDA A believes there is evidence of efficacy
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BB – “Perhaps based on bad phase 2”
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DJT – Well, we don’t know that

We don’t have the Freedom of Information Act information
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DJT – Remember, Bob is the one who told me during the 9/28/2013 Google+ Burzynski Discussion Hangout:

“You’re you’re you’re assuming”

“You’re you’re you’re assuming that”

“You’re assuming that”

“Um, I’m not assuming that”

“There is a correct answer here”

“You don’t know”

“You don’t know”

“You need to look into it”

“Alright ?”

“Before you dismiss it you have to look into it”

“Everytime somebody throws uh uh something to me,
I have to look into it”

“That’s just, it’s my responsibility as a reader”

“T t and what I would honestly expect and hope, is that you would be honest about this, to yourself, and and and that’s the thing we don’t, we often don’t realize that we’re not being honest with ourself

“I try to fight against it, constantly”

Bob just ASSUMED that the FDA approved phase 3 clinical trials for Burzynski “Perhaps based on bad phase 2”, but tells me NOT to ASSUME ?
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BB“He withdrew”

“He withdrew the the phase 3 clinical trial”

“I that before recruiting,
although I’ve seen lots of people say they were on a phase 3 clinical trial

“I wonder how that happened”
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DJT – Well, we know what happened in the movie because Eric particularly covered that when they tried to get what, what, was it 200 or 300 something institutions to take on a phase 3, and they refused
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1:48:01
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BB“Uh did do do you think that if they thought that he was a real doctor that they all would have refused like that ?
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DJT – Well, Eric gave the reasons that they said they would not take a particular uh phase 3

And so using that excuse that you you just gave there, I’m not even gonna buy that one, because that’s not one of the reasons
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Note how Bob pulls out the old “if they thought that he was a real doctor” line ?

Is Bob now claiming that Burzynski is NOT even a “real doctor” ?
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BB – “He’s changed things”
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DJT – Eric said they gave
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BB“That The Lancet is a top-tier journal like New England Journal of Medicine

“It’s basically be, besieged by uh 100′s of people submitting their, their, their reports”

“Um, it’s just, you know, let’s say he, someone has such a thin publishing record as Burzynski does, do you think that it’s likely that he will ever get in a top-tier journal ?

“What about the the Public Library of Science?”

“It’s not the only journal there”

“What about BMC Cancer ?”

“There’s lots of places that he can go”
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DJT – We’ll I’m
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BB“Um, and he doesn’t seem to to have evailed himself of that, as far as I can tell

“And I would know because he’d get rejected, or he’d be crowing, you know”
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1:49:02
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BB – “Either way, he’s gonna tell us what happens”

He told us what happened with The Lancet, you know”

“I don’t have any evidence that suggests to me that he’s even trying”
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Note how Bob refers to Burzynski’s numerous publications as “such a thin publishing record”

Bob, do I need to count all of these for you ? [9]
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DJT – Well, I’m, I’m sure that they’re going to keep you appraised just like they have in the past, just like Eric has done in the past

So

I mean, we’ll see what happens with the Japanese study [7]
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BB – “So let’s go back to this”

“How long will it take ?”

“How long will it take before you, the Japanese study’s interesting too because we should be able to find that in the Japanese science databases, and we can find, we can’t find it at all

“We can’t find it anywhere”

“And, and those are in English, so it’s not a language problem

“We can’t find that anywhere”

“We’ve asked”

“We asked Rick Schiff, for, for that study”

“And, and it hasn’t come to us

“He is now I believe on the Board of Directors, over there”
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1:50:00
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BB – “He should have access to this”

“We can’t get it”
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Bob, did you ask:

1. Annals of Oncology 2010;21:viii221 ?

2. European Society for Medical Oncology (ESMO), Colorectal cancer, Abstract: 3558, May 17, 2010 ?

3. Colorectal Cancer Association of Canada, COLORECTAL CANCER RESEARCH, Month Ending June 19, 2009
11. Antineoplaston Therapy Doubles 5-Year Survival Rate Following Curative Resection of Hepatic Mets (May 27/09) pg. 5 of 20 ?

4. Kurume University School of Medicine (Japan) Department of Surgery ?

5. Hideaki Tsuda ? [7]
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BB – “How how long will it take before you recognize that, nothing is forthcoming ?”

“How long would that take ?”
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DJT – Well that’s like me asking “How long is it going to take for y’all’s, y’all‘s Skeptics to respond to my questions ?”

Because y’all haven’t been forthcoming
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BB“Well, I mean, were talking about a blog here

“We’re talking about life”

“No, we’re talking about a blogger’s feelings in that case

“In in this case we’re talking about, 1,000′s of patients, over the course of of of generations, you know”

“This is important stuff”

“This is not eh eh equating what’s happening to to patients with what’s happening to you is is completely off-kilter as far as I can tell

“It’s nothing”

“It’s nothing like you not getting to say something on my web-site”

“You know”

“This is they they have thrown in with Burzynski, and they’ve trusted him, and he’s produced nothing

“Nothing of substance”
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1:51:00
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BB – “Nothing that that has made all of that um, uh, n nothing th th th that uh his peers would take seriously”

“The other thing that that that strikes me now is that, you know, you you you you keep saying that, well Eric is going to to share things with you”

“Does it ever concern you eh uh eh occur to you that Eric might not be reliable ?”
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Bob, do you want to have a contest to determine which of you is more “reliable” ?
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DJT – Well, he gave you The Lancet information and he posted the e-mail in the movie, and Josephine Jones posted a copy of it [6]
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BB“He then, and then he”

“And then he he, you know, the the the the dialogue that sprung up around that was, well see, he’s never going to get to get published”

“Well you’re just setting yourself up for wish fulfillment”

“You want him to be, persecuted, so you are ecstatic when he doesn’t get to publish, which is unfortunate for all the cancer patients, who really thought that one day, all the studies were going to be published”
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1:52:00
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DJT – Well, y’all are free to, you know, claim that all you want, because I don’t always agree with Eric, and uh, he’s free to express his opinion
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BB – “Where has Eric been wrong ?”
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DJT – Well I don’t necessarily believe, what Eric would say about, you know, The Lancet that refused to publish the 2nd one, for the reasons he stated, and which y’all have commented on, including Gorski

You know, I don’t necessarily agree with that

I am more agreeable to y’all, saying that, you know, they’re busy, they’ve got other things to do, but I’m kind of still laughing at their 1st response which he showed in the movie about how they felt about, you know his results would be better in some other publication

I thought that was kind of a ridiculous response to give someone
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BB“It’s it’s it’s it’s a form letter

“You know”

“They’re just saying, “No thanks””

““Thanks, but no thanks” is what they were saying, in the most generic way possible”

“Like I said, they’re besieged by researchers trying to publish
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1:53:05
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DJT – Well you would think that if its a form letter they would use the same form that they used the 2nd time

You know, they didn’t use the same wording that they used the 1st time

I would have think that, you know, their 2nd comment
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BB“So, so, possibly”

“So possibly what you are saying is that they in fact have read it, and after having read it they’ve rejected it”

“Is that what you’re saying ?”

“Because that’s what peer-review is”
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DJT – Nah, I’m not saying that they did that all

I’m just sayin’, you know, that they gave, 2 different responses, and I would think that the 2nd one they gave
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BB – “Do you know it was the same editor, that it came from the same desk ?”

“You can’t make that assumption that that the form letter will be the same form letter every time”

“I mean you just can’t

“I mean in in some ways we have a lot of non-information that you’re filling in, with what you expect, as as opposed to what’s actually really there, and I I I just think you’re putting too much uh stock in one uh, uh, in in in in this uh the publication kerfuffle
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1:54:16
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BB“Um”
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DJT – Well I find it funny, something along the lines of, you know, “We believe your message would be received better elsewhere, you know

I don’t see that as a normal response, a scientific publication would send to someone trying to publish something

I mean, to me that sounds, like, if you’re doing that, and you’re The Lancet Oncology, maybe you need to set some different procedures in place, ‘cuz you would think that with such a great scientific peer-reviewed magazine, that they would have structured things in as far as how they do their operations
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BB“Well, not necessarily

“I’ve been in any # of professional groups where the organization is just not optimal, and publications certainly th there are all sorts of pressures from all sorts of different places”
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1:55:08
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BB“I I have no problems whatsoever with seeing that this might not be completely uh um uh streamlining uniform processes as possible

“The fact that it’s not uniform, doesn’t have anything to do with Burzynski not publishing, not producing good data”

“Not just going to a, you know, god, even if, even if, let’s put it this way, even if he went to a pay to play type publication where you have to pay in order to get your manuscript accepted; and he has the money to do this, it wouldn’t take that much, and he were to put out a good protocol, and he were to show us his data, and he would make his, his his stuff accessible to us, then we could validate it, then we could look at it and say, “Yeah, this is good,” or “No, this is the problem, you have to go back and you have to fix this””

“Right ?”

