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Pete Cohen chats with Richard A. Jaffe, Esq.

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4/2012 – Pete Cohen chats with Rick Jaffe
(33:59) 11/9/2012
Richard A. Jaffe, Esq.
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How did you meet Dr. Burzynski?

A long time ago in 1988, um, he hired us to represent him in his Medical Board case, so, uh, started working for him then, and then there got to be more and more work, and, uh, at some point it was so much work, it was just easier for me to be down here
So I moved from New York to Texas, mostly just to, to represent him, and my wife was in the oil industry, so, it was a “no brainer” for her to move down here too

And how, were you intrigued by this whole case ?
I mean, did you work out straight away that this guy was genuine, and there was really something here ?

No (laugh)
How do you know, you know ?
At the time we represented, uh, a number of a alternative health practitioners around the country, and we heard a lot about Burzynski, but you don’t really know
I mean, um, um, there are a lot of stories out there
Every doctor seems to have a few patients, uh, that were helped
So initially, I mean, how do you know ?
His operation was larger than most of any, uh, health practitioners, alternative health practitioners in the country, and, uh, seemed a lot more sophisticated, but, uh, it’s not really until you dig in the medical records of the patients that you really see what’s going on
I mean, that’s what you really need
I mean,
It’s not really even, it’s
’cause this whole thing about anecdotal evidence, that everyone has testimony
so every doctor
You know what I mean ?
anybody
Even charlatans have testimony
people
one or two people
or 3 or 4 that’ll come, and say w
they were cured, and maybe, maybe the patients really believe that to be the case, but, um, oftentimes there’s other explanations
Prior treatment, um, the nature of the disease
Sometimes it’s such that their natural, the natural history is not straight linear, um, but after looking at some of the medical records, I mean, you know, I think
it’s just,
uh, anybody would become a believer, and indeed, I mean, government, government doctors have come down here and looked at

some of the records, and they were convinced that, that the treatment was causing remissions in some brain cancer patients

So, I mean, obviously lawyers, I imagine many lawyers all over the world would often take on a case, when they know, possibly the guy isn’t telling the truth, but they can see there’s still a story, and they, they, they, they, uh, represent that person, but for you, I suppose
that when you realized that there really was a story here, did you kind of get, emotionally caught up in this whole thing and think: “Right, th this guy’s got a cure for cancer, and I I need to bring this to, bring him to just, not bring him to justice, but, clear his name
Well, I think with Burzynski, more so than any client I’ve ever represented
He represents a unique constellation of medical services
He’s the only guy in the world doing what he’s doing with antineoplastons and now with this treatment, so, it’s really different
Uh, you know, with Burzynski, most of the patients, are in bad shape
They’re either dying, uh, they, or they have a disease for which there is no known cure, you know, like a lot of these brain tumors
So, even from the beginning, what’s different is their are many, many patients back then who were on the treatment, that uh, that felt that without this treatment they were going to die, and so that, that’s much different, than the average, any kind of lawsuit
Right ?
So th th these lawsuits, the Burzynski cases back then and now, uh, these cases matter, in a, in a deeper, and fundamental, and personal way than most anything, well I think that any lawyer does
I mean, any criminal defense lawyer, who defends an individual, is defending that person’s, uh, liberty
Alright ?
Versus incarceration
But here it, it wasn’t so much, or, it wasn’t exclusively about Burzynski, it was really about all these other patients, and they certainly believe they needed him, and, uh, uh, many of them, obviously did
So, so that, that, that’s a whole ‘nother dimension, which typically we lawyers don’t get involved in
So, I mean, it’s a responsibility but also a great privilege to be working on these kinds of cases

You’ve been representing him for how long ?

For a long time
Since 1988, continuously

And can you believe this is still going on ?

Well, you know, uh, it’s, you know, it’s, it’s just ongoing
I mean, until there’s a cure for cancer, for all cancer, either done by acknowledged

or, uh, uh, to be Burzynski’s cure or somebody else’s
I mean, this is ongoing
And I guess the problem is, you know, ultimately, there’s nobody yet
Not even Burzynski has the cure for every cancer or
even every stage, or even ev, every, ev, ev, every person that had cancer
So, because it’s such a tough battle, and because, it doesn’t work on everyone
So you have these open questions
Ah, so, so,
Yeah, I mean, I guess, I, I can’t believe he’s still messing around with these clinical trials
I mean, I think that if the drug didn’t have his name attached to it, it’d probably would have been approved by now
So, and I think, so that, that’s unfortunate, I think, that when you fight the FDA, and even if you win, you know, the F, the repercussions, you know, you know I, you know I
Hopefully the drug will be approved, sometime in the future, but, but who knows ?

So, um, why do you think, why was it, I mean, obviously I came over here as you know, for this case, which is now not going ahead at the moment
Why, why, why is that ?
Wha, what has the judge, said ?

Well, of course, you have to (under)stand, this case involves a different type of treatment
It doesn’t involve antineoplastons,the drug Dr. Burzynski invented, and your friend is receiving, and it involves a new approach to cancer, which is sort of like personalized medicine, where they take a bunch of FDA approved drugs, that have shown some promise, on a particular cancer, but are not, uh, approved for that indication, and based on these early clinical trials showing promising results for genetic testing they give these combinations of FDA approved drugs, off-label to patients, and that’s really what the, this case is about, and, uh, you know I think, I don’t think they, they never had a case
I mean, they never had a case
The, the main allegation, in each, of the 2 patients involved, is that they used this treatment, which wasn’t sufficiently tested, and was non-therapeutic, and whatnot, and we had a, what I would call a dry run
We presented the evidence to the Board, or 2 members of the Board, in both of these cases
In each, in each case, the Board members felt that the treatment, was within the standard of care, given the advanced condition of the patient, or one patient, and given how rare the other patient’s tumor was
So, we had our dry run in each case, and the Board found in our favor on the main charge
They had some technical issues with medical records or whatnot, and, uh, the Board basically said, they took the position, ok, agree to some kind of sanction on these little charges, or, or we’re going to go after you on everything
So, we refused the honor, and, uh, the Board then charged him with the same thing that they already cleared him with, or on, and, and so we had to do, you know, basically the same case again, and, uh, the irony in, is in these 2 cases Burzynski wasn’t even in the country
He was, he was, he was away for, uh, in both, for both cases, when the patientscame
So, uh, the question is how do you hold someone responsible
Even if you own the clinic, for treatment administered and prescribed, by other doctors, and that concept of vicarious liability does not, uh, exist in jurisprudence, and in the law governing professional re, responsibility, anywhere in this country
So, the Board’strying to start that
You know, I think they just got in over their heads, they
Most people just knuckle under
You know, most people don’t, are afraid to go to court, so they’ll sign anything just to, you know, not to go forward, but, you know, Burzynski faced serious stuff
I mean, he set, faced, 5, 10, 15 years in jail
So he wasn’t going to be intimidated, by the Medical Board, and he refused to give in
So when I told the Board at the time, and I told them all along, they have no case, and o on the merits they have no case
We already won, and they have no case now, and, and slowly I think, the Board is starting to understand that

And what sort of a person would you say Dr. Burzynski is ?

Well I think he’s a complicated person
I mean, I think, uh, uh, you know, he, I think like a lot of mavericks; I represent a lot of mavericks around the, uh, uh, country
One of the main characteristics of these guys, is that they have absolute and total certainty, in what they believe in, in what they do, um, and no doubt
Uh, they all think they’re right
They all think that history is going to vindicate them
Now, I’ve represented some people where I personally doubt (laugh) that, uh, uh, that belief, but not in Dr. Burzynski’s case
I mean, I think he’s all, he’s definitely helping people
He’s definitely, uh, uh, uh, making, extending people’s lives, and curing some people that otherwise would have died, and so I think he, and so I think he happens to be right
So, uh, you know, so, but, but he’s a human
He’s got a big ego
He thinks he’s, uh, he thinks he has made an important, contribute to medicine, and he’s not shy about sharing that sentiment
So, uh, I think, and I think that he’s, uh, not American
So he comes with a completely different mentality towards, say, the government
Alright, he grew up in communist Poland, where everyone, where everyone, has to work around, the government, and I think that’s much harder here, and, you know, I think he has expectations that, that he would have a lot more freedom, than it turned out he had, too, and he thought he would not have to deal with the kind of government, uh, rigamarole that you have to deal with in communist, Poland

And, and how do you think it might all pan out for him ?
I mean, I know you don’t have a crystal ball, but if you could look, 5 or 10 years down into the future, and, do you think that he will have got somewhere, to be accepted in the medical (?) of oncology ?

Well, I certainly hope so
I mean, 5, 10 years from now
I mean, I think, at a minimum, what’s going to happen, there will be many, many patients who will be alive, and continue to be alive because of him
Some, will have their lives extended
Some will be cured
Some wi, won’t be cured, and will die
So, I think that’s for sure, going to happen
You know, is there going to be an end to, uh, all this ?
We had a period of maybe 10 years where there was very little action with the Board, but, uh, you know, it’s hard, frankly, I mean, just in, and again my perspective, like I’m in a, like a, a sergeant in the trenches, in trench (laugh) warfare
So, it’s hard for me to see the big picture
I mean, I just keep fighting these battles, and there’s one, after another, after another
So this is really just the latest, and on there’s civil lawsuits, and then there are people on the Internet, and then, you know, there could be more Medical Board investigations
So, lo, look there are a lot of people who don’t like what he’s doing
They think what he’s doing is either unethical or wrong, or shouldn’t be giving drugs, these drugs to people, except under clinical trial conditions, and, you know, he has detractors, and he has a lot of supporters
I mean, uh, mostly amongst the patients he’s cured
So, I don’t know that, that, that is gonna resolve itself
I mean, ultimately, he’s one of the few people in the country, that, or maybe the only person in the country that does what he does, and, it’s not the way medicine is practiced, in this country, typically
Right, and, you know, I think what he does, is, is more, is more patient oriented, in a sense that, once you’ve been told you’re terminal, why should you just get the palliative care that a medical oncologist thinks, you know, they should be given
even though when, no one ever gets cured of chemotherapy, once it’s palliative, once you have stage 4, solid tumor

Mmm

I mean, they give chemotherapy for what they call palliative reasons, which means, not curative
So, this concept of giving, just conventional chemotherapy to make you feel better, extend your life 9 weeks, I mean, y, not everyone wants to do that
Some people want a shot for a real cure, and, you know, based on the evidence with antineoplastons
, I mean, he seems to be giving people that shot, and curing some of the people
So, you, you know, I don’t see how, this thing gets resolved
Up until the time that the
treatment, the
antineoplastons is approved by the FDA and, you know,
it’s, it’s hard to see a clear path, for that, for a lot of reasons, not the least of which is financial
I mean, it takes dozens of 10’s of millions of dollars

Mmm

or 10, 100’s of millions
So, I mean, someone has to finance the clinical trials
The drug companies aren’t interested right now
They’d just as soon, buy a drug that’s been fully tested
So, I mean, the drug company response has not been overwhelming, because, even though this phase 2 phase, have resolved, and, and, uh, they have excellent results, the drug companies want to wait and see
So, uh, it’s, it’s big money
I don’t think there’s any way in the world Dr. Burzynski, himself, can fund phase 3
I mean, he, he funded everything else now, but phase 3 are, is a much bigger stage involving dozens and 100’s of patients, and that’s just within the financial means of any individual

it seems like it’s unlikely that its going to happen right
I mean, even from the point of view of, what, with phase 3 trials, they’ll be with children

with brainstem gliomas, right
and the FDA’s saying they’ve got to have radiation

Yeah I, um,
I unfortunately, I haven’t been involved in that process
I just see the result, and I, I, I just don’t see how any parent agrees to that, you know

I don’t see how any parent agrees to it
I don’t see how clinical investigator, agrees to do it
Um, I don’t know
I got so, I got some questions of the FDA as to, why they forced him into this particular protocol
I mean, I don’t know
I don’t have any facts or evidence, but I, I, just doesn’t make any sense to me

what’s you’re about that ?

I don’t know
I mean, I, it just doesn’t seem to me, that it’s a, that it’s a fair clinical trial that

Mmm

either an investigator would find ethical, or a patient, or a family, would agree to have their patient treat, their, their kid treated under
I mean, it just doesn’t make any sense to me
I mean, it’s worse than
I mean, both phases, both phases, both arms of the study, you get radiation
It’s radiation alone versus radiation with his stuff
So, I mean, it just doesn’t make any sense to me, given, given the clinical, the phase 2 clinical trial results

So just a, so just a few things, like, you know I’m going to talk about big Pharma, and then talk about the FDA

Right

They talk about the many people as if they’re one person, but, you know, they’re obviously a collective group of individuals who work for an organization, right ?

