The MicHigANDer’s 12 days of Christmas

On the 1st day of Christmas, my true love gave to me

a communist wannabe Dezinformatzia officer Dr. David H. Gorski

On the 2nd day of Christmas, my true love gave to me

a “Show Me State” truth-hater, and a communist wannabe Dezinformatzia officer Dr. David H. Gorski

On the 3rd day of Christmas, my true love gave to me

a “who cares if you protected our ‘freedom of the press’ USA Today newspaper, “Show Me State” truth-hater, and a communist wannabe Dezinformatzia officer Dr. David H. Gorski

On the 4th day of Christmas, my true live gave to me

a “factually challenged” Wikipedia, “who cares if you protected our ‘freedom of the press’ USA Today newspaper, “Show Me State” truth-hater, and a communist wannabe Dezinformatzia officer Dr. David H. Gorski

On the 5th day of Christmas, my true love gave to me

Astugenal for free, a “factually-challenged” Wikipedia, “who cares if you protected our ‘freedom of the press’ USA Today newspaper, “Show Me State” truth-hater, and a communist wannabe Dezinformatzia officer Dr. David H. Gorski

On the 6th day of Christmas, my true love gave to me

Atengenal for you and me, Astugenal for free, a “factually-challenged” Wikipedia, “who cares if you protected our ‘freedom of the press’ USA Today newspaper, “Show Me State” truth-hater, and a communist wannabe Dezinformatzia officer Dr. David H. Gorski

On the 7th day of Christmas, my true love gave to me

Antineoplastons from sea to shining sea, Atengenal for you and me, Astugenal for free, a “factually-challenged” Wikipedia, “who cares if you protected our ‘freedom of the press’ USA Today newspaper, “Show Me State” truth-hater, and a communist wannabe Dezinformatzia officer Dr. David H. Gorski

On the 8th day of Christmas, my true love gave to me

Aminocare, Cengenal, Fengenal, Antineoplastons from sea to shining sea, Atengenal for you and me, Astugenal for free, a “factually-challenged” Wikipedia, “who cares if you protected our ‘freedom of the press’ USA Today newspaper, “Show Me State” truth-hater, and a communist wannabe Dezinformatzia officer Dr. David H. Gorski

On the 9th day of Christmas, my true love gave to me

F.D.A., N.I.H., N.C.I., Aminocare, Cengenal, Fengenal, Antineoplastons from sea to shining sea, Atengenal for you and me, Astugenal for free, a “factually-challenged” Wikipedia, “who cares if you protected our ‘freedom of the press’ USA Today newspaper, “Show Me State” truth-hater, and a communist wannabe Dezinformatzia officer Dr. David H. Gorski

On the 10th day of Christmas, my true love gave to me

Fabio Lanzoni, F.D.A., N.I.H., N.C.I., Aminocare, Cengenal, Fengenal, Antineoplastons from sea to shining sea, Atengenal for you and me, Astugenal for free, a “factually-challenged” Wikipedia, “who cares if you protected our ‘freedom of the press’ USA Today newspaper, “Show Me State” truth-hater, and a communist wannabe Dezinformatzia officer Dr. David H. Gorski

On the 11th day of Christmas, my true love gave to me

Barbara Burzynski, Fabio Lanzoni, F.D.A., N.I.H., N.C.I., Aminocare, Cengenal, Fengenal, Antineoplastons from sea to shining sea, Atengenal for you and me, Astugenal for free, a “factually-challenged” Wikipedia, “who cares if you protected our ‘freedom of the press’ USA Today newspaper, “Show Me State” truth-hater, and a communist wannabe Dezinformatzia officer Dr. David H. Gorski

On the 12th day of Christmas, my true love gave to me

Dr. Stanislaw R. Burzynski, Barbara Burzynski, Fabio Lanzoni, F.D.A., N.I.H., N.C.I., Aminocare, Cengenal, Fengenal, Antineoplastons from sea to shining sea, Atengenal for you and me, Astugenal for free, a “factually-challenged” Wikipedia, “who cares if you protected our ‘freedom of the press’ USA Today newspaper, “Show Me State” truth-hater, and a communist wannabe Dezinformatzia officer Dr. David H. Gorski

Happy “Freedom of Speech” Holidays and a Merry Christmas, everyone !

20131225-070337.jpg

Pete Cohen chats with Dr. Stanislaw Burzynski – Interview #2

======================================
Dr. B interview #2
2/7/2013 (10:31)
======================================
Why do you continue to do this ?
Why haven’t you just, given up ?

Because I am right
Why should I stop when I have 100’s of people who are cured

Mhmm

from incurable brain tumors
Ok
We have over 100 people, who are surviving over 5 years, just in the supervised clinical trials with brain tumors
So obviously this works (laughing)
It works in great way
So why should I stop because, some evil people like me to stop ?
It doesn’t make any sense
Evil will lose
So we are right, and we’re going to win
Not, uh, no matter how soon this will be established, but we are going to win

Well, for what it’s worth, and this is something, this is why I wanted to put myself, uh, in front of the camera with you
Obviously I spent 8 months, um, and I’ll try and not get too emotional about it, because that’s unprofessional (laughs)

Yes

but I spent, I spent a long time, looking into this, speaking to people,

Yes

You have very kindly given me access to everything here

Sure

Speak to anyone
Speak to patients
To see medical records, and I have, uh, been amazed by what I, what I’ve seen
I know the statistics are now showing, in the world, that one in two men, will have cancer
One in 3 women, will have cancer

Yes

It’s a, it’s a massive problem

That’s right

And I can see that you’ve genuinely found, uh, a cure for cancer

(?)