“So we really, every time we talk about the letter that he got, yeah that doesn’t have much to do with anything, really”
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1:56:02
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BB – “We wanna see the frickin’ data”

“And if he had a cure for some cancers that otherwise don’t have reliable treatments, he has an obligation to get that out there anyway he can

“And if if peer-review doesn’t, you know, play a, if peer-review can’t do it, you know, isn’t fast enough for him, then he should take it to the web, and he should send copies out to every pediatric, uh, you know, oncologist that there is

“That’s the way to do it”
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DJT – Well, I’m sure, I’m sure Gorski would have a comment about that, as he’s commented previously about how he thinks uh Burzynskishould publish
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1:57:10
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BB“It’s the, it’s the data itself

“If if Burzynski is is, is confident in his data, he will put it out there

“Right ?”

“One way or the other”
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DJT – Like I said before

Like I said before on my blog, you know, even if Burzynski publishes his phase 2 information, Gorski can just jump up and down and say, “Well, that just shows evidence of efficacy, you know, it’s not phase 3,
so it doesn’t really prove it”

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1:58:04
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DJT – So then he can go on, you know, for however many years he wants to
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2:01:00
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BB“Um, almost no treatment goes out without trials

“Massive amounts of data are required”
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Bob, do you think that’s the 2.5 million pages of clinical trial data that Fabio said Burzynski sent to the FDA ? [10]
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2:02:00
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BB“Uh, in in in that sense, you know, uh all the the the, you know, kind of back-peddling and and and trying to defend him is is going to, not going to help his case at all
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Bob, exactly where did I exhibit any “kind of back-peddling” ?
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2:03:03
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BB
“You are, honestly as far as I can tell you are doing the um, you know, you’re you’re ah throwing up uh, uh, uh, you’re giving me another uh invisible dragon in the garage, um”
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DJT – Well y’all, y’all can call things what y’all want

I mean, y’all can give these, fallacy arguments and all that garbage that y’all like, because that’s what y’all like to talk about instead of dealing with the issues

I mean, Gorski doesn’t want to deal with the issues
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2:04:11
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BB“Okay, so”

“What you’re telling me is that you trust the FDA to to be able to tell you when he’s not doing, good science, but also that you don’t trust the FDA”

“Do you see an inherent conflict there ?”
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DJT – How did I say I, I didn’t trust them ?
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BB“Well, when I, whenever I would ask about, like, why would these trials aren’t happening uh and, you know, you say well the the FDA’s arranged it

“The FDA’s in control”

“They sign off on these things”

“But they’re they’re they’re they’re at the same that they’re, they’re trustworthy they’re also not trustworthy depending on what you need for the particular argument at the time
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2:05:12
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BB – “You’re suggesting that they’re untrustworthy”
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DJT – No, I’m just sayin’ that I’ve raised questions and none of The Skeptics wanna to uh talk about ‘em [11]
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BB“Do you know that the FDA pulled out of the prosecution ?”

“Did you know that the FDA pulled out of the prosecution um of his criminal case, because they were backing a researcher ?”
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Bob, would that “researcher” be Dvorit D. Samid, who was in Burzynski: Cancer is Serious Business (Part I) ?
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DJT – Well, we know a lot stuff they did, but that still doesn’t impress me that they pulled out of the prosecution

I mean
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BB“Yeah, the the the it wasn’t the FDA who was pressing charges, it was a Federal prosecutor
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DJT – Right
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BB“Right”

“And and, they declined to provide information that the prosecution needed

“That’s important”

“That that that’s really important

“That he has been given the benefit of the doubt, and he has come up wanting, for decades now”
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DJT – Well I find it interesting a lot of this uh, a lot of these letters that were provided between, you know, the government and Burzynski, when the uh phase 2 study was going on, at the behest of the NCI

You know, anybody who reads that stuff knows, that when you just ignore the person that’s been doing, do treating their patients for 20 something years, or close to 20 years, and you change the protocol without his approval, and you don’t use the drugs in the manner that he knows works
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2:10:15
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BB“One of the interesting things about Doubting Thomas that I think you should definitely consider for yourself, is that at some point, when faced with the real opportunity to prove or disprove his assertions, he doubted himself”

“And that’s important”

“And that’s where you’re falling short in the analogy”
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DJT – Well, I think The Skeptics, Skeptics are falling short because, you know, they don’t own up to
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BB – “I’ve laid out exactly what it would take for me to turn on a fucking dime”

“I have, I have made it abundantly clear what I need

“Gorski has made it abundantly clear”

“Everybody else, Guy, and David, and Josephine Jones, uh, the Morgans, all of them have made it abundantly clear, what it would take to change our minds, and you’ve never done that”
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2:11:02
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BB“And even in this, this was an opportunity to do that

“To come up with a basis for understanding, where it’s like, you know what, If we can show this, you know, if we can show a this guy, that, that, there, that his standards are not being met, then, you know, we could possibly have some sort of ongoing dialogue after this”
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DJT – So I can say that since the Mayo Clinic (Correction: M.D. Anderson) finished their study in 2006, and it took them until 2013, to actually publish it, then I can say, well, Burzynski finished his in 2009, which was 3 years later, which would give Burzynski until 2016
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BB“Why wasn’t that study”
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DJT – for me to make up my mind (laughing)
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BB“Why wasn’t that, that that that, still . . again, it it doesn’t seem really to to approach the the the, main question here

“You know, um . . what are the standards that you have that it isn’t, what are your standards to show that it isn’t efficacious ?
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2:12:05
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DJT – Well I can say, well I’m going to have to wait, the same amount of time I had to wait for Mayo (Correction: M.D. Anderson) to publish their study; which was from 2006 to 2013
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BB“Why was the Mayo”

“Why was the Mayo (Correction: M.D. Anderson) study delayed ?”
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Note how Bob ASSUMES that the publishing of the final results of the M.D. Anderson study were delayed
——————————————————————
DJT – How do you know it was delayed ?
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BB“Well you said you had so many years before you finish it and go in”
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DJT – I mean, has anybody
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BB“Why, why did it take so long ?
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DJT – done a review of when a clinical trial is studied, and completed, and how long it took the people to publish it ?

You know

If they could point to me a study that’s done that, and say, well here’s the high end, here’s the low end of the spectrum, here’s the middle
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BB“I have something for you, okay ?”

“Send me that”

“Could you send me that study the way that it was published because um, just just send me the final study, um, to my e-mail address”
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DJT – Sure
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BB“Um, because, I can ask that question of those researchers, why was this study in this time, and what happened in-between”
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2:13:03
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BB – “Why did it take so long for it, for it to come out”
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DJT – Sure, but that’s not gonna, you know like, answer an overall question of, you know, somebody did a comparative study of all clinical trials, and, when they were finished, and at, and when the study was actually published afterwards

You know, that’s only gonna be one, particular clinical study
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BB“Right”

“Um, but it it would, perhaps, answer the question; because you’re using it as an example on the basis of which to dismiss criticism, whether or not, uh, it is the standard, and therefor you’re allowed to accept that Burzynski hasn’t published until 2016, or, um, it’s an anomaly, which is also a possibility, that most stuff comes out more quickly
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DJT – Well, we know that the Declaration of Helsinki doesn’t even give a standard saying, You must publish within x amount of years,” you know ?

So, I’ve yet to find a Skeptic who posted something that said, “Here are the standards, published here”
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2:14:07
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BB“I I, yeah, the other thing that David James points out is you know, why 2016 when he’s had 36 years already ?
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DJT – Again, we get back to, when the clinical trial is finished, not when Burzynski started
======================================
BB“Treating people”
======================================
DJT – I mean, you would expect to find a results to be published after, the final results are in
======================================
BB – “You would expect the Burzynski Patient Group to be a lot bigger after 36 years, and in fact is
======================================
DJT – You would expect some people would want to have confidentiality, and maybe not want to be included
======================================
BB – “So, if you’re unsure about this stuff, if you’re unsure about the the time to publication, why are you defending it so hard, other than saying, “I don’t know, I really need to”
======================================
DJT – Why am I unsure ?
======================================
BB“Uh about the
======================================
DJT – (laughing) I just gave you an example
======================================
BB“The reasons, the reasons for which that he’s, no, why are you defending him so hard, when you’re unsure ?
——————————————————————
2:15:02
======================================
DJT – Oh, who said I was unsure ?