Well, I mean, I think, the concern is, that the FDA now, by statute is, in no small part funded, by the pharmaceutical industry
It’s like “Pay as you go”
So the, the pharmaceutical ind, industry now, pays for, the processing of the clinical trials by the FDA
So, and then you have the whole concept of the revolving door
You have a lot of government officials going into the drink, uh, drug companies
So I think that’s another problem
So, I mean, you know, I think conspiracy is too strong of a word, m, but, you know, I will say, I don’t think the system’s set up, for an individual like Burzynski, to get a drug approved
I, I, I just don’t see
There’s no support for that
I mean, the days
I mean, it’s like, Einstein, you know ?
He sat in a patent office, and, and doodled, and had his little theory
He could never get his, stuff published today, you know ?
Where did he go to school
?
Where was he teaching, you know ?
So Burzynski has a lot of the same problems
They say he doesn’t publish, but, they won’t let him publish
So, uh, or they won’t let him publish , in, in the mainstream journals
So, I, I, I think though, I think the, I think the system, has a strong bias, against a guy with a discovery
So, that’s not quite saying, there’s a conspiracy, but it’s, it’s sort of along the same lines, and, you know, the conspiracy implies some kind of, um, intentionality on the part of one or two, or some small group or coterie of people, and I don’t know, I don’t think that’s really the case
I think what happens is, the institutions are such that, they allow certain things, and disallow certain things
Alright ?
I think that’s just
there’s no
I don’t think there’s any 2, 3, 4, or some, coterie of Rocka, they’re like a Rockefeller conspiracy
People are saying that there are 12 industrials
That they control the world
I mean, I don’t see that happening, but, the whole system is such that, you know, it’s, it’s
I guess what, uh
The, there’s a book by, uh, a, a, Thomas Kuhn, the Structure of Scientific Revolutions, and he talks about, normal science, and how science progresses, in terms of paradigm shifts
So, normal scientific medicine, works, uh, by big institutions doing, studies about combinations of drugs, after drug companies, invent mostly, modifications of existing drugs, and, less commonly, completely new drugs, and, uh, less commonly, different classes of drugs
So, you have a whole, you have a whole pipeline from a drug company, a whole, uh, uh, mechanism of testing, by the universities, funded by the pharmaceutical company, uh, all the pharmaceutical companies, and that, that just doesn’t lend itself, to one guy, sitting someplace in Houston, or wherever, and having a drug, put through that process
That just doesn’t happen
Burzynski is, so far as I can tell, the only person, to ever completed, a phase 2 trials on a drug he invented
I don’t think that’s ever happened, before, and I don’t think it’ll ever happen again

Ah, was it ’98, was it the chairman, uh

Kessler ?

Kessler
I saw, an interview he gave, press, a press conference where he was explaining about, being able to fast-track
The FDA trying to make it possible to fast-track, you know, drugs that have shown, you know, positive, rather than going through all of this sort of clinical trial, and there’s a guy in the, in the press conference who started asking questions about Burzynski

Right

and you could just see quite clearly he was very uncomfortable

Right

asking questions about, uh, about Dr. Burzynski
How do you think someone like him,
would view, someone like Dr. Burzynski ?

Not favorably
I think that, uh,

Do you think they must know ?
Do you think they must, even he, let’s just say, if he were on his own, he, he knows there’s something there
That he’s obviously got something

I,
I don’t know, uh
I think, that, the guys in conventional medicine, because Burzynski came from orthodox medicine
He was at Baylor
He was a researcher at Baylor
So, I think, they’re not going to Burzynski, is that, he didn’t go about it, the way, other physicians would have done it, other scientists would have done it
So normally what would happen, is, uh, uh, I mean, I think the critical, point in his story is that, when he was at Baylor, and his, uh, professor was supporting him, this Unger, left, you know, they had space for him
They wanted him to go in the Oncology, uh, Department, but, they wanted the patent, to his drug, and he wouldn’t do it
So, that would have been the more conventional approach
You give up the patent rights, you become part of the team, then some big institution, uh, uh, shepherds the drug through, and then they find some drug company support, who will split the patent with the university
So, had he done that, uh, you know, I think the drug woulda been approved by now, but, you know, it was his drug
He came to America with it, and he wasn’t going to give it all away
So, I mean, I just think that’s, you know, I mean and that’s, you know, I think he wasn’t expecting that kind of thing in America
Maybe in communist Poland, but not in America
So I think that really, you know, set him down the path of being a, a, an alternative health practitioner

And wha, wha, what was it like for you when, uh, winning, the case, in was it, 199, 3, 1998 ?

’97

1997

Well, you know, there wasn’t just one case
I mean, I mean, it was everyone
I mean, I analogize it to, like whack-a-mole, or whack-a-rat, you know
You have, like a rat come out of, of a hole, and you bang him, and one comes out of this hole, and all of a sudden you’ve got 2, and then 3, and, so, you know, during the early ’90’s, I mean, I mean, there were 3 grand juries, uh, we had the Medical Board action, which went to hearing in ’93
The Texas Department of Health sued him in ’92
Half a dozen insurance companies had sued, uh, uh, sued him for, for some, for Racketeering
Uh, Texas Air Quality Department went after him
I’m trying to think who else
So, all of this happened, over the course of 3, or 4, or 5 years, and it was just, continuous, and so, one agency would, would get active, and then, they get beaten down
Then somebody else would come, uh, come up, and surface, and indeed, I mean, you know, it, you know, some of them flat out said they were waiting to see what happened, with this oth, wha, what happened with this other agency, and they weren’t gonna do anything, and then when they got tired, they decided, that this new agency had to do something
So, I mean, that was flat out, what happened
So, yeah, I mean, it culminated in the criminal case, I suppose, but even there it was up and down
I mean, the judge ordered, uh, ordered, prohibited him from giving the treatment to anybody else, because the Texas Medical Board case, ultimately went against us, and then we had to go Congress, and Congress forced the FDA to put all his patients on clinical trials which made the Medical B, Board case moot, and then we won the criminal case
So, after we won the criminal case in, uh, ’97, things got quiet for a little bit
So that, that, that was good
I mean, it was quiet
I mean, relatively quiet, and then, uh, lately in the last couple years it’s been very active again

So the worst case scenario would have been
What would have been the worst case scenario ?

For when ?

And this, this
What could have happened this week if the case had gone ahead ?

Well, the worst case scenario would be, there would be a finding, that, that it’s a depart, it’s a departure from the standard of care to use, uh, off-label drugs, that haven’t been approved by the
FDA for an indicated use, and you can’t use the combination of the drugs until someone gives the stamp of approval saying that their safe and effective, which means, you know, you couldn’t, it couldn’t, you couldn’t give the treatment anymore to patients
So you have 100’s of patients that are on this multi-agent gene-targeted therapy, and ultimately that form of treatment is only available at the Burzynski Clinic
I mean, I don’t think that even clinical trials
Burzynski, depending on how you look at it, he’s a few years ahead of, of, uh, well, even the clinical trials
I mean, they’re some clinical trials now on different kinds of cancer where they’re doing 1, 2, or 3 agents
He’ll use 4 or 5, albeit, lesser dosages
So he’s treated 1,000’s of patients like that, but there’s no place else in the world where people can get, the treatment
So it’s kinda the same thing as back in the ’90’s
We have people on drugs, uh, which are unavailable, uh, and, only available through Burzynski
So, if he couldn’t give them, to people, then they wouldn’t get ’em, and, they’re terminal, and, they’re doing well
I mean, or they’re not going to do as well, or they’re going to die
So, it’s, I guess it, it’s sort of the same thing here, ah, uh, only, uh, the irony is all these drugs are, approved by the FDA, and most cancer patients get off-label, uh, drugs
Drugs off-label
So that’s, very common in cancer
It’s just that not common with the drug used on these patients, and in the combinations used

So, this finally
Whe, when you’ve, uh, won these cases, I mean, there must be, it must be good, right ?
It must be good feeling

I had a good feeling last week
I mean, I mean, you know, or I’ve been working non-stop, for months, every day
I mean, there’s no day off in this kind of stuff
It’s just constant
It’s just, his war
There’s always something to do, and then I’m a solo practitioner
So, when the judge cut the heart of the Board’s case out, I’ve been telling the Board, that they can’t, that they have no basis to, to, to bring charges against him, for several years, since 2010
, 2009, and they’re not listening, and, and, I was pretty sure that once you had a judge look at the case, they would, rule in our favor, you know, but the problem is the Board is, like a law unto themselves, and they think they can do anything, and, uh, they just changed the law, in September
So actually, the Board has no recourse
They, they used to be able to change findings of facts, and conclusions of law, but as of September, 2011, they can no longer do so
So, if the, judges’ ruling s, uh, stands, as I think they will, their only remedy is going to be to appeal to a State District Court, and they’re not used to that, because they, like exercising, uh, complete authority
So, they’re in a new position, and I’m sure this is the 1st case, that they’ve ever, not gotten what they want to, from, from a judge, administrative law judge, and not being able to correct it
So, I mean, that, this is a good ti, completely new experience for the Board, and I feel bad for them (both: laughing)

You, you, you do
As a Board they all sit down, and as a group of people, and talk about Dr. Burzynski, and, and, and work out how they’re gonna bring him down, and then ?

Well, that’s more the conspiracy
I, I, I, I think that, some of the Board members, may know of him
He, but, but, but like I say, he’s appeared in front of these informal settlement conferences, and basically, individually they, I mean, exonerate him, of, of the main charges, but I, I, I think that, you know, when we talk about the Board, the Board other than these a, acting informal settlement conferences, where you have one Board member, and one member of some district disciplinary review committee, we’re not really talking about the Board members, these doctors, and lay members of the Board, we’re talking about the Board staff, and that’s the lawyers and administrators of the Board, and I think, you know, I don’t know
I have some, uh, uh, they need to clean house
I mean, they’re getting some very, very bad legal advice, and I, I just think the legal advice at the top, is, is, is horrible, and, and they need to make some dramatic changes, and I think it would be better for the people of Texas if they, just did some house cleaning with the administrative staff there

And what do you think about the way that, uh, Dr. Burzynski’s been , what’s the word, in England, he’s got a very bad press there

(Alright ?)

and, um, why do you think that is ?

Uh, why, well, I mean, look
I mean, I think, people have opinions
They’re,
they have the right to express opinions
I mean, I think, uh, some of his agents did some things that I think, were not wise, in retrospect
I mean

Mhmm

Uh,

The stuff with the, this kid, this blogger

Yes

(?)

And I think that, uh
I think you have to be very careful, about what you tell people that are expressing opinions, and, you know, I mean, I, I, I think, you know, I think there’s a reason why, lawyers get involved in these cases, and should be involved, and I think what happens is, you know, I think there was a, you know, a well meaning, individual, who just went too far, and I think stirred things up unnecessarily so
You know, I mean, I think someone who had some legal training, acting on Burzynski’s behalf, might not have made some of the, you know, just faux pas that were made
So, I mean, that stirred, some things up, and I think

(?) stirred something up that was already there ?
You know, ’cause, I know, I’ve spoken to so many people in the U.K., and, uh, and you find very few people that have anything positive to say
In fact, a friend of mine who’s a famous doctor on television, when I was here, he was on British television with a little girl, and her father, who were trying to, uh, raise money to, um, come over here and, um, in fact, they couldn’t come anywhere, come, they couldn’t come anyway, because, the, uh, FDA said that this type of brain tumor, she couldn’t be treated anyway
But this doctor, who’s a friend of mine said, uh, Dr. Burzynski is, you know, he’s a medical pioneer
He’s, uh, uh, he said that and then literally, for 2 months, non-stop, I think especially on Twitter, they said that he never should have said this, and the guy is a quack, and he’s a, he’s a fraud, and

So your, your friend got in trouble for saying that he’s a pioneer ?

He didn’t get in trouble, but I mean he got a lot of bad press, for speaking on television with this child next to him, saying that, Dr. Burzynski was, you know, a pioneer, and pioneers often have a hard time, and

Right, right

And, you know, you look at Twitter, uh, you probably don’t
You could be (laugh) and you just see, it’s probably, probably the only, 30, hard, hard core people, who spend, all of their time, trying to

Yeah, I think that’s right
I think it’s a very small group, of people, that are making pretend it’s a big movement
I mean, we’ve looked, at some of the traffic
We’ve analyzed some of the traffic
I don’t even think it’s 30
I think it’s more like, 3, or 4, or 5, that are creating things, and then someone had some friend who’s an actor, who has, you know, 3 million followers, and all
So it’s really a very small group of people, but historically, medical doctors who have stood up for Burzynski, have had negative consequences
We had, someone from the National Cancer Institute, NIH testify, this Nick Patronas, and he got in a lot of trouble for doing that
So, you know, it’s not, it’s, unfortunately, you know, speaking up for Burzynski can have, uh, negative career consequences, or, or just some bad P.R., but that’s, part of being a pioneer
It doesn’t mean that, uh, Burz, I mean, if anything, I mean, it shows, it shows that’s like the medical mafia
Yeah
So, that’s what I call, the church of medical orthodoxy
So, that’s what I call
So

Well I, I think it’s gonna be so interesting when I get this film broadcasted, to see what kind of reaction we get
It, it’s just a story I felt I had to (?)

Where are, where are you going to try and get it ?

I’m going to try and get it
I know people at the BBC

Right

I’ve worked in television
So I’m going to try

Oh really, (?)

I’m gonna try those avenues, but you know what ?
Even if it doesn’t

You have cable
You have some kind of public access ?

Yeah
I’ve, I’ve worked in television for years
So I’ve, I have a very good stab at getting it out there, but if I don’t, I’ll get it broadcasted on the Internet

Oh sure
You do, do a YouTube or something, or do what Merola did as a documentary

(?)

That’s had an amazing impact

Yeah
He’s making a sequel
Eric was just over in England

Oh really ?

I looked after him when he came over

Yeah
He wanted to talk to some of the patients and doctors

Eric, I said, ah, you know, so, we’ll see
But listen, I really appreciate the opportunity to ah

Ok, no problem

really, to be able to talk to you
======================================

======================================
http://www.richardjaffe.com
======================================

Critiquing Wikipedia: Burzynski Clinic – 2013 BBC documentary, Curing cancer or ‘selling hope’ to the vulnerable?

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Wikipedia must be too busy accusing me of using multiple Internet I.P. addresses to try and change every wiki article under the sun, instead of keeping their Burzynski article up-to-date

I await the in-depth analysis which breaks down my blog, Twitter, and Internet activity, showing that it was humanly possible for me to do all that has been claimed

But then again, maybe I’m NOT human !

HAL ?

Is that you HAL ?

Anywho, WP took a crack at addressing the British Broadcasting Corporation’s (BBC) Panorama documentary [1]

I did some critiques on the documentary article, documentary, and WP’s “credible source,” Dr. David H. Orac … Gorski [2-4]

“Burzynski exploits a legal loophole”by treating patients” with antineoplastons do so as part of a clinical trial, so the drug does not need a licence” for twenty years.” [66]

“Legal loophole” ?

Really ??

Not so much

It’s the law

“The Skeptics™” have had years to get it changed in Congress if it were a “legal loophole”

“According to Watford Observer, the mother of Luna Petagine, a young girl with a brain tumor, “cast doubt” on Burzynski’s “expensive treatment.” [67]

“Expensive treatment” ?

Based on what objective criteria ? [5-6]

The Reading Post said, the “Panorama investigation shown on Monday questioned whether the Burzynski Clinic was ‘selling hope’to families” which doubted the statistics provided by the Burzynski Clinic. [68]

Based on what objective criteria ?

“They say 776 patients with brain tumours were treated in trials before 2008.”

“And that 15.5% had survived more than five years, which compares favourably to other treatments.” [6] (see #13)

Where’s Wikipedia’s survival rates for:

a) Chemotherapy

b) Radiation Therapy

c) Radiotherapy

d) Other

and their comparison of possible adverse effects of chemotherapy, radiation therapy, radiotherapy, other, compared to antineoplastons ?

The issues I had with the documentary were:

1. “The report includes interviews with experts like Professor Richard Grundy of Nottingham Children’s Hospital”

“Prof Richard Grundy treats children with cancer, and runs one of the UK’s biggest research projects into brain tumours.”

“He says it is “unethical” for Dr Burzynski not to share his findings:”

In my ‘opinion,’ it is “unethical” for Professor Grundy to NOT share his findings re Dr. Burzynski’s 2003-2010 phase 2 clinical trial preliminary reports [7]

2. “Unfortunately the results from Dr Burzynski’s clinic are not published in any form that’s acceptable to the scientific community.””

Explain [7]

3. Dr Jeanine Graf

“She sometimes treats patients from the Burzynski Clinic who have become critically ill, but she has never known any of them survive.”

How many patients ?

Richard Bilton asked for numbers from Burzynski, so he should be consistent and have asked Dr. Graf the same question

4. “He must believe in what he’s doing, but I have not been convinced by the existing scientific literature that his therapy has any efficacy.”

Where is Dr. Graf’s “in-depth” review of Dr. Burzynski’s above-listed publications ? [7]
======================================
REFERENCES:
======================================
[1] – Wikipedia: Burzynski Clinic – Legal Issues: 2013 BBC documentary, Curing cancer or ‘selling hope’ to the vulnerable?
——————————————————————
http://en.wikipedia.org/wiki/Burzynski_Clinic
——————————————————————
http://en.m.wikipedia.org/wiki/Burzynski_Clinic
——————————————————————
http://en.wikipedia.org/w/index.php?title=Burzynski_Clinic&mobileaction=toggle_view_desktop
======================================
[2] – 6/4/2013 – The British are Coming, The British are Coming: Critiquing
“Curing cancer or ‘selling hope’ to the vulnerable?”:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/06/04/the-british-are-coming-the-british-are-coming-critiquing-curing-cancer-or-selling-hope-to-the-vulnerable/
======================================
[3] – 6/7/2013 – IT MAY NOT BE SCIENCE: Critiquing “Curing cancer or ‘selling hope’ to the vulnerable?”:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/06/07/it-may-not-be-science-critiquing-curing-cancer-or-selling-hope-to-the-vulnerable/
======================================
[4] – 8/4/2013 – Critiquing Dr David H. “Orac”
Gorski, M.D., Ph.D, LIAR: Stanislaw Burzynski versus the BBC:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/08/04/critiquing-dr-david-h-orac-gorski-m-d-ph-d-liar-stanislaw-burzynski-versus-the-bbc/
======================================
[66] – Richard Bilton

——————————————————————
http://www.radiotimes.com/episode/wxxjy/panorama–cancer-hope-for-sale—panorama
——————————————————————
there for posterity on YouTube
�
http://t.co/YOlSjCg1d0
——————————————————————
THIS IS IT!
�
http://fb.me/LYCqmKrh
——————————————————————
http://t.co/6cDJapt6eM
——————————————————————
http://t.co/nFpwlQg275
======================================
[67] – Watford Observer
——————————————————————
http://www.watfordobserver.co.uk/news/10470494.print/
======================================
[5] – 4/25/2013 – Burzynski: Costs of Cancer treatments:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/04/25/burzynski-costs-of-cancer-treatments/
======================================
[6] – 7/18/2013 – Critiquing: In which the latest movie about Stanislaw Burzynski “cancer cure” is reviewed…with Insolence:
——————————————————————
See #10
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/07/18/critiquing-in-which-the-latest-movie-about-stanislaw-burzynski-cancer-cure-is-reviewed-with-insolence-2/
======================================
[68] – Reading Post
——————————————————————
http://www.getreading.co.uk/news/amelia-saunders-family-mislead-burzynski-4051287
======================================
[7] – 8/7/2013 – Burzynski: Phase II Clinical Trials Preliminary Reports:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/08/07/burzynski-phase-ii-clinical-trials-preliminary-reports/
======================================

Yes! Weekly: Burzynski: Cancer is Serious Business Part II

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6/20/2013 Mark Burger published a review:
——————————————————————
http://www.yesweekly.com/triad/article-16162-burzynski-cancer-is-.html
——————————————————————
As could be expected, The Skeptics™
showed up
======================================
ANONYMOUS: “I’m afraid you’ve fallen for Dr Burzynski’s PR efforts here”
——————————————————————
LIE: The documentary film is by Eric Merola, NOT “Dr. Burzynski’s Public Relations”
======================================
ANONYMOUS: “In reality, Dr B is a quack and a charlatan of the worst order, and the movie is nothing more than a desperate attempt to try to sell his snake oil to the gullible”
——————————————————————
LIE: After reading through the comments, this sounds like the infamous lying Professor Robert J. (Bob) Blaskiewicz of University of Wisconsin, Eau Claire, “infamy”, who is a charlatan of the first order, and belabors his ignorance by referring to “snake oil”, which as far as I know, has never been approved for phase III clinical trials, unlike Dr. Burzynski’s antineoplastons A10 (Atengenal) and AS2-1 (Astugenal)
——————————————————————
Bob Blaskiewicz (Blatherskitewicz), Faux Skeptic Exposed!:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/06/07/bob-blaskiewicz-blatherskitewicz-faux-skeptic-exposed/
======================================
ANONYMOUS: “You have to ask why he’s never published any data showing that his treatment works”
——————————————————————
LIE: What people should ask is why does “Professor” @rjblaskiewicz and his other Skeptic pals continue posting idiotic statements like this on the Internet and social media (Twitter) ?
——————————————————————
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/
======================================
ANONYMOUS: “Well, if you believe everything the movie tells you, then perhaps you think it’s because of a huge global conspiracy that prevents him from publishing in any journal anywhere in the world”
——————————————————————
If you want to talk Jesse Ventura type “conspiracy theory”:

1. Why are The Skeptics™ like you too afraid to debate ?

2. Why did your “pal” David H. “Orac” Gorski, MD, PhD, FACS block me on his blog for questioning his infallibility ?

3. Why did Forbes delete my comments when I questioned The Skeptics™? regarding your “pal” Gorski’s “bud”, Peter A. Lipson, MD’s article ?

4. Why did The Skeptics™ Josephine Jones block me from her blog ?

5. Why did The Skeptics™ Adam Jacobs block me from his blog ?

6. Why did The Skeptics™ Guy Chapman block me from his blog ?

7. Why did The Skeptics™ Keir Liddle block me from his blog ?

8. Why do The Skeptics™ whine to Twitter in order to get Twitter to suspend the accounts of people who question them ?

9. Why did Wikipedia block me, using lame excuses ?

10. Why did reddit act like wiki’s little bitch and delete my posts and block my comments because this reddiot davidreiss666 whined like a little bitch ?
——————————————————————
overview for DidymusJudasThomas (reddit.com)

submitted 4 days ago by davidreiss666 to reportthespammers

1 comment
======================================
ANONYMOUS: “Even if you are sufficiently conspiracy minded to believe that’s true, then it still doesn’t explain why he hasn’t published his results on the clinicaltrials dot gov website, where most of his trials are recorded as either “ongoing”, “withdrawn”, or “unknown status””
——————————————————————
Did you NOT appear on the below blog talk radio show with your “pal” Gorski who said at 29:00 that Burzynski should NOT publish the information himself ?
——————————————————————
Ep09 – Talking Burzynski – David Gorski and Bob Blaskiewicz 05/29/2013
Skeptic Canary Show – BlogTalkRadio
May 29, 2013 … This week, join your hosts as we talk about Dr. Stanislaw Burzynski and the Burzynski Clinic. Well be joined by two special guest, Doctor David Gorski and Bob Blaskiewicz
http://www.blogtalkradio.com/…/ep09–talking-burzynski–david-gorski-and-bob-blaskiewicz
——————————————————————
http://www.blogtalkradio.com/skepticcanary/2013/05/29/ep09–talking-burzynski–david-gorski-and-bob-blaskiewicz
——————————————————————
http://goo.gl/7pWIj
——————————————————————
http://bit.ly/15lv5zG
——————————————————————
Critiquing the #SkepticCanary: “The Skeptics™” (SkeptiCowards©) Bob Blatherskitewicz and the so-called, “self-proclaimed” “CANCER RESEARCHER”:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/06/03/critiquing-the-skepticcanary-the-skeptics-skepticowards-bob-blatherskitewicz-and-the-so-called-self-proclaimed-cancer-researcher/
======================================
ANONYMOUS: “Only one of his trials is recorded as being completed, and that one doesn’t reveal it’s results”
——————————————————————
Did you notice that your above 5/29/2013 appearance was BEFORE this article was published 6/20/2013 ?
======================================
ANONYMOUS: “The fact is that Burzynski keeps is actual research data an extremely closely guarded secret”
——————————————————————
Like THIS ?
——————————————————————
Critiquing: Dr. David H. “Orac” Gorski, M.D., Ph.D, L.I.A.R.:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/08/07/critiquing-dr-david-h-orac-gorski-m-d-ph-d-l-i-a-r/
======================================
ANONYMOUS: “If is treatment were actually effective, do you seriously think he’d do that?”
——————————————————————
RATS!!!. Like this ?
——————————————————————
Burzynski: Oh, RATS!!!
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/07/26/the-lancet-oncology-peer-review-team-d-12-01519-fail-2/
======================================
ANONYMOUS: “Burzynski likes to cultivate his conspiracy theories because it helps his business of scamming vulnerable cancer patients”
——————————————————————
Is that like The Skeptics™ like to LIE to people ?
——————————————————————
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/
======================================
ANONYMOUS: “For Burzynski, at least, cancer is indeed serious business”
——————————————————————
And for you, it must be a joke, considering how you are too much of a coward to debate questions like these
——————————————————————
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/
======================================
JEFF: “it has been tested independently in other countries, as the film shows”
======================================
ANONYMOUS: “The Japanese study remains unpublished, Jeff, just like all the over 60 studies Burzynski has started”

“Even if it were published, it would need to be replicated”
——————————————————————
Really ? Why not try pointing out where these studies were replicated before the FDA allowed these drugs to be used ?
——————————————————————
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/
======================================
ANONYMOUS: “Merola manipulated by voice, face and even what I said in his movie and never asked for my comments”

“Sure, he misrepresented me to my new employers, but that doesn’t actually count as consulting me, now does it?”