I just gave you an example
——————————————————————
Note how Bob ASSUMES that I’m “unsure” when I had the same answer since 0:32:07 [12]

Bob, who approves “Accelerated Approval” ?

1. FDA ?

2. A peer-reviewed scientific journal ?

3. The Skeptics™ ?

Bob, It’s your unlucky [13]
======================================
REFERENCES:
======================================
[1] – September 28, 2013 “The Skeptics™” Burzynski discussion: By Bob Blaskiewicz – 2:19:51
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/10/04/september-28-2013-the-skeptics-burzynski-discussion-by-bob-blaskiewicz-21951/
======================================
[2] – FDA grants Orphan Drug Designation (ODD) for A10 and AS2-1:
——————————————————————
http://www.burzynskiresearch.com/assets/PressRelease_12022008_BZYR(2).pdf
——————————————————————
josephinejones (@_JosephineJones), D Nile ist http://josephinejones.wordpress.com/2013/01/23/happy-birthday-dr-burzynski-and-goodbye-antineoplastons/comment-page-1/#comment-8921
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/09/23/josephinejones-_josephinejones-d-nile-ist-httpjosephinejones-wordpress-com20130123happy-birthday-dr-burzynski-and-goodbye-antineoplastonscomment-page-1comment-8921/
======================================
[3] – The Skeptics @Majikthyse reveals madjik research skilz:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/09/26/the-skeptics-majikthyse-reveals-madjik-research-skilz/
======================================
[4] – Critiquing David H. Gorski, MD, PhD, FACS http://www.sciencebasedmedicine.org/editorial-staff/david-h-gorski-md-phd-managing-editor/
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/08/21/critiquing-david-h-gorski-md-phd-facs-www-sciencebasedmedicine-orgeditorial-staffdavid-h-gorski-md-phd-managing-editor/
======================================
[5] – The Lancet Oncology
——————————————————————
http://www.thelancet.com/journals/lanonc/onlinefirst
——————————————————————
http://www.thelancet.com/journals/lanonc/issue/current
======================================
[6] – FINALLY, one of “The Skeptics™” has the “Balls” to do what even Dr. David H. “Orac” Gorski would NOT do:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/09/12/finally-one-of-the-skeptics-has-the-balls-to-do-what-even-dr-david-h-orac-gorski-would-not-do/
======================================
[7] – Burzynski – The Antineoplaston Randomized Japan Phase II Clinical Trial Study:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/03/28/burzynski-the-antineoplaston-randomized-japan-phase-ii-clinical-trial-study/
======================================
[8] – Critiquing: National Cancer Institute (NCI) at the National Institutes of Health (NIH) CancerNet “fact sheet”:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/09/19/critiquing-national-cancer-institute-nci-at-the-national-institutes-of-health-nih-cancernet/
======================================
[9] – Stanislaw Rajmund Burzynski Publications:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/03/16/stanislaw-rajmund-burzynski-publications/
======================================
[10] – Critiquing: In which the latest movie about Stanislaw Burzynski “cancer cure” is reviewed…with Insolence:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/07/18/critiquing-in-which-the-latest-movie-about-stanislaw-burzynski-cancer-cure-is-reviewed-with-insolence-2/
======================================
[11] – QUESTIONS the Critics and Cynics, “The Skeptics™” do NOT want to ANSWER:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/06/23/questions-the-critics-and-cynics-the-skeptics-do-not-want-to-answer/
======================================
[12] – The Biggest Loser: “The Skeptics™” Guy Chapman (guychapman @vGuyUK @SceptiGuy) http://www.chapmancentral.co.uk/blahg/ – September 28, 2013 “The Skeptics™” Burzynski discussion: By Bob Blaskiewicz – 2:19:51
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/10/18/the-biggest-loser-the-skeptics-guy-chapman-guychapman-vguyuk-sceptiguy-httpwww-chapmancentral-co-ukblahg-september-28-2013-the-skeptics/
======================================
[13] – Burzynski: Why has the FDA NOT granted Accelerated Approval for Antineoplastons A10 (Atengenal) and AS2-1 (Astugenal) ?:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/07/28/burzynski-why-has-the-fda-not-granted-accelerated-approval-for-antineoplastons-a10-astengenal-and-as2-1-astugenal/
======================================

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Complete response of a recurrent, multicentric malignant glioma in a patient treated with phenylbutyrate

Complete response of a recurrent, multicentric malignant glioma in a patient treated with phenylbutyrate
——————————————————————
http://www.ncbi.nlm.nih.gov/pubmed/12241121/
——————————————————————
J Neurooncol. 2002 Sep;59(3):239-42
——————————————————————
http://www.ncbi.nlm.nih.gov/m/pubmed/12241121/
——————————————————————
Journal of Neuro-Oncology
Volume 59, Issue 3 , pp 239-242
——————————————————————
http://link.springer.com/article/10.1023%2FA%3A1019905127442
——————————————————————
DOI
10.1023/A:1019905127442
Journal of Neuro-Oncology 59: 239–242, 2002
2002 Kluwer Academic Publishers. Printed in the Netherlands
——————————————————————
http://ketonutrition.net/wp-content/uploads/2013/01/Baker_Complete_response_of_GBM_with_Phenylbutyrate_2002.pdf
——————————————————————
Neuro-Oncology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA
======================================
REFERENCES:
======================================
6. Gore SD, SAMID D, Weng LJ: Impact of the putative differentiating agents sodium phenylbutyrate and sodium phenylacetate on proliferation, differentiation, and apoptosis of primary neoplastic myeloid cells. Clin Cancer Res 3(10): 1755–1762, 1997
——————————————————————
7. Ram Z, SAMID D, Walbridge S, Oshiro EM, Viola JJ, Tao-Cheng JH, Shack S, Thibault A, Myers CE, Oldfield EH: Growth inhibition, tumor maturation, and extended survival in experimental brain tumors in rats treated with phenylacetate. Cancer Res 54: 2923–2927, 1994
——————————————————————
8. Thibault A, SAMID D, Cooper MR, Figg WD, Tompkins AC, Patronas N, Headlee DJ, Kohler DR, Venzon DJ, Myers CE: Phase I study of phenylacetate administration twice daily to patients with cancer. Cancer 75: 2932–2938, 1995
——————————————————————
9. SAMID D, Hudgins WR, Shack S, Liu L, Prasanna P, Myers CE: Phenylacetate and phenylbutyrate as novel, non-toxic differentiation inducers. Adv Exp Med Biol 400A: 501–505, 1997
——————————————————————
10. Chang SM, Kuhn JG, Robins HI, Schold SC, Spence AM, Berger MS, Mehta MP, Bozik ME, Pollack I, Schiff D, Gilbert M, Rankin C, Prados MD: Phase II study of phenylacetate in patients with recurrent malignant glioma: a North American Brain Tumor Consortium report. J Clin Oncol 17(3): 984–990, 1999
http://m.jco.ascopubs.org/content/17/3/984.full.pdf
SAMID D References
——————————————————————
11. Buckner JC, Malkin MG, Reed E, Cascino TL, Reid JM, Ames MM, Tong WP, Lim S, Figg WD: Phase II study of antineoplastons A10 (NSC 648539) and AS2-1 (NSC 620261) in patients with recurrent glioma. Mayo Clin Proc 74(6): 641–642, 1999
——————————————————————
12. SAMID D, Ram Z, Hudgins WR, Shack S, Liu L, Walbridge S, Oldfield EH, Myers CE: Selective activity of phenylacetate against malignant gliomas: resemblance to fetal brain damage in phenylketonuria. Cancer Res 54: 891–895, 1994
======================================
Antineoplastons: Phenylacetylglutaminate (PG or PAG), Phenylacetate (PN), and Phenylbutyrate (PB):
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/06/17/phenylacetylglutaminate-pg-or-pag-phenylacetate-pn-and-phenylbutyrate-pb/
======================================
Phenylbutyrate (PB):
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/06/18/phenylbutyrate-pb/
======================================
Phenylacetate (PN):
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/06/18/phenylacetate-pn/
======================================
Phenylacetylglutamine (PG or PAG):
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/06/18/phenylacetylglutamine-pg-or-pag/
======================================
Burzynski, China, and Dvorit D. Samid:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/02/21/burzynski-china-dvorit-d-samid/
======================================
Critiquing: Dr. David H. “Orac” Gorski and The Skeptics™ http://www.scienceblogs.com/Insolence
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/08/08/critiquing-dr-david-h-orac-gorski-and-the-skeptics/
======================================

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

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

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

“Burzynski … antineoplastons … “:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