“The “birthday surprise” in the movie was a fundraiser for a children’s cancer research hospital that raised over $15K, something I’m rather proud of, actually”
——————————————————————
Nice TRY with your LIE
——————————————————————
Critiquing Bob Blaskiewicz (#Burzynski Cancer is Serious Business, Part II):
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/03/26/critiquing-bob-blaskiewicz-burzynski-cancer-is-serious-business-part-ii/
======================================
ANONYMOUS: “I’d encourage you to look at the other side of the story at The OTHER Burzynski Patient Group”

“These are far more typical outcomes”
——————————————————————
Do you mean this one of a number of your blogs which I just critiqued ?
——————————————————————
Critiquing https://theotherburzynskipatientgroup.wordpress.com
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/08/24/critiquing-httpstheotherburzynskipatientgroup-wordpress-com/
======================================
ANONYMOUS: “You might also see what Merola got wrong/faked at the anp4all website”
——————————————————————
Oh, do NOT worry

I will critique this one also, and let people see what YOU got wrong
======================================
ADAM JACOBS: “Jeff, you say it has been “tested independently in other countries”, but how do you know?”

“Because the movie says so?”

“Well, it would, wouldn’t it?”

“Come back and tell me about these so-called “independent tests” when they’ve been published”

“Until then, there is no reliable evidence that they actually happened”
——————————————————————
Adam Jacobs also known as @DianthusMed also known as Dianthus Medical of London, why don’t YOU come back and tell me when YOU learn how to read ?
——————————————————————
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/
======================================
TOMMIE TAYLOR: “The worst conspiracy in the world and the most profitable is the mainstream medical procedures of surgery, chemotherapy, and radiation”

“Chemo and radiation destroy the immune system to the point that the body cannot heal”

“It is a crime against humanity to allow only these therapies”
======================================
ADAM JACOBS: “You do know that Burzynski uses chemotherapy, don’t you?”

“Antineoplastons themselves are a form of chemotherapy, but actually most of Burzynski’s patients don’t get ANPs anyway: they just get conventional chemotherapy”
——————————————————————
Adam, have you blocked anyone else from your blog since you blocked me because you are a coward ?
——————————————————————
The Burzynski Skeptics:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/08/18/the-burzynski-skeptics/
======================================

Critiquing David H. Gorski, MD, PhD, FACS www.sciencebasedmedicine.org/editorial-staff/david-h-gorski-md-phd-managing-editor/

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Critiquing David H. Gorski, MD, PhD, FACS http://www.sciencebasedmedicine.org/editorial-staff/david-h-gorski-md-phd-managing-editor/

“Our only goal is to promote high standards of science in medicine”
——————————————————————
http://www.sciencebasedmedicine.org/editorial-staff/
——————————————————————
So proclaims Science Based Medicine . org

6/10/2013 Gorski published:
======================================
BBC Panorama investigates Stanislaw Burzynski
——————————————————————
http://www.sciencebasedmedicine.org/bbc-panorama-investigates-stanislaw-burzynski/
======================================
“Burzynski hasn’t published anything other than case reports, tiny case series, and unconvincing studies, mostly (at least over the last decade or so) in crappy journals not even indexed on PubMed”
——————————————————————
Gorski’s above statement makes me wonder if PhD’s are handed out to any hack that requests one

Burzynski has published at least 4 publications which list all of the patients and information like:
======================================
[2] 16. 2003
(Pgs. 95-96) data charts
(Pg. 95)
Case
Sex
Age
Date of initial diagnosis
Tumor histology
Tumour location
Tumour size
Previous therapies
Karnofsky performance status
KPS baseline
Date of recurrence
(Pg. 96)
Start date
Stop date
Days on treatment
Dosage
Response
Status / date of death
Progression date
Survival time (weeks) from start
Time (weeks) to progression
Last contact
======================================
[9] 17. 2004
(Pgs. 316 + 318-321) data charts
(Pg. 316)
Gender
Age
Tumour histology
Tumour size (total of measured lesions)
Previous therapies
Karnofsky performance status
(Pg. 318)
Case
Age at admission
Sex
Ethnicity
Date of initial diagnosis
Pathology code
Visual Pathway Glioma (VPG)
Karnofsky baseline
Previous treatment
Multicentric tumour location
(Pg. 319)
” ”
(Pg. 320)
Case
Start date
Stop date
Days on treatment
Average dosage (IV treatment / PO treatment)
(Pg. 321)
Case
Response
Maximum response date
Time to maximum response (months)
Radiological PD as of 1/03/04
Progression Free Survival (PFS) (year)
Status
Karnofsky Performance Status (KPS) baseline
Karnofsky Performance Status (KPS) follow-up
Reason for withdrawal
Survival time from diagnosis (years)
======================================
[10] 18. 6/2005
(Pgs. 169 + 171.–.172) data charts
(Pg. 169)
Gender
Tumor type
Tumor spread
Previous therapies
Age
Karnofsky performance status
(Pg. 171)
Case
Protocol
Gender
Age at Admission (years)
Ethnicity
Date of Initial Diagnosis
Tumor Type
Tumor Dissemination
Karnofsky Performance Status (KPS) Baseline
Previous treatment
(Pg. 172)
Case
Start Date
Stop Date
Days on Treatment
Average Dosage g/kg/d (A10 / AS2-1)

Case
Response
Radiological PD
Progression Free Survival (PFS) (month)
Status
Karnofsky Performance Status (KPS) Baseline
Karnofsky Performance Status (KPS) Follow-up
Reason for Withdrawal
Overall Survival from Diagnosis (OSD) (month)
Overall Survival from Start (OSS) (month)
======================================
[12] 19. 3/2006
(Pgs. 42-45) data charts
(Pg. 42)
Gender
Age
Tumor history
Tumor size at baseline
Previous therapies
Karnofsky Performance Status
(Pg. 43)
Case
Protocol
Sex
Age (years)
Date of Initial Diagnosis
Tumor Type
Tumor Dissemination
Recurrence
Karnofsky Performance Status (KPS) Baseline
Previous Treatment
(Pg. 44)
Case
Start Date
Stop Date
Days On
Average Dosage g/kg/d (A10 / AS2-1)
(Pg. 45)
Case
Response
Radiological PD
Progression Free Survival (PFS) (months)
Status
Karnofsky Performance Status (KPS) Baseline
Karnofsky Performance Status (KPS) Follow-Up
Reason for Withdrawal
Overall Survival from Diagnosis (OSD) (month)
Overall Survival from Start of antineoplaston(OST) (month)
======================================
Maybe Gorski should try “deconstructing” some of these, especially the ones where patients did NOT have chemotherapy or radiation therapy

I’ve even provided a handy reference list

But by George, I’m George Dubya dubious that Gorski can handle it, given his track record
� � � � � � � � � � � � � � � � �
[18] 12/2009 (Pg. 923)
1 – Special Exception (SE)
——————————————————————
[3] 1. 3/2004 (Pg. 52)
10 – subgroup
——————————————————————
[3] 1. 3/2004 (Pg. 55)
10 – Japan
——————————————————————
[11] 7. 7/2005 (Pg. 300)
10 – children
——————————————————————
[2] 16. 2003 (Pg. 98)
11 – Special Exception (SE)
——————————————————————
[7] 4. 10/2004 (Pg. 427)
11 – children
4 – children Study (ST)
7 – children Special Exception (SE)
——————————————————————
[1] 1. 10/2003 (Pg. 358)
12 – children
——————————————————————
[2] 16. 2003 (Pg. 91)
1st 12 – Study (ST)
——————————————————————
[4] 4. 9/2004 (Pg. 257)
12
——————————————————————
[9] 17. 2004 (Pg. 316)
1st 12 – children
——————————————————————
[15] 10. 6/2008 (Pg. 450)
1st 12 – children
——————————————————————
[10] 18. 6/2005 (Pgs. 169 + 176)
13 – children
——————————————————————
[8] 5. 10/2004 (Pg. 428)
17
——————————————————————
[20] 14. 6/2010 (Pg. ii95)
17
——————————————————————
[12] 19. 3/2006 (Pgs. 40-41 + 46)
18
——————————————————————
[3] 1. 3/2004 (Pg. 50)
19 – children
——————————————————————
[3] 1. 3/2004 (Pg. 55)
19 – Japan
——————————————————————
[14] 8. 10/2006 (Pg. 466)
19
——————————————————————
[16] 10/2008 (Pg. 821)
20
——————————————————————
[17] 12/2008 (Pg. 1067)
20
——————————————————————
[21] 15. 11/2010 (Pg. iv72)
20
——————————————————————
[5] 2. 10/2004 (Pg. 384)
22
——————————————————————
[6] 3. 10/2004 (Pg. 386)
31 – Special Exception (SE)
——————————————————————
[19] 13. 12/2009 (Pg. 951)
40
——————————————————————
[19] 13. 12/2009 (Pg. 951)
52 – Special Exception SE)
——————————————————————
[3] 1. 3/2004 (Pg. 55)
56 – Japan
——————————————————————
[6] 3. 10/2004 (Pg. 386)
60
——————————————————————
[3] 1. 3/2004 (Pg. 52)
62
——————————————————————
[3] 1. 3/2004 (Pg. 53)
80
——————————————————————
[13] 2006
30 (Pg. 173)
335 – children (Pg. 174)
1652 – adults (Pg. 174)
� � � � � � � � � � � � � � � � �
[18] 12/2009 (Pg. 923)
1 – evaluable Special Exception (SE)
——————————————————————
[2] 16. 2003 (Pg. 91)
1st 10 – evaluable Study (ST)
——————————————————————
[3] 1. 3/2004 (Pg. 52)
10 – evaluable subgroup
——————————————————————
[3] 1. 3/2004 (Pg. 55)
10 – evaluable Japan
——————————————————————
[11] 7. 7/2005 (Pg. 300)
10 – evaluable children
——————————————————————
[2] 16. 2003 (Pg. 98)
11 – evaluable Special Exception (SE)
——————————————————————
[7] 4. 10/2004 (Pg. 427)
11 – evaluable children
4 – evaluable children Study (ST)
7 – evaluable children Special Exception (SE)
——————————————————————
[1] 1. 10/2003 (Pg. 358)
12 – evaluable children
——————————————————————
[9] 17. 2004 (Pg. 316)
1st 12 – evaluable children
——————————————————————
[15] 10. 6/2008 (Pg. 450)
1st 12 – evaluable children
——————————————————————
[10] 18. 6/2005 (Pgs. 169 + 176)
13 – evaluable children
——————————————————————
[21] 15. 11/2010 (Pg. iv72)
13 – evaluable
——————————————————————
[8] 5. 10/2004 (Pg. 428)
17 – evaluable
——————————————————————
[20] 14. 6/2010 (Pg. ii95)
17 – evaluable
——————————————————————
[3] 1. 3/2004 (Pg. 51)
18 – evaluable children
——————————————————————
[12] 19. 3/2006 (Pgs. 40-41 + 46)
18 – evaluable
——————————————————————
[3] 1. 3/2004 (Pg. 55)
19 – evaluable Japan
——————————————————————
[14] 8. 10/2006 (Pg. 466)
19 – evaluable
——————————————————————
[16] 10/2008 (Pg. 821)
20 – evaluable
——————————————————————
[17] 12/2008 (Pg. 1067)
20 – evaluable
——————————————————————
[5] 2. 10/2004 (Pg. 384)
22 – evaluable
——————————————————————
[6] 3. 10/2004 (Pg. 386)
31 – evaluable Special Exception (SE)
——————————————————————
[19] 13. 12/2009 (Pg. 951)
52 – evaluable Special Exception SE)
——————————————————————
[3] 1. 3/2004 (Pg. 55)
56 – evaluable Japan
——————————————————————
[6] 3. 10/2004 (Pg. 386)
60 – evaluable
——————————————————————
[3] 1. 3/2004 (Pg. 52)
62 – evaluable
——————————————————————
[3] 1. 3/2004 (Pg. 53)
80 – evaluable
——————————————————————
[13] 2006
30 – evaluable (Pg. 173)
335 – children (Pg. 174)
1652 – adults (Pg. 174)
� � � � � � � � � � � � � � � � �
[1] 1. 10/2003 (Pg. 358)
escalating doses of ANP intravenous injections (IV) and subsequently capsules (po)
——————————————————————
[2] 16. 2003 (Pg. 91)
Patients received escalating doses of antineoplaston A10 and AS2-1 by intravenous bolus injections
——————————————————————
[2] 16. 2003 (Pg. 93)
Antineoplaston therapy was administered in gradually escalating doses by intermittent bolus injections 6 times a day using a portable Provider 6000 dual-channel pump (Abbott Laboratories, North Chicago, IL, USA)
——————————————————————
[5] 2. 10/2004 (Pg. 384)
ANP was given in escalating doses by intravenous bolus injections
——————————————————————
[9] 17. 2004 (Pg. 317)
Gradually escalating doses were administered by intermittent bolus injections 6 times a day using a portable Provider 6000 dual channel pump (Abbott Laboratories, North Chicago, IL, USA)
——————————————————————
[12] 19. 3/2006 (Pg. 40)
Antineoplastons A10 (A10I) and AS2-1 injections, were given in escalating doses by intravenous injections
——————————————————————
[20] 14. 6/2010 (Pg. ii95)
Patients received escalating doses of intravenous A10 and AS2-1 6 times daily
12 or more weeks – ANP
or
at least 4 weeks – ANP but developed progressive disease (PD)
——————————————————————
[21] 15. 11/2010 (Pg. iv72)
Patients received escalating doses of intravenous ANP 6 times daily
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 93)
Dose escalation was necessary to prevent peritumoral oedema
——————————————————————
[9] 17. 2004 (Pg. 317)
Gradual dose escalation was necessary to prevent peritumoral oedema
——————————————————————
[12] 19. 3/2006 (Pg. 44)
ANP was given by intravenous injections in escalating doses to prevent peritumoral oedema
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 93)
Treatment consisted of daily intravenous injections of antineoplaston A10 (300 mg / mL) and AS2-1 (80 mg / mL) through a Broviac or equivalent catheter
——————————————————————
[4] 4. 9/2004 (Pgs. 257-260)
he was admitted for administration of intravenous antineoplastons A10 and AS2-1 through a subclavian venous catheter by intermittent bolus injections 6 times per day using a portable pump
——————————————————————
[7] 4. 10/2004 (Pg. 427)
intravenous injection of ANP
——————————————————————
[8] 5. 10/2004 (Pg. 428)
intravenous infusions of ANP
——————————————————————
[9] 17. 2004 (Pg. 317)
300 mg / ML – Daily intravenous injections of A10
——————————————————————
[9] 17. 2004 (Pg. 317)
80 mg / ML – Daily intravenous injections of AS2-1
——————————————————————
[9] 17. 2004 (Pg. 317)
administered through a subclavian venous catheter
——————————————————————
[9] 17. 2004 (Pg. 315)
ANP intravenously initially and subsequently orally
——————————————————————
[10] 18. 6/2005 (Pg. 169)
intravenous infusions of 2 formulations of ANP, A10 and AS2-1
——————————————————————
[10] 18. 6/2005 (Pg. 170)
IV ANP
——————————————————————
[11] 7. 7/2005 (Pg. 300)
ANP was given intravenously daily through a subclavian venous catheter and double channel infusion pump
——————————————————————
[12] 19. 3/2006 (Pg. 42)
Treatment involved daily intravenous injections of A10I and AS2-1
——————————————————————
[12] 19. 3/2006 (Pg. 42)
The injections were administered every 4 hours through a subclavian venous catheter via a dual-channel infusion pump
——————————————————————
[14] 8. 10/2006 (Pg. 466)

ANP was given intravenously daily through a subclavian venous catheter and a double-channel infusion pump
——————————————————————
[15] 10. 6/2008 (Pg. 450)
Treatment consisted of intravenous infusions of antineoplastons (ANP) A10 and AS2-1
——————————————————————
[16] 10/2008 (Pg. 821)
ANP was administered intravenously daily through a subclavian central venous catheter by a double-channel infusion pump
——————————————————————
[17] 12/2008 (Pg. 1067)
ANP was administered intravenously daily through a subclavian venous catheter via a double-channel infusion pump
——————————————————————
[18] 12/2009 (Pg. 923)
The patient received intravenous injections of ANP every 4 hours through a subclavian central venous catheter via a double channel infusion pump followed by PO ANP only
——————————————————————
[18] 12/2009 (Pg. 923)
6/8/2000 – PO ANP
——————————————————————
[18] 12/2009 (Pg. 923)
IV ANP
——————————————————————
[19] 13. 12/2009 (Pg. 951)
ANP was administered daily through a subclavian venous catheter via a double channel infusion pump
� � � � � � � � � � � � � � � � �
[9] 17. 2004 (Pg. 317)
Intravenous injections were discontinued after determination of CR, PR, or stable disease (SD)
——————————————————————
[9] 17. 2004 (Pg. 317)
After discontinuation of injections, the patients continued A10 and AS2-1 in 0.5g capsules
——————————————————————
[18] 12/2009 (Pg. 923)
7/8/2004 – discontinued
——————————————————————
[18] 12/2009 (Pg. 923)
2/1999 – CR
� � � � � � � � � � � � � � � � �
[5] 2. 10/2004 (Pg. 384)
4.3 months – median duration of administration
——————————————————————
[21] 15. 11/2010 (Pg. iv72)
4.4 months – median duration of treatment
——————————————————————
[14] 8. 10/2006 (Pg. 466)
4 1/2 months – median duration of i.v. ANP
——————————————————————
[12] 19. 3/2006 (Pg. 40)
5 months – median duration of antineoplaston administration
——————————————————————
[8] 5. 10/2004 (Pg. 428)
5.2 months – administered median
——————————————————————
[19] 13. 12/2009 (Pg. 951)
5.4 months – median duration of treatment (ST)
——————————————————————
[19] 13. 12/2009 (Pg. 951)
5.6 months – median duration of treatment (SE)
——————————————————————
[7] 4. 10/2004 (Pg. 427)

5.7 months – average duration of ANP
——————————————————————
[16] 10/2008 (Pg. 821)
5.7 months – median duration of treatment
——————————————————————
[2] 16. 2003 (Pgs. 91 + 96)
6 months – median duration of treatment
——————————————————————
[17] 12/2008 (Pg. 1067)
6.5 months – median duration of treatment
——————————————————————
[1] 1. 10/2003 (Pg. 358)