——————————————————————
10 / 100% – experienced 35 recurrence-free intervals
——————————————————————
Recurrence-free intervals during antineoplaston AS2-1 administration SIGNIFICANTLY LONGER than without
——————————————————————
Patients who experienced recurrence-free intervals with and without antineoplaston AS2-1 SHOWED LONGER INTERVALS during antineoplaston AS2-1 administration
——————————————————————
2 patients in stage I showed LONGER RECURRENCE-FREE INTERVALS than those in more advanced stages
——————————————————————
Antineoplastons AS2-1 couldn’t prevent recurrence of HCC but PROLONGED RECURRENCE-FREE INTERVAL between regional treatments and IMPROVED SURVIVAL RATE OF PATIENTS
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[39] 2003 Case of survival for nearly 8 years after treatment of unresectable multiple liver metastases from colon cancer, using microwave ablation and NONTOXIC ANTITUMOR AGENT, antineoplastons
——————————————————————
72-year-old man diagnosed with adenocarcinoma of ascending colon and 14 bilateral liver metastases underwent right hemicolectomy combined with microwave ablation of 6 metastatic liver tumors
——————————————————————
Antineoplaston A10 given intravenously, followed by oral antineoplaston AS2-1
——————————————————————
Computed tomography scans done 1 and 4 years after initial diagnosis showed recurrent tumors
——————————————————————
Patient underwent 2nd and 3rd microwave ablation of recurrent tumors, and has survived for nearly 8 years WITHOUT SUFFERING ANY SERIOUS ADVERSE EFFECTS
——————————————————————
Currently FREE FROM CANCER
——————————————————————
Demonstrates potential effectiveness of NONTOXIC ANTITUMOR AGENT, antineoplastons, for controlling liver metastases from colon cancer
� � � � � � � � � � � � � � � �
======================================
Burzynski has made it clear that PHENYLACETATE, by itself, does NOT achieve the results of antineoplastons (PHENYLACETATE, PHENYLGLUTAMINATE, PHENYLACETYLISOGLUTIMINATE, PHENYLBUTYRATE)
======================================
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======================================
[40] 2003
——————————————————————
Pg. 92
——————————————————————
Antineoplaston A10 and AS2-1 are synthetic derivatives of phenylacetate (PN) acid, glutamine and isoglutamine
——————————————————————
A10 is sterile solution of sodium phenylacetylisoglutiminate (isoPG) in 4 : 1 ratio
——————————————————————
Antineoplaston AS2-1 is sterile solution of sodium phenylacetate (PN) and phenylacetylglutaminate (PG) in 4 : 1 ratio
——————————————————————
Pg. 93
======================================
combination of antineoplaston A10 and AS2-1 used instead of single drugs
——————————————————————
Based on previous observations, combination treatment has provided better results than single drugs
——————————————————————
Pg. 97
——————————————————————
active ingredient of antineoplaston AS2-1 is PHENYLACETATE,
——————————————————————
Pg. 98
——————————————————————
known to modulate expression of ras oncogenes and tumor suppressor gene p53
——————————————————————
ras oncogene protein p21ras
——————————————————————
farneslyation of p21ras, which is inhibited by antineoplaston AS2-1
——————————————————————
Antineoplaston AS2-1 also activates p53 gene
——————————————————————
protein p53 activates p21 gene, which directs synthesis of p21WAF1/Cip1 protein
——————————————————————
Induction of p21WAF1/Cip1 suppresses human glioma cell proliferation
——————————————————————
proposed mechanism of action of 2 ingredients of antineoplaston A10, sodium phenylacetylglutamine (PG) and sodium phenylacetylisoglutimine (IsoPG), is inhibition of glutamine incorporation into proteins of neoplastic cells
——————————————————————
Antineoplaston A10 has demonstrated 5 effects related to therapeutic indication in patients with brain tumors: cytostatic, antimitogenic, antiproliferative and inhibitory effects, and differentiation of tumors
——————————————————————
[22-25]
——————————————————————
Initial clinical studies with antineoplaston therapy included testing of separate ingredients phenylacetate (PN) (antineoplaston AS5) and phenylacetylglutaminate (PG) (antineoplaston AS2-5)
——————————————————————
[26-28]
——————————————————————
studies failed to show marked anticancer activity of phenylacetate (PN) in malignant glioma, confirmed by phase II study by North
——————————————————————
Pg. 99
——————————————————————
American Brain Tumor Consortium
——————————————————————
[29]
——————————————————————
Based on results, further studies of phenylacetate (PN) as single agent in patients with malignant glioma were not recommended
——————————————————————
subsequent study by Buckner et al.
——————————————————————
[30]
——————————————————————
confirmed conclusion because patients receiving antineoplaston AS2-1 didn’t respond to treatment
——————————————————————
main difference between Buckner’s study is dosage of antineoplaston A10, which was approximately 50 times lower in Buckner’s study
——————————————————————
[31]
——————————————————————
2 patients who participated in our study (cases 3 and 8) developed recurrence on lower dosages of antineoplaston A10, but responded again with Complete Response (CR) when dosage of antineoplaston A10 was increased
——————————————————————
In these 2 patients, antineoplaston AS2-1 didn’t seem to have effect on 2nd response, which suggests antineoplaston A10 rather than antineoplaston AS2-1 is main active drug
� � � � � � � � � � � � � � � �
[41] 8/2005 Antineoplastons such as A10 include naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH OF CELLS
——————————————————————
Findings indicate antineoplaston A10 ANTITUMOR EFFECT could be utilized as effective therapy for breast cancer patients
� � � � � � � � � � � � � � � �
[42] 2006 Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which CONTROL NEOPLASTIC GROWTH
——————————————————————
Antineoplaston A10 (3-pehnylacetylamino-2,6-piperidinedion) is first chemically identified antineoplastons and when administered orally is hydrolysed in pancreatic juice to PHENYLACETYLGLUTAMINE and PHENYLACETYLISOGLUTAMINE in ration of 4 to 1
——————————————————————
These metabolites are water soluble and have ANTITUMOR EFFECT, are further degraded to PHENYLACETIC acid
——————————————————————
Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETYLISOGLUTAMINE in ratio of 4 to 1 formulated as Antineoplaston A10 injectable formulation
——————————————————————
Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid in ratio of 1 to 4 also shown to have ANTITUMOR EFFECT in tissue culture study, then formulated as Antineoplaston AS2-1
——————————————————————
Reported CYTOSTATIC INHIBITORY EFFECT of A10 on HUMAN HEPATOCELLULAR CARCINOMA CELLS and differentiation inducing effect of AS2-1 on various TUMOR CELLS suggest potential benefit for treatment of HUMAN HEPATOCELLULAR CARCINOMA since this TUMOR recurs frequently despite initial successful treatment
——————————————————————
BOTH AGENTS INHIBITED CELL PROLIFERATION and increased number of cells in G0 and G1 phases and Antineoplaston AS2-1 induced apoptosis, we also describe clinical experience of hepatocellula carcinoma (HCC) patient whose tumor, after incomplete trancathere arterial embolization (TAE) for 7cm 7cm HCC, has been stable for more than 15 months during which time he has been taking Antineoplaston AS2-1 continuously WITHOUT ANY SERIOUS ADVERSE EFFECTS
� � � � � � � � � � � � � � � �
[43] 1/2008 Novel mechanism through which all-trans retinoic acid (ATRA) and antineoplaston, ANTICANCER DRUG, CAUSED CELL GROWTH INHIBITION IN BREAST CANCER CELLS through effects on intracellular pathways
——————————————————————
Antineoplaston caused down-regulation of PKCalpha protein expression, resulting in INHIBITION of ERK MAPK phosphorylation, with resultant INHIBITION of Rb phosphorylation leading to G(1) arrest
� � � � � � � � � � � � � � � �
[44] 10/1/2010 As degradation product of Antineoplaston A10 in vivo, PHENYLACETYL GLUTAMINE showed ANTITUMOR ACTIVITIES
——————————————————————
Designed and radiosynthesized PHENYLACETYL GLUTAMINE derivative, achieved under mild reaction condition
——————————————————————
radiochemical purity of (S)-2-((S)-2-(4-(3-fluoropropyl)benzamido)-3-phenylpropanamido)pentanedioic acid ([18F]FBPPA) was 98%, and best radiochemical yield was up to 46%
——————————————————————
results revealed it might become potential PET imaging agent for DETECTING TUMORS
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� � � � � � � � � � � � � � � �
References:
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[1] 7/1971
� � � � � � � � � � � � � � � �
Neish, W. J. P. Phenylacetic acid as a potential therapeutic agent for the treatment of HUMAN CANCER. Experientia (Basel), 27: 860-861, 1971
http://www.ncbi.nlm.nih.gov/pubmed/5139518/
Experientia. 1971 Jul;27(7):860-1
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[2] 1976
� � � � � � � � � � � � � � � �
Biological active peptides in human urine: III. Inhibitors of the growth of human leukemia, osteosarcoma, and HeLa cells
http://www.ncbi.nlm.nih.gov/m/pubmed/1066715
S R Burzynski, …
Physiol Chem Phys 8(1):13-22 (1976), PMID .1066715
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[3] 1990
� � � � � � � � � � � � � � � �
BURZYNSKI, S. R., Kubove E., Burzynski, B. Treatment of hormonally refractory CANCER of the prostate with ANTINEOPLASTON AS2-1. Drugs Exp. Clin. Res., 16: 361-369, 1990
http://www.ncbi.nlm.nih.gov/pubmed/2152694/
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[4] 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
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Cancer Res 1992;52:1988-1992
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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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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
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SAMID D, Shack S, Ti-Sherman L PHENYLACETATE-A novel nontoxic inducer of TUMOR CELL differentiation. Cancer Res 52:1988, 1992
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[5] 9/15/1992
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SAMID, D., Yeh, A., and Prasanna, P. Induction of erythroid differentiation and fetal
hemoglobin production in HUMAN leukemic cells treated with PHENYLACETATE. Blood, 80: 1576-81, 1992
http://www.ncbi.nlm.nih.gov/pubmed/1381630/
SAMID D, Yen A, Prasanna P . Induction of erythroid differentiation and fetal hemoglobin production in HUMAN leukemic cells treated with PHENYLACETATE . Blood. 1992;80:1576
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Blood, 80: 1576-1581, 1992
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Blood. 1992 Sep 15;80(6):1576-81
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.full.pdf
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD
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[6] 5/1993
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SAMID D, Shack S , Myers CE . Selective growth arrest and phenotypic reversion of prostate CANCER CELLS in vitro by nontoxic pharmacological concentrations of PHENYLACETATE . J. Clin. Invest . 1993;91:2288
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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC288233/