9.5 months – median duration of IV ANP
——————————————————————
[11] 7. 7/2005 (Pg. 300)
9 1/2 months – median duration of administration
——————————————————————
[9] 17. 2004 (Pgs. 315 + 320)
16 months (1 year 4 months) average duration of intravenous ANP
——————————————————————
[15] 10. 6/2008 (Pg. 450)
16.5 months – median
——————————————————————
[9] 17. 2004 (Pg. 320)
19 months – average duration of oral ANP
——————————————————————
[10] 18. 6/2005 (Pgs. 168 + 170)
20 months (1 year 8 months) administered average duration
� � � � � � � � � � � � � � � � �
[1] 1. 10/2003 (Pg. 358)
28.6 months – median duration of po ANP
After obtaining at least minor response (SD), the treatment continued with po ANP
——————————————————————
[4] 4. 9/2004 (Pg. 257)
655 consecutive days – administration of antineoplastons A10 and AS2-1 with the exception of a few short interruptions
� � � � � � � � � � � � � � � � �
[16] 10/2008 (Pg. 821)
5.69 g/kg/day – median average dosage of A10
——————————————————————
[17] 12/2008 (Pg. 1067)
5.8 g/kg/day – median average dosages of A10
——————————————————————
[21] 15. 11/2010 (Pg. iv72)
6.0 g/kg/day – median average dosages of A10
——————————————————————
[5] 2. 10/2004 (Pg. 384)
6.37 g/kg/day – average dosage of Antineoplaston A10
——————————————————————
[1] 1. 10/2003 (Pg. 358)
7.95 g/kg/day – average dosage of A10
——————————————————————
[9] 17. 2004 (Pgs. 315 + 320)
7.95 g/kg/day – average dosage of A10
——————————————————————
[15] 10. 6/2008 (Pg. 450)
8.36 g/kg/day – average dosage of A10
——————————————————————
[19] 13. 12/2009 (Pg. 951)
9.0 g/kg/day – median of average dosages of A10 (ST)
——————————————————————
[14] 8. 10/2006 (Pg. 466)
9.2 g/kg/day – average dosage of A10
——————————————————————
[12] 19. 3/2006 (Pg. 40)
9.22 g/kg/day – average dosage of A10I
——————————————————————
[8] 5. 10/2004 (Pg. 428)
9.4 g/kg/d – median of average dosages of A10
——————————————————————
[19] 13. 12/2009 (Pg. 951)
9.4 g/kg/day – median of average dosages of A10 (SE)
——————————————————————
[10] 18. 6/2005 (Pgs. 168 + 170)
10.30 g/kg/day – average dosage of A10
——————————————————————
[7] 4. 10/2004 (Pg. 427)
10.6 g/kg/d – median of average dosages of A10
——————————————————————
[2] 16. 2003 (Pg. 91)
11.3 g/kg/day – average dosage of A10
——————————————————————
[11] 7. 7/2005 (Pg. 300)
12.16 g/kg/day – average dosage of A10
======================================
[2] 16. 2003 (Pg. 96)
5.3-16.1 g/kg/day – dosage of A10
� � � � � � � � � � � � � � � � �
[1] 1. 10/2003 (Pg. 358)
0.28 g/kg/d – average dosage of A10 and AS2-1
After obtaining at least minor response (SD), the treatment continued with po ANP
——————————————————————
[9] 17. 2004 (Pg. 320)
0.28 g/kg/day – average dosage of A10 and AS2-1
� � � � � � � � � � � � � � � � �
[4] 4. 9/2004 (Pg. 257)
8.15 g/kg/d – maximum dosage of A10
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 96)
11.3 g/kg/day – average maximum dosage of A10
——————————————————————
[12] 19. 3/2006 (Pg. 42)
13.37 g/kg/day – maximum dosage of A10I (SD = 7.36 g/kg/day)
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 93)
20 g/kg/day – highest tolerated or effective dosage of A10 not exceeding
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 96)
331.4 kg – maximum total dose of A10
� � � � � � � � � � � � � � � � �
[5] 2. 10/2004 (Pg. 384)
0.24 g/kg/day – average dosage of Antineoplaston AS2-1
——————————————————————
[17] 12/2008 (Pg. 1067)
0.24 g/kg/day – median average dosages of AS2-1
——————————————————————
[16] 10/2008 (Pg. 821)
0.28 g/kg/day – median average dosage of AS2-1
——————————————————————
[19] 13. 12/2009 (Pg. 951)
0.3 g/kg/day – median of average dosages of AS2-1 (ST and SE)
——————————————————————
[21] 15. 11/2010 (Pg. iv72)
0.3 g/kg/day – median average dosages of AS2-1
——————————————————————
[12] 19. 3/2006 (Pg. 40)
0.31 g/kg/day – average dosage of AS2-1
——————————————————————
[14] 8. 10/2006 (Pg. 466)
0.32 g/kg/day – average dosage of AS2-1
——————————————————————
[9] 17. 2004 (Pgs. 315 + 320)
0.33 g/kg/day – average dosage of AS2-1
——————————————————————
[1] 1. 10/2003 (Pg. 358)
0.34 g/kg/d – average dosage of AS2-1
——————————————————————
[15] 10. 6/2008 (Pg. 450)
0.37 g/kg/day – average dosage of AS2-1
——————————————————————
[10] 18. 6/2005 (Pgs. 168 + 170)
0.38 g/kg/day – average dosage of AS2-1
——————————————————————
[2] 16. 2003 (Pg. 91)
0.4 g/kg/day – average dosage of AS2-1
——————————————————————
[7] 4. 10/2004 (Pg. 427)
0.4 g/kg/d – median of average dosages of AS2-1
——————————————————————
[8] 5. 10/2004 (Pg. 428)
0.4 g/kg/d – median of average dosages of AS2-1
——————————————————————
[11] 7. 7/2005 (Pg. 300)
0.41 g/kg/day – average dosage of AS2-1
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 96)
0.2-0.6 g/kg/day – dosage of AS2-1
� � � � � � � � � � � � � � � � �
[4] 4. 9/2004 (Pg. 257)
0.35 g/kg/d – maximum dosage of
AS2-1
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 96)
0.4 g/kg/day – average maximum dosage of AS2-1
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 93)
0.4 g/kg/day – highest tolerated or effective dosage of AS2-1 not exceeding
� � � � � � � � � � � � � � � � �
[12] 19. 3/2006 (Pg. 42)
0.49 g/kg/day – maximum dosage of AS2-1 (SD = 0.26 g/kg/day)
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 96)
23.9 kg – maximum total dose of AS2-1
� � � � � � � � � � � � � � � � �
[1] 1. 10/2003 (Pg. 358)
1 / 9% – nonevaluable due to only 4 weeks of treatment and lack of follow-up scans
This patient died while on treatment due to a brain infarct and was counted as a treatment failure
——————————————————————
[7] 4. 10/2004 (Pg. 427)
1 – nonevaluable
——————————————————————
[9] 17. 2004
1 – nonevaluable due to only receiving 4 weeks of ANP and no follow-up scans
This patient died while receiving ANP due to a nonhemorrhaging brain infarction and was considered a treatment failure (Pg. 320)
(only 4 weeks after initiation of ANP Pg. 321)
(There was no evidence that these were treatment related deaths Pg. 321)
——————————————————————
[2] 16. 2003 (Pg. 96)
Patient 2 unable to be evaluated because didn’t have follow-up MRI to determine response
——————————————————————
[2] 16. 2003 (Pg. 96)
Patient 11 unable to be evaluated because died of intratumoral hemorrhage and her duration of treatment was too short to short for evaluation of response
——————————————————————
[8] 5. 10/2004 (Pg. 428)
2 – nonevaluable due to lack of follow-up scans
——————————————————————
[7] 4. 10/2004 (Pg. 427)
3 Special Exception (SE) – nonevaluable
——————————————————————
[21] 15. 11/2010 (Pg. iv72)
7 – couldn’t be evaluated due to an inadequate duration of treatment and lack of follow-up magnetic resonance imaging (MRI) scans
——————————————————————
[19] 13. 12/2009 (Pg. 951)
12 – not evaluable due to too short a duration of treatment and lack of follow-up MRIs
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 97)
4 – died from the tumour
4 – died from aspiration pneumonia
2 – intratumoral bleeding
——————————————————————
[7] 4. 10/2004 (Pg. 427)
One CR patient developed recurrence after premature discontinuation of ANP and obtained a 2nd CR after ANP was restarted
This patient who initially had multiple metastases to the brain and spinal cord died due to aspiration pneumonia and was confirmed by autopsy as disease free
——————————————————————
[9] 17. 2004
1 patient who had stable disease discontinued ANP against medical advice and died 4.5 years later (Pgs. 315 + 320)
(There was no evidence that these were treatment related deaths Pg. 321)
——————————————————————
[10] 18. 6/2005
1 patient passed away after 6 years, 10 months from the start of the treatment (3 years after discontinuation of ANP)
The cause of death was recurrent pneumonia, possibly due (Pg. 170)
to chronic immunosuppression from chemotherapy administered prior to ANP (patient 1) (Pg. 172)
——————————————————————
[12] 19. 3/2006 (Pg. 45)
The deaths of 12 patients were most likely tumor related
——————————————————————
[12] 19. 3/2006 (Pg. 45)
There was a single death due to a pulmonary embolism
——————————————————————
[12] 19. 3/2006 (Pg. 45)
2 cases of death possibly resulting from aspiration pneumonia
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 97)
The 2 surviving patients weren’t previously treated with chemotherapy and radiation therapy and didn’t develop pneumonia or intratumoral bleeding
——————————————————————
[10] 18. 6/2005 (Pg. 169)
6 hadn’t received prior chemotherapy or radiation
——————————————————————
[10] 18. 6/2005 (Pg. 175)
6 long-term
——————————————————————
[12] 19. 3/2006 (Pgs. 40-41)
6 – didn’t have radiation therapy or chemotherapy
——————————————————————
[16] 10/2008 (Pg. 821)
No patients received radiation or chemotherapy before starting ANP, but 6 patients underwent surgery and 14 had biopsy only
——————————————————————
[18] 12/2009 (Pg. 923)
The tumor was inoperable
� � � � � � � � � � � � � � � � �
[2] 16. 2003
Patient 3 (Pg. 95)
Patient 8 (Pg. 95)
Case 10 (Pgs. 96-97)
——————————————————————
[3] 1. 3/2004
Case Study, Patient 1 (Pgs. 50-51)
Case Study, Patient 2 (Pgs. 51-52)
Case Study, Patient 3 (Pgs. 53-54)
Case Study, Patient 4 (Pg. 54)
Case Study, Patient 5 (Pg. 55)
——————————————————————
[9] 17. 2004
Case 8 (Pgs. 321-322)
Case 10 (Pgs. 321 + 323)
——————————————————————
[10] 18. 6/2005 (Pgs. 172-173)
Patient 4
——————————————————————
[10] 18. 6/2005 (Pgs. 173-174)
Patient 11
——————————————————————
[12] 19. 3/2006 (Pgs. 45-46)
Case Report Patient 12
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 94)
Trial design – Fleming
——————————————————————
[9] 17. 2004 (Pg. 317)
Trial design – Fleming
� � � � � � � � � � � � � � � � �
======================================
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:
https://twitter.com/gorskon/status/318056135645073408
——————————————————————
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”)

Maybe #ScienceBasedMedicine needs to change this
——————————————————————
“Our only goal is to promote high standards of science in medicine”
======================================
� � � � � � � � � � � � � � � � �
References:
� � � � � � � � � � � � � � � � �
http://www.burzynskiclinic.com/scientific-publications.html
� � � � � � � � � � � � � � � � �
[1] 1. 10/2003 (Pg. 358)
——————————————————————
Interim Reports on Clinial Trials:
NEURO-ONCOLOGY
Phase II study of Antineoplastons A10 and AS2-1 (ANP) in children with recurrent and progressive multicentric glioma
A preliminary report
http://www.burzynskiclinic.com/images/stories/Publications/970.pdf
Neuro-Oncology. 2003; 5: 358
Volume 5 Issue 4 October 2003
======================================
[2] 16. 2003 (Pgs. 91-101)
——————————————————————
Interim Reports on Clinial Trials
BT-11 – BRAIN STEM GLIOMA
Special exception (SE) to BT-11
DRUGS IN R&D
Phase II study of antineoplaston A10 and AS2-1 in patients with recurrent diffuse intrinsic brain stem glioma:
a preliminary report
recurrent diffuse intrinsic brain stem glioma
Drugs in R and D
(Drugs in Research and Development)
http://www.ncbi.nlm.nih.gov/pubmed/12718563
Drugs In R and D / Drugs in Research and Development:
http://www.ncbi.nlm.nih.gov/m/pubmed/12718563
Drugs R D. 2003;4(2):91-101
http://www.burzynskiclinic.com/images/stories/Publications/960.pdf
Drugs in R&D 2003;4:91-101
======================================
[3] 1. 3/2004 (Pgs. 47-58)
——————————————————————
Review Articles on Clinical Trials:
INTEGRATIVE CANCER THERAPIES
The Present State of Antineoplaston Research
http://www.burzynskiclinic.com/images/stories/Publications/994.pdf
Integrative Cancer Therapies 2004;3:47-58
Volume 3, No. 1, March 2004
DOI: 10.1177/1534735-403261964
======================================
[4] 4. 9/2004 (Pgs. 257-261)
——————————————————————
Case Reports:
INTEGRATIVE CANCER THERAPIES
Special exception (SE) to BT-11 BRAIN STEM GLIOMA
Long-term survival and complete response of a patient with recurrent diffuse intrinsic brain stem glioblastoma multiforme
http://www.burzynskiclinic.com/images/stories/Publications/1145.pdf
Integrative Cancer Therapies 2004;3:257-261
Volume 3, Number 3 September 2004
======================================
[5] 2. 10/2004 (Pg. 384)
——————————————————————
Interim Reports on Clinial Trials:
NEURO-ONCOLOGY
BT-20 Patients With GLIOBLASTOMA MULTIFORME (GBM)
Phase II study of Antineoplastons A10 and AS2-1 (ANP) in recurrent glioblastoma multiforme
http://www.burzynskiclinic.com/images/stories/Publications/1218.pdf
Neuro-Oncology. 2004; 6: 384
Volume 6 Issue 4 October 2004
Abstracts from the Society for Neuro-Oncology Ninth Annual Meeting, Toronto, Ontario, Canada, November 18-21, 2004
======================================
[6] 3. 10/2004 (Pg. 386)
——————————————————————
Interim Reports on Clinial Trials:
(DBSG) (Study (ST) and Special Exception (SE))
NEURO-ONCOLOGY
Long-term survivals in phase II studies of Antineoplastons A10 and AS2-1 (ANP) in patients with diffuse intrinsic brain stem glioma
http://www.burzynskiclinic.com/images/stories/Publications/1219.pdf
Neuro-Oncology. 2004; 6: 386
Volume 6 Issue 4 October 2004
======================================
[7] 4. 10/2004 (Pg. 427)
——————————————————————
Interim Reports on Clinial Trials:
(AT/RT of CNS) (Study (ST) and Special Exception (SE))
NEURO-ONCOLOGY
BT-14 CHILDREN WITH RHABDOID TUMOR OF THE CENTRAL NERVOUS SYSTEM
Phase II studies of antineoplastons A10 and AS2-1 (ANP) in children with atypical teratoid/rhabdoid tumors (AT/RT) of the central nervous system
A preliminary report
http://www.burzynskiclinic.com/images/stories/Publications/1146.pdf
Neuro-Oncology. 2004; 6: 427
Volume 6 Issue 4 October 2004
Abstracts from the Eleventh International Symposium on Pediatric Neuro-Oncology, Boston, Massachusetts, June 13-16, 2004
======================================
[8] 5. 10/2004 (Pg. 428)
——————————————————————
Interim Reports on Clinial Trials:
NEURO-ONCOLOGY
BT-12 CHILDREN WITH PRIMITIVE NEUROECTODERMAL TUMORS (PNET)
Treatment of primitive neuroectodermal tumors (PNET) with antineoplastons A10 and AS2-1 (ANP)
Preliminary results of phase II studies
http://www.burzynskiclinic.com/images/stories/Publications/1147.pdf
Neuro-Oncology. 2004; 6: 428
Volume 6 Issue 4 October 2004
Abstracts from the Eleventh International Symposium on Pediatric Neuro-Oncology
======================================
[9] 17. 2004 (Pgs. 315-326)
——————————————————————
Interim Reports on Clinial Trials:
DRUGS IN R&D
Drugs in R and D
(Drugs in Research and Development)
Pg. 317
BT-13 – children with low-grade astrocytoma
BT-23 – children with visual pathway gliomas
Phase II study of antineoplaston A10 and AS2-1 in children with recurrent and progressive multicentric glioma
A Preliminary Report
http://www.ncbi.nlm.nih.gov/pubmed/15563234
Drugs R&D 2004;5(6):315-326
http://www.ncbi.nlm.nih.gov/m/pubmed/15563234
Drugs R D. 2004;5(6):315-26
http://www.burzynskiclinic.com/images/stories/Publications/1194.pdf
======================================
[10] 18. 6/2005 (Pgs. 168-177)
——————————————————————
Interim Reports on Clinial Trials:
INTEGRATIVE CANCER THERAPIES
BT-12 children with PRIMITIVE NEUROECTODERMAL TUMORS (PNET)
CAN-01 (CAN-1) PATIENTS WITH REFRACTORY MALIGNANCIES
Long-term survival of high-risk pediatric patients with primitive neuroectodermal tumors treated with Antineoplastons A10 and AS2-1
http://www.ncbi.nlm.nih.gov/pubmed/15911929
Integrative Cancer Therapies 2005;4(2):168-177
http://www.ncbi.nlm.nih.gov/m/pubmed/15911929
Integr Cancer Ther. 2005 Jun;4(2):168-77
http://www.burzynskiclinic.com/images/stories/Publications/1220.pdf
DOI: 10.1177/1534735405276835
http://m.ict.sagepub.com/content/4/2/168.long?view=long&pmid=15911929
Volume 4 Number 2 June 2005
======================================
[11] 7. 7/2005 (Pg. 300)
——————————————————————
Interim Reports on Clinial Trials:
BT-11 BRAIN STEM GLIOMA
Targeted therapy with ANP in children less than 4 years old with inoperable brain stem gliomas. Neuro-Oncology. 2005; 7:300
http://www.burzynskiclinic.com/images/stories/Publications/1224.pdf
Volume 7 Issue 3 July 2005
Abstracts from the World Federation of Neuro-Oncology Meeting
======================================
[12] 19. 3/2006 (Pgs. 40-47)
——————————————————————
Interim Reports on Clinial Trials:
BT-03