http://m.jci.org/articles/view/116457
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[7] 2/15/1994
� � � � � � � � � � � � � � � �
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
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Cancer Res. 1994 Feb 15;54(4):891-5
http://www.ncbi.nlm.nih.gov/m/pubmed/8313377/
Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
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[8] 4/1/1994
� � � � � � � � � � � � � � � �
A phase I and pharmacokinetic study of intravenous PHENYLACETATE in PATIENTS with CANCER
http://www.ncbi.nlm.nih.gov/pubmed/8137283/
Cancer Res 54(7):1690-4 (1994), PMID.8137283
http://www.ncbi.nlm.nih.gov/m/pubmed/8137283
Cancer Res April 1, 1994 54:1690
http://cancerres.aacrjournals.org/content/54/7/1690
Cancer Res. 1994 Apr 1;54(7):1690-4.
http://m.cancerres.aacrjournals.org/content/54/7/1690.abstract
Cancer Res . 1994;54:
http://cancerres.aacrjournals.org/content/54/7/1690
Clinical Pharmacology Branch, National Cancer Institute, NIH, Bethesda, Maryland
http://m.cancerres.aacrjournals.org/content/54/7/1690.full.pdf
A A Thibault, …, D D SAMID et al.
http://cancerres.aacrjournals.org/content/54/7/1690.full.pdf?sid=78d246d7-a4ee-4980-bdaf-b299dc98cbe8
Thibault A, Cooper MR, Figg WD, Venzon DJ, Sartor O, Tompkins AE, et al. (SAMID D)
↵1 This study was supported in part by a grant from Elan Pharmaceutical Research Co.
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[9] 6/1/1994
� � � � � � � � � � � � � � � �
Growth inhibition, TUMOR maturation, and extended survival in experimental BRAIN TUMORS in rats treated with PHENYLACETATE.
http://www.ncbi.nlm.nih.gov/pubmed/8187079/
Ram Z, SAMID D, Walbridge S, et al:
http://www.ncbi.nlm.nih.gov/m/pubmed/8187079/
Cancer Res 54:2934-2927, 1994
http://m.cancerres.aacrjournals.org/content/54/11/2934.abstract?ijkey=03bc67e581ef77536842806b949046916458d548&keytype2=tf_ipsecsha
Cancer Res. 1994 Jun 1;54(11):2923-7.
http://m.cancerres.aacrjournals.org/content/54/11/2923.abstract
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland
http://m.cancerres.aacrjournals.org/content/54/11/2923.full.pdf
Cancer Res. 1994 Jun 1;54(11):2923-7
http://cancerres.aacrjournals.org/content/54/11/2923
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[10] 1994
� � � � � � � � � � � � � � � �
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
� � � � � � � � � � � � � � � �
[11] 2/8/1995
� � � � � � � � � � � � � � � �
PHENYLACETATE synergizes with retinoic acid in inducing the differentiation of human neuroblastoma cells.
http://www.ncbi.nlm.nih.gov/pubmed/7829265/
Int J Cancer. 1995 Feb 8;60(4):507-14
http://www.ncbi.nlm.nih.gov/m/pubmed/7829265/
Department of Pathology and Laboratory Medicine (Neuropathology), UCLA School of Medicine
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910600414/abstract
Int J Cancer 60:507-514, 1995
Int J Cancer. 1995 Feb 8;60(4):507-14.
International Journal of Cancer
Volume 60, Issue 4, pages 507–514, 8 February 1995
Article first published online: 17 JUL 2006
DOI: 10.1002/ijc.2910600414
Sidell N, Wada R, Han G, et al: (SAMID D)
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[12] 4/1995
� � � � � � � � � � � � � � � �
Disposition of PHENYLBUTYRATE and its metabolites, PHENYLACETATE and PHENYLACETYLGLUTAMINE.
J Clin Pharmacol 35:368-373, 1995 Abstract
http://www.ncbi.nlm.nih.gov/pubmed/7650225/
J Clin Pharmacol 35:368-373, 1995 Abstract
http://www.ncbi.nlm.nih.gov/m/pubmed/7650225/
The Journal of Clinical Pharmacology
Volume 35, Issue 4, pages 368–373, April 1995
http://m.jcp.sagepub.com/content/35/4/368.abstract?ijkey=74bff0d86ce76b404728762fe2a1bfde1641fa41&keytype2=tf_ipsecsha
J Clin Pharmacol. 1995 Apr;35(4):368-73
http://onlinelibrary.wiley.com/doi/10.1002/j.1552-4604.1995.tb04075.x/abstract;jsessionid=DFDEF1599D764E2845EC2897269C198B.d01t01
Article first published online: 8 MAR 2013
http://jcp.sagepub.com/content/35/4/368
Piscitelli SC, Thibault A, Figg WD, et al: (SAMID D)
DOI: 10.1002/j.1552-4604.1995.tb04075.x
Pharmacy Department, National Institutes of Health, Bethesda, Maryland, USA
http://m.jcp.sagepub.com/content/35/4/368.abstract?ijkey=74bff0d86ce76b404728762fe2a1bfde1641fa41&keytype2=tf_ipsecsha
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[13] 5/1995
� � � � � � � � � � � � � � � �
The effect of Antineoplaston, a new ANTITUMOR AGENT on MALIGNANT BRAIN TUMORS
http://www.ncbi.nlm.nih.gov/pubmed/7474850
Kurume Med J. 1995;42(3):133-40
http://www.ncbi.nlm.nih.gov/m/pubmed/7474850
Department of Neurosurgery, Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/3/42_3_133/_article
Tsuda H (Japan)
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/3/42_3_133/_article/references
Burzynski References: 1 – 2 and 4
SAMID Reference: 7 (who learned from Burzynski re PHENYLACETATE)
Lee (Japan) A-10 Reference: 3
Nishidi (Japan) A-10 Reference: 6
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/3/42_3_133/_pdf
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[14] 6/15/1995
� � � � � � � � � � � � � � � �
Phase I study of PHENYLACETATE administered twice daily to PATIENTS with CANCER. Cancer 75:2932-8, 1995
http://www.ncbi.nlm.nih.gov/pubmed/7773944/
Cancer 75(12):2932-8 (1995), PMID.7773944
http://www.ncbi.nlm.nih.gov/m/pubmed/7773944
A A Thibault, D D SAMID, … C E CE Myers
Cancer. 1995 Jun 15;75(12):2932-8
Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
Thibault A, SAMID D, Cooper MR, et al:
Thibault, A., SAMID, D., Cooper, M. A., Figg, W. 0., Tompkins, A. C., Patronas, N., Headlea, 0. J., Kohler, 0. A., Venzon, 0. J., and Myers, C. E. Cancer (Phila.), 75: 2932-2938, 1995.
http://onlinelibrary.wiley.com/doi/10.1002/1097-0142(19950615)75:12%3C2932::AID-CNCR2820751221%3E3.0.CO;2-P/abstract
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[15] 7/1995
� � � � � � � � � � � � � � � �
Transcriptional upregulation of TGF-α by PHENYLACETATE and PHENYLBUTYRATE is associated with differentiation of HUMAN MELANOMA CELLS
http://www.ncbi.nlm.nih.gov/pubmed/7578983/
Liu L., Hudgins W. R., Miller A. C., Chen L. C., SAMID D.
http://www.sciencedirect.com/science/article/pii/S1043466685700610
Cytokine, 7: 449-456, 1995.
Cytokine Volume 7, Issue 5, July 1995, Pages 449–456
Cytokine. 1995 Jul;7(5):449-56.
a Clinical Pharmacology Branch, National Cancer Institute, Armed Forces of Radiation Research Institute, Bethesda, Maryland, USA
b Radiation Biochemistry Department, Armed Forces of Radiation Research Institute, Bethesda, Maryland, USA
http://dx.doi.org/10.1006/cyto.1995.0061
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[16] 9/27/1995
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Increased susceptibility of ras-transformed cells to PHENYLACETATE is associated with inhibition of p21ras isoprenylation and phenotypic reversion. Int J Cancer 63:124-129, 1995
http://www.ncbi.nlm.nih.gov/pubmed/7558439/
Int J Cancer. 1995 Sep 27;63(1):124-9
http://www.ncbi.nlm.nih.gov/m/pubmed/7558439/
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD, USA
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910630122/abstract
Int J Cancer 63:124-129, 1995
Int J Cancer. 1995 Sep 27;63(1):124-9.
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910630122/references
International Journal of Cancer
Volume 63, Issue 1, Article first published online: 17 JUL 2006
DOI: 10.1002/ijc.2910630122
Shack S, Chen L-C, Miller AC, et al: (SAMID D)
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910630122/abstract
Shack, S., Chen, L-C., Miller, A. C., Danesi, A., and SAMID, D. Int. J. Cancer, 63: 124-129, 1995
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[17] 10/1995
� � � � � � � � � � � � � � � �
Stockhammer G, Manley GT, Johnson R, et al: (SAMID D) Inhibition of proliferation and induction of differentiation in medulloblastoma and astrocytoma-derived cell lines with PHENYLACETATE. J Neurosurg 83:672-681, 1995
http://www.ncbi.nlm.nih.gov/pubmed/7674018/
J Neurosurg. 1995 Oct;83(4):672-81
http://www.ncbi.nlm.nih.gov/m/pubmed/7674018/
Cotzias Laboratory of Neuro-Oncology, Memorial Sloan-Kettering Cancer Center, New York, New York, USA
http://thejns.org/doi/abs/10.3171/jns.1995.83.4.0672?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed&
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[18] 10/12/1995
� � � � � � � � � � � � � � � �
Cytostatic activity of PHENYLACETATE and derivatives against TUMOR CELLS:
Correlation with lipophilicity and inhibition of protein prenylation.
http://www.ncbi.nlm.nih.gov/pubmed/7488244/
Biochem Pharmacol. 1995 Oct 12;50(8):1273-9
http://www.ncbi.nlm.nih.gov/m/pubmed/7488244/
Biochem Pharmacol 50:1273-1279, 1995
http://www.sciencedirect.com/science/article/pii/0006295295020133
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD, USA
� � � � � � � � � � � � � � � �
[19] 1995
� � � � � � � � � � � � � � � �
Toxicological study on antineoplastons A-10 and AS2-1 in cancer patients
Kurume Med J. 1995;42(4):241-9
http://www.ncbi.nlm.nih.gov/pubmed/8667595
Tsuda H
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://www.ncbi.nlm.nih.gov/m/pubmed/8667595
Burzynski References: 1 – 3 and 5
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_article
Nishida et al. (Japan) A-10 Reference: 4 and 7
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_article/references
Muldoon et al. A-10 Reference: 6
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_pdf
� � � � � � � � � � � � � � � �
[20] 2/1996
� � � � � � � � � � � � � � � �
Lipid metabolism as a target for BRAIN CANCER therapy:
Synergistic activity of lovastatin and sodium PHENYLACETATE against human glioma cells
http://www.ncbi.nlm.nih.gov/pubmed/8592143/
J Neurochem 66:710-716, 1996
http://www.ncbi.nlm.nih.gov/m/pubmed/8592143/
J Neurochem. 1996 Feb;66(2):710-6.
http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.1996.66020710.x/abstract
DOI: 10.1046/j.1471-4159.1996.66020710.x
http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.1996.66020710.x/abstract;jsessionid=913EBF64F1FA2FD0D08BD94FDDE391D5.d03t01
Article first published online: 23 NOV 2002
http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.1996.66020710.x/abstract;jsessionid=E929EA030144CC973FECF4DAA1D9D50C.d01t04
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland, USA
Prasanna P, Thibault A, Liu L, et al: (SAMID D)
� � � � � � � � � � � � � � � �
[21] 5/1996
� � � � � � � � � � � � � � � �
PHENYLACETATE is an inhibitor of prostatic growth and development in culture.
http://www.ncbi.nlm.nih.gov/pubmed/8627880/
J Urol 155:1762-1770, 1996
http://www.ncbi.nlm.nih.gov/m/pubmed/8627880/
J Urol. 1996 May;155(5):1762-70
Lipshutz JH, SAMID D, Cunha GR:
The Journal of Urology
Volume 155, Issue 5, Pages 1762-1770, May 1996
Department of Medicine, University of California, San Francisco, USA
� � � � � � � � � � � � � � � �
[22] 1996
� � � � � � � � � � � � � � � �
Inhibitory effect of antineoplaston A10 and AS2-1 on human hepatocellular carcinoma
Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/pubmed/8755117
Kurume Med J. 1996;43(2):137-47
http://www.ncbi.nlm.nih.gov/m/pubmed/8755117
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article
Burzynski References: 1 – 3, 5 and 7
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article/references
SAMID Reference: 13 (who learned from Burzynski re PHENYLACETATE)
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_pdf
Nishida et al. (Japan) A10 Reference: 4 and 10
Muldoon et al. A10 Reference: 8
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[23] 8/23/1996
� � � � � � � � � � � � � � � �
Pineau T, Hudgins WR, Liu L, et al: (SAMID D) Activation of a human peroxisome proliferator-activated receptor by the ANTITUMOR agent PHENYLACETATE and its analogs. Biochem Pharmacol 52:659-667, 1996
http://www.ncbi.nlm.nih.gov/pubmed/8759039/
Biochem Pharmacol. 1996 Aug 23;52(4):659-67
http://www.ncbi.nlm.nih.gov/m/pubmed/8759039/
Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD, USA
http://www.sciencedirect.com/science/article/pii/0006295296003401
� � � � � � � � � � � � � � � �
[24] 9/1996
� � � � � � � � � � � � � � � �
The differentiating agent PHENYLACETATE increases prostate-specific antigen production by prostate cells
http://www.ncbi.nlm.nih.gov/pubmed/8827086/
Prostate 29:177-182, 1996
http://www.ncbi.nlm.nih.gov/m/pubmed/8827086/
Prostate. 1996 Sep;29(3):177-82
Walls R, Thibault A, Liu L, et al: (SAMID D)
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland, USA
� � � � � � � � � � � � � � � �
[25] 12/1996
� � � � � � � � � � � � � � � �
Gorospe M, Shack S, Guyton KZ, et al: (SAMID D)
Up-regulation and functional role of p21Waf1/Cip1 during growth arrest of HUMAN BREAST CARCINOMA MCF-7 cells by PHENYLACETATE. Cell Growth Differ 7:1609-1615, 1996
http://www.ncbi.nlm.nih.gov/pubmed/8959328/
Cell Growth Differ. 1996 Dec;7(12):1609-15
http://www.ncbi.nlm.nih.gov/m/pubmed/8959328/
Laboratory of Cellular and Molecular Biology, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, Maryland, USA
http://cgd.aacrjournals.org/cgi/reprint/7/12/1609.pdf
� � � � � � � � � � � � � � � �
[26] 5/1996
� � � � � � � � � � � � � � � �
Shack, S., Miller, A., Liu, L., Prasanna, P., Thibault, A., and SAMID, D.. Vulnerability of multidrug-resistant TUMOR CELLS to the aromatic fatty acids PHENYLACETATE and PHENYLBUTYRATE. Clin. Cancer Res., 2: 865-872, 1996
http://www.ncbi.nlm.nih.gov/pubmed/9816242/
Clin Cancer Res. 1996 May;2(5):865-72
http://www.ncbi.nlm.nih.gov/m/pubmed/9816242/
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892, USA
http://m.clincancerres.aacrjournals.org/content/2/5/865.abstract

http://m.clincancerres.aacrjournals.org/content/2/5/865.full.pdf
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[27] 8/1997
� � � � � � � � � � � � � � � �
Miller AC, Whittaker T, Thibault A, et al: (SAMID D)
Modulation of radiation response of HUMAN TUMOR CELLS by the differentiation inducers, PHENYLACETATE and PHENYLBUTYRATE. Int J Radiat Biol 72:211-218, 1997
http://www.ncbi.nlm.nih.gov/pubmed/9269314/
Int J Radiat Biol. 1997 Aug;72(2):211-8
http://www.ncbi.nlm.nih.gov/m/pubmed/9269314/
Armed Forces Radiobiology, Research Institute, Bethesda, MD, USA
� � � � � � � � � � � � � � � �
[28] 11-12/1997
� � � � � � � � � � � � � � � �
Antineoplaston AS2-1 for maintenance therapy in liver cancer
H Tsuda phase I clinical trial
http://www.ncbi.nlm.nih.gov/pubmed/21590224
Oncol Rep. 1997; 4:1213- 1216
http://www.ncbi.nlm.nih.gov/m/pubmed/21590224
Oncol Rep. 1997 Nov-Dec;4(6):1213-6
http://www.spandidos-publications.com/or/4/6/1213
Oncol Rep 4 (6):1213-6 (1997)
Oncology Reports
4 (6):1213-6
KURUME UNIV,SCH MED,DEPT SURG,KURUME,FUKUOKA,JAPAN. KURUME UNIV,SCH MED,DEPT INTERNAL MED,KURUME,FUKUOKA,JAPAN. KURUME UNIV,SCH MED,DEPT RADIOL,KURUME,FUKUOKA,JAPAN
� � � � � � � � � � � � � � � �
[29] 1997
� � � � � � � � � � � � � � � �
PHENYLACETATE and PHENYLBUTYRATE as novel, nontoxic differentiation inducers
http://www.ncbi.nlm.nih.gov/pubmed/9547596
Adv Exp Med Biol (1997), PMID.9547596
http://www.ncbi.nlm.nih.gov/m/pubmed/9547596
Adv Exp Med Biol. 1997;400A:501-5
http://link.springer.com/chapter/10.1007%2F978-1-4615-5325-0_67
DOI
10.1007/978-1-4615-5325-0_67
http://link.springer.com/content/pdf/10.1007%2F978-1-4615-5325-0_67.pdf
Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury 2
Advances in Experimental Medicine and Biology Volume 400, 1997, pp 501-505
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD USA
D D SAMID, W R WR Hudgins, … C E CE Myers
� � � � � � � � � � � � � � � �
[30] 5 – 6/1998
� � � � � � � � � � � � � � � �
Quick response of advanced cancer to chemoradiation therapy with antineoplastons
H Tsuda A10 and AS2-1 – I
http://www.ncbi.nlm.nih.gov/pubmed/9538158
Oncol. Rep. 1998;5:597–600
http://www.ncbi.nlm.nih.gov/m/pubmed/9538158
Oncol Rep. 1998 May-Jun;5 (3):597-600
http://www.spandidos-publications.com/or/5/3/597
5 (3):597-600
Oncol Rep 5 (3):597-600 (1998)
Oncology Reports
Department of Anesthesiology, Kurume University, School of Medicine, Kurumeshi, Fukuokaken, Japan
� � � � � � � � � � � � � � � �
[31] 11-12/1998
� � � � � � � � � � � � � � � �
Antineoplaston treatment for advanced hepatocellular carcinoma
H Tsuda – A10 I – I
http://www.ncbi.nlm.nih.gov/pubmed/9769368
Oncol Rep. 1998;5:1363-1367
http://www.ncbi.nlm.nih.gov/m/pubmed/9769368
Oncol Rep. 1998 Nov-Dec;5 (6):1363-7
http://www.spandidos-publications.com/or/5/6/1363
Oncol Rep 5 (6):1363-7 (1998)
5 (6):1363-7
Oncology Reports, Spandidos Publications
Department of Radiology, Kumabe Hospital, Kurume University School of Medicine, Kurumeshi, Fukuokaken, Japan
� � � � � � � � � � � � � � � �
[32] 3/1999
� � � � � � � � � � � � � � � �
Phase II study of PHENYLACETATE in patients with recurrent MALIGNANT GLIOMA:
a North American Brain Tumor Consortium report
http://www.ncbi.nlm.nih.gov/pubmed/10071293/
J Clin Oncol. 1999 Mar;17(3):984-90
http://www.ncbi.nlm.nih.gov/m/pubmed/10071293/
J Clin Oncol 17(3):984-90 (1999), PMID.10071293
http://m.jco.ascopubs.org/content/17/3/984.long
S M Chang, J G Kuhn, … M D Prados
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[33] 7/3/2000
� � � � � � � � � � � � � � � �
(A10) – Potential utility of antineoplaston A-10 levels in breast cancer
http://www.ncbi.nlm.nih.gov/pubmed/10814881
Cancer Lett 155:67-70, 2000
http://www.ncbi.nlm.nih.gov/m/pubmed/10814881
Cancer Lett 155(1):67-70 (2000)
http://www.cancerletters.info/article/S0304-3835(00)00408-0/abstract
Cancer Lett. 2000 Jul.3;155(1):67-70
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DOI: 10.1016/S0304-3835(00)00408-0
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Cancer Letters, Elsevier Science
Department of Pharmacognosy, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