BT-11 BRAIN STEM GLIOMA (BSG)
BT-18
6. MIXED GLIOMA
ADULT PATIENTS WITH MIXED GLIOMA
“mixed glioma”, a type of primary malignant brain tumor (PMBT)
BT-22
8. CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
CAN-01 (CAN-1)
PATIENTS WITH REFRACTORY MALIGNANCIES
Burzynski, S.R., Janicki, T.J., Weaver, R.A., Burzynski, B. Targeted therapy with Antineoplastons A10 and AS2-1 of high grade, recurrent, and progressive brainstem glioma. Integrative Cancer Therapies 2006;5(1):40-47
http://www.ncbi.nlm.nih.gov/pubmed/16484713
Integr Cancer Ther. 2006 Mar;5(1):40-7
http://www.ncbi.nlm.nih.gov/m/pubmed/16484713
DOI: 10.1177/1534735405285380
http://www.burzynskiclinic.com/images/stories/Publications/5825.pdf
�
http://m.ict.sagepub.com/content/5/1/40.long?view=long&pmid=16484713
======================================
[13] 2006 (Pgs. 167-168)
——————————————————————
http://www.burzynskiclinic.com/images/stories/Publications/1252.pdf
======================================
[14] 8. 10/2006 (Pg. 466)
——————————————————————
Interim Reports on Clinial Trials:
BT-11 BRAIN STEM GLIOMA
Treatment of multicentric brainstem gliomas with antineoplastons (ANP) A10 and AS2-1. Neuro-Oncology. 2006; 8:466
http://www.burzynskiclinic.com/images/stories/Publications/2105.pdf
Volume 8 Issue 4 October 2006
Abstracts for the Eleventh Annual Meeting of the Society for Neuro-Oncology (SNO)
======================================
[15] 10. 6/2008 (Pg. 450)
——————————————————————
NEURO-ONCOLOGY
Interim Reports on Clinical Trials:
(OPG)
BT-23 – CHILDREN WITH VISUAL PATHWAY GLIOMA
Phase II study of antineoplastons A10 and AS2-1 (ANP) in children with optic pathway glioma:
A preliminary report
http://www.burzynskiclinic.com/images/stories/Publications/7287.pdf
Neuro-Oncology 2008; 10:450
Volume 10 Issue 3 June 2008
======================================
[16] 10/2008 (Pg. 821)
——————————————————————
NEURO-ONCOLOGY
Phase II study of antineoplastons A10 and AS2-1 (ANP) in patients with newly diagnosed anaplastic astrocytoma:
A preliminary report
http://www.burzynskiclinic.com/images/stories/Publications/7853.pdf
Neuro-Oncology 2008; 10:821
Volume 10 Issue 5 October 2008
======================================
[17] 12/2008 (Pg. 1067)
——————————————————————
NEURO-ONCOLOGY
Phase II study of antineoplastons A10 and AS2-1 infusions (ANP) in patients with recurrent anaplastic astrocytoma
http://www.burzynskiclinic.com/images/stories/Publications/7898.pdf
Neuro-Oncology 2008; 10:1067
Volume 10 Issue 6 December 2008
======================================
[18] 12/2009 (Pg. 923)
——————————————————————
Case Reports:
NEURO-ONCOLOGY
Over a 10-year survival and complete response of a patient with diffuse intrinsic brainstem glioma (DBSG) treated with antineoplastons (ANP)
http://www.burzynskiclinic.com/images/stories/Publications/8638.pdf
Neuro-Oncology 2009; 11:923
Volume 11 Issue 6 December 2009
======================================
[19] 13. 12/2009 (Pg. 951)
——————————————————————
Interim Reports on Clinial Trials:
BT-11 BRAIN STEM GLIOMA
(Study (ST) and Special Exception (SE))
Phase II study of antineoplastons A10 and AS2-1 in patients with brainstem glioma
Protocol BC-BT-11
http://www.burzynskiclinic.com/images/stories/Publications/8639.pdf
Neuro-Oncology 2009, 11:951.
Volume 11 Issue 6 December 2009
Abstracts from the Third Quadrennial Meeting of the World Federation of Neuro-Oncology (WFNO) and the Sixth Meeting of the Asian Society for Neuro-Oncology (ASNO), May 11-14, 2009, Yokohama, Japan
======================================
[20] 14. 6/2010 (Pg. ii95)
——————————————————————
Interim Reports on Clinical Trials:
BT-13 – CHILDREN WITH LOW GRADE ASTROCYTOMA
A Phase II Study of Antineoplaston A-10 and AS-1 Injections in children with low-grade astrocytomas
http://www.burzynskiclinic.com/images/stories/Publications/8397.pdf
Neuro-Oncology 2010; 12, ii95.
Volume 12 Issue 6 June 2010
Antineoplaston A10 (Atengenal)
Antineoplaston AS2-1 (Astugenal)
======================================
[21] 15. 11/2010 (Pg. iv72)
——————————————————————
Interim Reports on Clinical Trials:
BT-18 – ADULT PATIENTS WITH MIXED GLIOMA
Preliminary Results of a Phase II Study of Antineoplastons A10 and AS2-1 (ANP) in Adult Patients with Recurrent Mixed Gliomas
http://www.burzynskiclinic.com/images/stories/Publications/8637.pdf
Neuro-Oncology 2010; 12:iv72.
Volume 12 Supplement 4 November 2010
======================================