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[34] 8/31/2000
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Immune modulatory potentials of antineoplaston A-10 in breast cancer patients
http://www.ncbi.nlm.nih.gov/pubmed/10893443
Cancer Lett 157: 2000
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Cancer Lett 157 (1):57-63 (2000)
http://www.cancerletters.info/article/S0304-3835(00)00472-9/abstract
Cancer Lett. 2000 Aug.31;157(1):57-63
http://www.sciencedirect.com/science/article/pii/S0304383500004729
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http://dr-labouzeid.webs.com/A10-Cancer%20Letters%20157.pdf
Cancer Lett 157: 57-63, 2000
Cancer Letters – Elsevier
Cancer Letters, Elsevier Science
DOI: 10.1016/S0304-3835(00)00472-9
Department of Pharmacognosy, Faculty of Pharmacy, Mansoura University, Egypt

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[35] 12/2000
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(antineoplaston A10) – Novel piperidinedione analogs as inhibitors of breast cancer cell growth
http://www.ncbi.nlm.nih.gov/pubmed/11199474
333 (12):431-4 (2000)
http://www.ncbi.nlm.nih.gov/m/pubmed/11199474
DOI: 10.1002/1521-4184(200012)333:123.0.CO;2-M
http://onlinelibrary.wiley.com/doi/10.1002/1521-4184(200012)333:12%3C431::AID-ARDP431%3E3.0.CO;2-M/abstract
Arch Pharm (Weinheim), John Wiley & Sons, Inc.
Department of Medicinal Chemistry, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

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[36] 8/2001
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A phase Idose escalation and bioavailability study of oral sodium PHENYLBUTYRATE in patients with refractory solid tumor malignancies
http://www.ncbi.nlm.nih.gov/pubmed/11489804
Clin Cancer Res 7(8):2292-300 (2001), PMID.11489804
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Clin Cancer Res. 2001 Aug;7(8):2292-300
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J Gilbert, S D Baker, … M A Carducci
SAMID References: 2-3, 5-6, 15 and 22
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[37] 2002
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A novel strategy for remission induction and maintenance in cancer therapy
H Tsuda A10 and AS2-1
http://www.ncbi.nlm.nih.gov/pubmed/11748457
Oncol Rep 2002;9:65–8
http://www.ncbi.nlm.nih.gov/m/pubmed/11748457
Oncol. Rep. 2002;9:65-68
http://www.spandidos-publications.com/or/9/1/65
Oncol Rep 9(1):65-8 (2002)
Oncology Reports, Spandidos Publications
Department of Anesthesiology, Kurume University, School of Medicine, Fukuoka-ken, Japan
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[38] 3 – 4/2003
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The preventive effect of antineoplaston AS2-1 on HCC recurrence
Hideaki H TSUDA Phase II Clinical Trial
http://www.ncbi.nlm.nih.gov/pubmed/12579278
Oncol Rep. 2003 Mar-Apr;10(2):391-7
http://www.ncbi.nlm.nih.gov/m/pubmed/12579278
Oncol Rep. 2003;10:391-397
http://www.spandidos-publications.com/or/10/2/391
Spandidos Publications
http://www.burzynskiclinic.com/images/stories/Publications/964.pdf
Oncology Reports 10: 391-397, 2003
Oncol Rep 10 (2):391-7 (2003)
Oncol Rep 2003;10:391–7
Department of Anesthesiology, Kurume Daiichi Social Insurance Hospital, Kushihara Kurumeshi, Fukuoka, Japan
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[39] 2003
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Long-term survival following treatment with antineoplastons for colon cancer with unresectable multiple liver metastases: report of a case
http://www.ncbi.nlm.nih.gov/pubmed/12768372
Long-Term Survival Following Treatment with Antineoplastons for Colon Cancer with Unresectable Multiple Liver Metastases:
Report of a Case
Hideaki Tsuda A10 and AS2-1 – Phase II Clinical Trial
http://www.springerlink.com/content/b48ch3ha165nbrqp
Surg Today. 2003;33(6):448-53
http://link.springer.com/article/10.1007%2Fs10595-002-2503-2
Surg Today 2003; 33:448–53
http://link.springer.com/content/pdf/10.1007%2Fs10595-002-2503-2
Surg Today. 2003; 33:448-453
http://link.springer.com/article/10.1007%2Fs10595-002-2503-2?LI=true
33 (6):448-53
http://link.springer.com/content/pdf/10.1007%2Fs10595-002-2503-2
Surgery Today, Springer
http://sciencelinks.jp/j-east/article/200313/000020031303A0389449.php
Surg Today 2003
http://sciencelinks.jp/j-east/article/200313/000020031303A0389449.php
DOI: 10.1007/s10595-002-2503-2
http://ci.nii.ac.jp/naid/10015483373
Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan
http://ci.nii.ac.jp/naid/10015483373
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[40] 2003
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Drugs in R and D
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http://www.ncbi.nlm.nih.gov/m/pubmed/12718563
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(Drugs in Research and Development)
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Drugs R D. 2003;4(2):91-101
Drugs in R&D 2003;4:91-101
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[41] 8/2005
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Antineoplaston induces G1 arrest by PKCα and MAPK pathway in SKBR-3 breast cancer cells
Hideaki H TSUDA Antineoplaston A10
http://www.ncbi.nlm.nih.gov/pubmed/16012735
Antineoplaston induces G1 arrest by PKCo and MAPK pathway in SKBR-3 breast cancer cells
http://www.ncbi.nlm.nih.gov/m/pubmed/16012735
Antineoplaston induces G(1) arrest by PKCalpha and MAPK pathway in SKBR-3 breast cancer cells
http://www.spandidos-publications.com/or/14/2/489
Oncol Rep. 8/2005; 14(2):489-94
http://gyouseki.kurume-u.ac.jp/PDF/ichiran_2005.pdf
Oncol Rep 14(2):489-94 (2005)
http://research.kurume-u.ac.jp/K90RES.php?scode=49485632873864
Oncol Rep. 2005; 14:489–94
http://onlinelibrary.wiley.com/doi/10.1002/iub.574/abstract
Oncol. Rep. 14, 489–494
http://onlinelibrary.wiley.com/doi/10.1002/iub.574/full
Oncology Reports, 8/2005, Volume 14 Number 2
Pages: 489-494
http://onlinelibrary.wiley.com/store/10.1002/iub.574/asset/574_ftp.pdf?v=1&t=hbr9z60q&s=0b1c1e8655db9c54b45dbf72062e8b11cb7895ac
Oncology Reports, Spandidos Publications
Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan
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[42] 2006
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Inhibitory Effect of Antineoplaston A10 and AS2-1 on Human Hepatocellular Carcinoma
Tsuda H, et al
http://www.ncbi.nlm.nih.gov/pubmed/8755117
Kurume Med J. 1996;43(2):137-47
http://www.ncbi.nlm.nih.gov/m/pubmed/8755117
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article
Kurume Medical Journal
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_pdf
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[43] 1/2008
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Preclinical studies of molecular-targeting diagnostic and therapeutic strategies against breast cancer
http://www.ncbi.nlm.nih.gov/pubmed/18224398
antineoplaston
http://www.ncbi.nlm.nih.gov/m/pubmed/18224398
Breast Cancer 15(1):73-8 (2008)
DOI: 10.1007/s12282-007-0015-y
http://link.springer.com/article/10.1007%2Fs12282-007-0015-y
Breast Cancer. 2008;15(1):73-8. doi: 10.1007/s12282-007-0015-y
http://www.springerlink.com/content/p724x34746l56v73
15(1):73-8
http://ci.nii.ac.jp/naid/10021288533
Breast Cancer: January 2008, Volume 15, Issue 1, pp 73-78
Department of Surgery, Kurume University, Fukuoka, Japan
Burzynski Reference: 12
Tsuda (Japan) Antineoplaston Reference: 13
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[44] 10/2010
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Antineoplaston A10 phenylacetyl glutamine (PG)
http://www.springerlink.com/content/tj0177485773007t
(S)-2-((S)-2-(4-(3-[18F]fluoropropyl)benzamido)-3-phenylpropanamido)pentanedioic acid labeled with 18F
http://link.springer.com/article/10.1007%2Fs10967-010-0633-2?LI=true
(S)-2-((S)-2-(4-(3-[18 F] fluoropropyl) benzamido)-3-phenylpropanamido) pentanedioic acid labeled with 18 F
http://www.springerlink.com/content/tj0177485773007t
Journal of Radioanalytical and Nuclear Chemistry, 2010, 286, 1, 135
http://link.springer.com/article/10.1007%2Fs10967-010-0633-2
October 2010, Volume 286, Issue 1, pp 135-140
http://link.springer.com/article/10.1007/s10967-010-0633-2/fulltext.html
DOI
10.1007/s10967-010-0633-2

http://onlinelibrary.wiley.com/doi/10.1021/js960120y/abstract
Burzynski References: 5. – 6.
http://www.springerlink.com/content/tj0177485773007t
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Burzynski, China, and Dvorit D. Samid

12/17/2012 – China
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3524164
CDA-2 (cell differentiation agent 2), a URINARY preparation

CDA-2 and its main component PHENYLACETYLGLUTAMINE (PG or PAG)

Antineoplaston AS2-5 is PHENYLACETYLGLUTAMINE (PAG or PG)

Antineoplaston AS2-1 is a 4:1 mixture of phenylacetic acid (PA) and PHENYLACETYLGLUTAMINE (PAG or PG)

Antineoplastons AS2-5 and AS2-1 are derived from Antineoplaston A10

BURZYNSKI Reference: 22.
antineoplaston AS21

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0052117
National Cancer Institute, at the National Institutes of Health cancer . gov web-site re Antineoplastons:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page5
PHENYLACETYLGLUTAMINE (PAG or PG)

Antineoplaston AS2-5 is PHENYLACETYLGLUTAMINE (PAG or PG)

Antineoplaston AS2-1 is a 4:1 mixture of phenylacetic acid (PA) and PHENYLACETYLGLUTAMINE (PAG or PG)

Antineoplastons AS2-5 and AS2-1 are derived from Antineoplaston A10

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

4/1994 – Dvorit D. SAMID et al.
A phase I … study of intravenous phenylacetate (PN) in patients with cancer

Cancer Res 54(7):1690-4 (1994), PMID 8137283

Cancer Res. 1994 Apr 1;54(7):1690-4

Clinical Pharmacology Branch, National Cancer Institute, NIH, Bethesda, Maryland
http://www.ncbi.nlm.nih.gov/m/pubmed/8137283
Phenylacetate (PN) elimination was accounted for by conversion to PHENYLACETYLGLUTAMINATE (PG or PAG), which was excreted in the urine

4/1995 – Dvorit D. SAMID et al.
Disposition of Phenylbutyrate (PB) and its metabolites Phenylacetate (PN) and PHENYLACETYLGLUTAMINATE (PG or PAG)

J Clin Pharmacol 35(4):368-73 (1995), PMID 7650225

J Clin Pharmacol. 1995 Apr;35(4):368-73

Pharmacy Department, National Institutes of Health, Bethesda, Maryland, USA
http://www.ncbi.nlm.nih.gov/m/pubmed/7650225
PHENYLACETYLGLUTAMINATE (PG or PAG) and Phenylacetate (PN) are metabolites of Phenylbutyrate (PB) and are constituents of AS2-1