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

Posted on by
Reply

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:
https://twitter.com/gorskon/status/318056135645073408
——————————————————————
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
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[25] 12/1996 PHENYLACETATE (PA) and related aromatic fatty acids constitute novel class of relatively nontoxic antineoplastic agents
————————————————————
Using human breast carcinoma MCF-7 cells as model, we show PA-induced growth arrest associated with enhanced expression of cyclin-dependent kinase inhibitor p21Waf1/Cip1 …
————————————————————
induction of p21WAF1/CIP1 mRNA by PA independent of cellular p53 status
————————————————————
PA effectively induced p21WAF1/CIP1 mRNA and growth inhibition of wild-type mouse embryonal fibroblasts
————————————————————
findings strongly support role for p21Waf1/Cip1 in PA-mediated inhibition of cell growth
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[26] 1996 Cytotoxic chemotherapies often give rise to multidrug resistance, which remains major problem in CANCER management
————————————————————
In pursuit of alternative treatments for chemoresistant TUMOR CELLS, we tested response of multidrug-resistant (MDR) TUMOR CELL lines to aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB), 2 differentiation inducers currently in clinical trials
————————————————————
Both compounds induced cytostasis and maturation of multidrug-resistant BREAST, OVARIAN, and COLON CARCINOMA CELLS with no significant effect on cell viability
————————————————————
MDR cells generally more sensitive to GROWTH ARREST by PA and PB than parental counterparts
————————————————————
PA and PB potentiated the cytotoxic activity of doxorubicin against MDR cells
————————————————————
Taken together, our in vitro data indicate PA and PB, differentiation inducers of aromatic fatty acid class, may provide alternative approach to treatment of MDR TUMORS
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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
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[29] 1997 PHENYLACETATE and analogs represent new class of pleiotropic growth regulators that alter TUMOR CELL biology by affecting GENE EXPRESSION at both transcriptional and post transcriptional levels
————————————————————
Based on findings, NaPA and NaPB entered clinical trials at NATIONAL CANCER INSTITUTE
————————————————————
Ongoing phase I studies with NaPA, involving adults with PROSTATE and BRAIN CANCER, confirmed therapeutic levels can be achieved with no significant toxicities, and provide preliminary evidence for benefit to patients with advanced disease (Thibault et al., submitted)
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[30] 5 – 6/1998 Antineoplastons A10 and AS2-1 EXHIBIT GROWTH INHIBITION OF CANCER CELLS by diverse modes of action
——————————————————————
Observed ANTITUMOR RESPONSES within 2-3 weeks of combination treatment of chemoradiation therapy and antineoplastons A10 and AS2-1 in phase I clinical study conducted in Kurume University Hospital
——————————————————————
Reviewed 3 clinical cases of advanced cancer (multiple metastatic lung cancer, thalamic glioma and primary lung cancer) in which we believed antineoplaston A10 and AS2-1 may be contributing to RAPID ANTITUMOR RESPONSE
——————————————————————
Possible use of this combination for induction therapy in advanced cancer
� � � � � � � � � � � � � � � �
[31] 11-12/1998 Antineoplaston A10 injection (antineoplaston A10 I) exhibited CYSTOSTATIC GROWTH INHIBITION OF HUMAN HEPATOCELLULAR CARCINOMA (HCC) CELLS in vitro and showed minimum adverse effects in phase I clinical trial
——————————————————————
2 cases of advanced HCC treated with antineoplaston A10 I
——————————————————————
Both cases showed interesting responses to antineoplaston A10 I
——————————————————————
One showed massive coagulation necrosis of tumors after intra-arterial infusion of antineoplaston A10 I and other showed RESOLUTION of portal vein TUMOR thrombosis with systemic infusion of antineoplaston A10 I
——————————————————————
Usefulness of anti-neoplaston A10 I in terminal staged HCC is discussed
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[32] 3/1999 determine response rate, time to treatment failure, and toxicity of phenylacetate in patients with recurrent malignant glioma …
————————————————————
Adult patients
————————————————————
43 – enrolled 12/1994-12/ 1996
40 – assessable
————————————————————
Reversible symptoms
————————————————————
fatigue
somnolence
were primary toxicities
————————————————————
only mild hematologic toxicity
————————————————————
30 / 75% – failed treatment within 2 months
————————————————————
7 / 17.5% – stable disease
————————————————————
3 – 7.5% – response defined as more than 50% reduction in tumor
————————————————————
Median time to treatment failure
————————————————————
2 months
————————————————————
35 – died
————————————————————
median survival
————————————————————
8 months
————————————————————
PHENYLACETATE HAS LITTLE ACTIVITY at this dose schedule in PATIENTS with RECURRENT MALIGNANT GLIOMA
————————————————————
Further studies with drug would necessitate evaluation of different dose schedule
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[33] 7/3/2000 Antineoplastons first described by Burzynski are naturally occurring peptides and amino acid derivatives, which CONTROL NEOPLASTIC GROWTH
——————————————————————
data suggest strong inverse association of urinary antineoplaston A-10 level with breast cancer
————————————————————
finding was stimulus for further investigations of antineoplaston A-10 levels in some benign as well as other malignant diseases to determine utility of approach as predictive test for women at risk of developing breast cancer
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[34] 8/31/2000 Antineoplastons are naturally occurring CYTODIFFERENTIATING AGENTS
—————————————————————
Findings confirm presence of immune defects among patients with breast cancer and results should stimulate development of new strategies to induce and augment immunity for treatment of breast cancer
—————————————————————
Antineoplaston A-10 may provide rational basis for designing trials to employ its immune modulatory potentials as adjuvant therapy in breast cancer patients
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[35] 12/2000 4 new piperidinedione A10 analogs synthesized and tested for antimitotic activity on human breast cancer cell line against prototype A10 and antibreast cancer drug tamoxifen
—————————————————————
“3B” and “3D” were several-fold more potent ANTIPROLIFERATIVE AGENTS than A10 and tamoxifen and had significantly higher capacity to bind DNA than A10
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[36] 8/2001 No partial remission or complete remission was seen, but 7 patients had stable disease for more than 6 months while on drug
————————————————————
PB may have role as cytostatic agent and should be additionally explored in combination with cytotoxics and other novel drugs
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[37] 2002 p53 tumor suppressor gene plays important role in protecting cells from developing undesirable proliferation
——————————————————————
Mutant p53 gene or malfunctioning p53 protein found in more than 50% of cancer cells impedes DNA repair or apoptosis induction
——————————————————————
May be why some cancers gain resistance to chemotherapy and radiation and become more resistant after frequent cancer treatments
——————————————————————
non-toxic p53 gene activator would induce cancer cell apoptosis and help damaged cancer cells to recover
——————————————————————
combination use of chemotherapeutics or radiation with non-toxic p53 gene activator will be crucial in cancer therapy, damaging DNA with chemotherapeutics or radiation on one hand and promoting apoptosis induction with p53 gene activator on the other
——————————————————————
Strategy would be most efficient for remission induction and maintenance CANCER therapy
——————————————————————
Antineoplastons are naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH
——————————————————————
Antineoplaston A10 and AS2-1 are chemically identified and synthesized antineoplastons PROVEN TO INHIBIT CANCER CELL GROWTH by arresting cell cycle in G1 phase and INHIBITING TUMOR GROWTH by reducing mitosis
——————————————————————
Agents thought to be good candidates for clinically easily applicable non-toxic p53 gene activators
——————————————————————
CASES OF ADVANCED CANCER RESPONDED WELL to combination treatment using chemotherapeutics and irradiation with antineoplaston A10 and AS2-1 in clinical trials being conducted in Kurume University Hospital
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[38] 3 – 4/2003 Phase II clinical trail to clarify whether antineoplaston AS2-1, mixture of sodium salts of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid at ratio of 1:4, prolongs recurrence-free interval of HCC patients who undergo frequent treatments for recurrence
——————————————————————
10 patients enrolled in trial
2 in stage I
6 in stage II
1 in stage III
1 in stage IV-B
at initial diagnosis
——————————————————————
10 / 100% – experienced 35 recurrence-free intervals
——————————————————————
Recurrence-free intervals during antineoplaston AS2-1 administration SIGNIFICANTLY LONGER than without
——————————————————————
Patients who experienced recurrence-free intervals with and without antineoplaston AS2-1 SHOWED LONGER INTERVALS during antineoplaston AS2-1 administration
——————————————————————
2 patients in stage I showed LONGER RECURRENCE-FREE INTERVALS than those in more advanced stages
——————————————————————
Antineoplastons AS2-1 couldn’t prevent recurrence of HCC but PROLONGED RECURRENCE-FREE INTERVAL between regional treatments and IMPROVED SURVIVAL RATE OF PATIENTS
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[39] 2003 Case of survival for nearly 8 years after treatment of unresectable multiple liver metastases from colon cancer, using microwave ablation and NONTOXIC ANTITUMOR AGENT, antineoplastons
——————————————————————
72-year-old man diagnosed with adenocarcinoma of ascending colon and 14 bilateral liver metastases underwent right hemicolectomy combined with microwave ablation of 6 metastatic liver tumors
——————————————————————
Antineoplaston A10 given intravenously, followed by oral antineoplaston AS2-1
——————————————————————
Computed tomography scans done 1 and 4 years after initial diagnosis showed recurrent tumors
——————————————————————
Patient underwent 2nd and 3rd microwave ablation of recurrent tumors, and has survived for nearly 8 years WITHOUT SUFFERING ANY SERIOUS ADVERSE EFFECTS
——————————————————————
Currently FREE FROM CANCER
——————————————————————
Demonstrates potential effectiveness of NONTOXIC ANTITUMOR AGENT, antineoplastons, for controlling liver metastases from colon cancer
� � � � � � � � � � � � � � � �
======================================
Burzynski has made it clear that PHENYLACETATE, by itself, does NOT achieve the results of antineoplastons (PHENYLACETATE, PHENYLGLUTAMINATE, PHENYLACETYLISOGLUTIMINATE, PHENYLBUTYRATE)
======================================
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[40] 2003
——————————————————————
Pg. 92
——————————————————————
Antineoplaston A10 and AS2-1 are synthetic derivatives of phenylacetate (PN) acid, glutamine and isoglutamine
——————————————————————
A10 is sterile solution of sodium phenylacetylisoglutiminate (isoPG) in 4 : 1 ratio
——————————————————————
Antineoplaston AS2-1 is sterile solution of sodium phenylacetate (PN) and phenylacetylglutaminate (PG) in 4 : 1 ratio
——————————————————————
Pg. 93
======================================
combination of antineoplaston A10 and AS2-1 used instead of single drugs
——————————————————————
Based on previous observations, combination treatment has provided better results than single drugs
——————————————————————
Pg. 97
——————————————————————
active ingredient of antineoplaston AS2-1 is PHENYLACETATE,
——————————————————————
Pg. 98
——————————————————————
known to modulate expression of ras oncogenes and tumor suppressor gene p53
——————————————————————
ras oncogene protein p21ras
——————————————————————
farneslyation of p21ras, which is inhibited by antineoplaston AS2-1
——————————————————————
Antineoplaston AS2-1 also activates p53 gene
——————————————————————
protein p53 activates p21 gene, which directs synthesis of p21WAF1/Cip1 protein
——————————————————————
Induction of p21WAF1/Cip1 suppresses human glioma cell proliferation
——————————————————————
proposed mechanism of action of 2 ingredients of antineoplaston A10, sodium phenylacetylglutamine (PG) and sodium phenylacetylisoglutimine (IsoPG), is inhibition of glutamine incorporation into proteins of neoplastic cells
——————————————————————
Antineoplaston A10 has demonstrated 5 effects related to therapeutic indication in patients with brain tumors: cytostatic, antimitogenic, antiproliferative and inhibitory effects, and differentiation of tumors
——————————————————————
[22-25]
——————————————————————
Initial clinical studies with antineoplaston therapy included testing of separate ingredients phenylacetate (PN) (antineoplaston AS5) and phenylacetylglutaminate (PG) (antineoplaston AS2-5)
——————————————————————
[26-28]
——————————————————————
studies failed to show marked anticancer activity of phenylacetate (PN) in malignant glioma, confirmed by phase II study by North
——————————————————————
Pg. 99
——————————————————————
American Brain Tumor Consortium
——————————————————————
[29]
——————————————————————
Based on results, further studies of phenylacetate (PN) as single agent in patients with malignant glioma were not recommended
——————————————————————
subsequent study by Buckner et al.
——————————————————————
[30]
——————————————————————
confirmed conclusion because patients receiving antineoplaston AS2-1 didn’t respond to treatment
——————————————————————
main difference between Buckner’s study is dosage of antineoplaston A10, which was approximately 50 times lower in Buckner’s study
——————————————————————
[31]
——————————————————————
2 patients who participated in our study (cases 3 and 8) developed recurrence on lower dosages of antineoplaston A10, but responded again with Complete Response (CR) when dosage of antineoplaston A10 was increased
——————————————————————
In these 2 patients, antineoplaston AS2-1 didn’t seem to have effect on 2nd response, which suggests antineoplaston A10 rather than antineoplaston AS2-1 is main active drug
� � � � � � � � � � � � � � � �
[41] 8/2005 Antineoplastons such as A10 include naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH OF CELLS
——————————————————————
Findings indicate antineoplaston A10 ANTITUMOR EFFECT could be utilized as effective therapy for breast cancer patients
� � � � � � � � � � � � � � � �
[42] 2006 Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which CONTROL NEOPLASTIC GROWTH
——————————————————————
Antineoplaston A10 (3-pehnylacetylamino-2,6-piperidinedion) is first chemically identified antineoplastons and when administered orally is hydrolysed in pancreatic juice to PHENYLACETYLGLUTAMINE and PHENYLACETYLISOGLUTAMINE in ration of 4 to 1
——————————————————————
These metabolites are water soluble and have ANTITUMOR EFFECT, are further degraded to PHENYLACETIC acid
——————————————————————
Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETYLISOGLUTAMINE in ratio of 4 to 1 formulated as Antineoplaston A10 injectable formulation
——————————————————————
Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid in ratio of 1 to 4 also shown to have ANTITUMOR EFFECT in tissue culture study, then formulated as Antineoplaston AS2-1
——————————————————————
Reported CYTOSTATIC INHIBITORY EFFECT of A10 on HUMAN HEPATOCELLULAR CARCINOMA CELLS and differentiation inducing effect of AS2-1 on various TUMOR CELLS suggest potential benefit for treatment of HUMAN HEPATOCELLULAR CARCINOMA since this TUMOR recurs frequently despite initial successful treatment
——————————————————————
BOTH AGENTS INHIBITED CELL PROLIFERATION and increased number of cells in G0 and G1 phases and Antineoplaston AS2-1 induced apoptosis, we also describe clinical experience of hepatocellula carcinoma (HCC) patient whose tumor, after incomplete trancathere arterial embolization (TAE) for 7cm 7cm HCC, has been stable for more than 15 months during which time he has been taking Antineoplaston AS2-1 continuously WITHOUT ANY SERIOUS ADVERSE EFFECTS
� � � � � � � � � � � � � � � �
[43] 1/2008 Novel mechanism through which all-trans retinoic acid (ATRA) and antineoplaston, ANTICANCER DRUG, CAUSED CELL GROWTH INHIBITION IN BREAST CANCER CELLS through effects on intracellular pathways
——————————————————————
Antineoplaston caused down-regulation of PKCalpha protein expression, resulting in INHIBITION of ERK MAPK phosphorylation, with resultant INHIBITION of Rb phosphorylation leading to G(1) arrest
� � � � � � � � � � � � � � � �
[44] 10/1/2010 As degradation product of Antineoplaston A10 in vivo, PHENYLACETYL GLUTAMINE showed ANTITUMOR ACTIVITIES
——————————————————————
Designed and radiosynthesized PHENYLACETYL GLUTAMINE derivative, achieved under mild reaction condition
——————————————————————
radiochemical purity of (S)-2-((S)-2-(4-(3-fluoropropyl)benzamido)-3-phenylpropanamido)pentanedioic acid ([18F]FBPPA) was 98%, and best radiochemical yield was up to 46%
——————————————————————
results revealed it might become potential PET imaging agent for DETECTING TUMORS
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References:
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[1] 7/1971
� � � � � � � � � � � � � � � �
Neish, W. J. P. Phenylacetic acid as a potential therapeutic agent for the treatment of HUMAN CANCER. Experientia (Basel), 27: 860-861, 1971
http://www.ncbi.nlm.nih.gov/pubmed/5139518/
Experientia. 1971 Jul;27(7):860-1
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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
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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
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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
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SAMID, D., Ram, Z., Hudgins, W. R., Shack, S., Liu, L., Waibridge, S., Oldfield, E. H., and Myers, C. E. Selective activity of PHENYLACETATE against MALIGNANT GLIOMAS: resemblance to fetal brain damage in phenylketonuria. Cancer Res., 54: 891-895, 1993
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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
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
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
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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
http://www.sciencedirect.com/science/article/pii/S0304383500004080
DOI: 10.1016/S0304-3835(00)00408-0
http://www.sciencedirect.com/science/article/pii/S0304383500004080
Cancer Letters, Elsevier Science
Department of Pharmacognosy, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt
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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
http://www.ncbi.nlm.nih.gov/m/pubmed/10893443
Cancer Lett 157 (1):57-63 (2000)
http://www.cancerletters.info/article/S0304-3835(00)00472-9/abstract
Cancer Lett. 2000 Aug.31;157(1):57-63
http://www.sciencedirect.com/science/article/pii/S0304383500004729
(Cancer Lett., 2000, 157, 57)
http://dr-labouzeid.webs.com/A10-Cancer%20Letters%20157.pdf
Cancer Lett 157: 57-63, 2000
Cancer Letters – Elsevier
Cancer Letters, Elsevier Science
DOI: 10.1016/S0304-3835(00)00472-9
Department of Pharmacognosy, Faculty of Pharmacy, Mansoura University, Egypt
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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
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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 R D. 2003;4(2):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)
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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
� � � � � � � � � � � � � � � �
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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