You know, it might not work for everyone, but if you’re given the su

Yeah

given the support

Yes

If you’re given, uh, the, uh, I don’t know, just the support basically, and the funds maybe, you could really, do some work, that could change, the whole (nature ?)

Absolutely, and then we can get better, and better
Of course, what you have now is not yet the finished products
We understand that
That’s something we can substantially improve
The response rate can be improved
So, certainly, all of this can be done, but, obviously, we need the resources
We need time to do it, and most of my time is spent with such silly thing like, uh, uh, protecting ourselves against attacks from, the people who are hired to destroy us
Ok
Obviously, there are some companies who are working on the payroll of pharmaceutical business, who are trying to smear us
To spread bad publicity about us
To generate lies about us
These people are criminals, and they are still flourishing
The end for them will come soon, but they are still hurting the other people
because the other people will not take treatment
They will not come, and they will die
Ok
There is no cure for, uh, uh, malignant brain tumors which are inoperable, ok, and we can cure at least, good percent of these people
We presented, our results, at many, many, 1st class
scientific congresses, like nuero-oncology congresses, cancer congresses, and it’s important for U.K.
I showed you yesterday, eh, presentation on brainstem glioma in children

Yeah, I have it here

and at the same, uh, Congress, in Edinburgh, we presented also another, eh, eh, paper, on the treatment of glioblastoma multiforme, and the survival on, about 88 patients, in glioblastoma multiforme
So obviously, I make, I make this available to everybody , they would like to listen, come to my presentation
They, they, they know about it, but they don’t want to know about it

Why not ?

(laughs) Because they are working
They are slaves of the big pharmaceutical cartels, ok, and on the payroll of big companies
They hate to see somebody else outside, the slavery, who can do it
I’m free man
I can, ah, do the research because, I am spending my own money for it
I don’t need to beg pharmaceutical companies or government to give me the money
I can do it on my own
They hate it
These people
They hate it because they have slave mentality

Mmm

They arch their back for scraps of money from the table, of some powerful companies, from the government, and they, how can you deal with s, slaves
They don’t want to see something new because this would disrupt, slavery system
Ok
So, current medical education s, system is manufacturing robots
They don’t think on their own, they use only what, the government, or the lawyers of the government, or what the administrators will tell them to do, ok, and if they don’t then they get punished, ok (laughs), and that’s a great system for a ph, pharmaceutical companies, because obviously they can make a lot of money, but it’s not a great system for people who have cancer because they don’t have good results

So you’ve presented at these conferences, and people don’t come up to you afterwards and say:

Mhmm

“I want to come and see what you’re doing
I’ve got to see this for myself”

Ah, well, uh, at each of these Congresses I meet a few doctors who are top specialists in their area who will come to me and say: “Ok, this looks very interesting
We’d like to know more about it
Please send me some, eh, results and a few cases that I can review,”
and that’s what you do

Yeah

You send them these cases, and that’s the end of it
I don’t hear from them anymore because they’re afraid to move any

Mmm

further, ok, because they know if they move further, they get punished
They don’t receive grants
They’d be scrutinized by their peers
They’re afraid
Ok (laughs)

Yeah

They work for us

Yeah

they work for us undercover
We have over 100 telephone callers who used to work with us, but they don’t want anybody to know about it because they’d be immediately attacked by the other guys

And the pharmaceutical world as well

Ah, well, the other guys are obviously working for cartels
Uh, they’re on the payroll, a, oh, of big business, which is cancer business, and they don’t want to lose it
Uh, in average, uh, city you might have say about 20 oncologists
One of them may work for us, but he does not no, want to tell anybody that he’s doing this because he would be destroyed by the other guys
These 20 guys will jump on him and he will, won’t have practice anymore
Ok

Yeah

So that’s, uh, the travesty, but, uh, uh, I believe that this is coming to the end
Ultimately, su, more and more doctors will learn what we do

Yeah

and more and more patients will benefit, and the breakthrough will come, but before the breakthrough will come, you have the toughest time

Mmm

because, the opposition is mounting the attacks
Whenever we came up with an announcement that was in the 20th century, we have such and such success, you are furiously attacked by the other guys, who are on payroll, uh, of cartels
Ok (laughs), for no apparent reason
You should be congratulated but we are attacked, because they see we are going to win, and they hate to see this because this means they won’t see money anymore for them, ok, or at least they think they won’t, they won’t have their payroll anymore
—————————————————————
Dr. Burzynski on publishing (6:18)
—————————————————————
So why does, why does, ev, everyone hide behind this thing of saying about publishing, because that’s the thing you hear all the time

Well, we cannot publish until the time is right (laughs)

Yeah

If you would like to publish the results of, of a
10 year survival, for instance

Mmm

Which we have
Nobody has over 10 year survival in
malignant brain tumor, but we do, and if you like to do it right, it takes time to prepare it, and that’s what we do now
What we publish so far
We publish numerous, uh, publications which were, interim reports when we are still continuing clinical trials
Now we are preparing, a number of publications for final reports
Eh, many of my publications were rejected by known publi, by known journals like

Why ?

like Lancet, like JAMA,
like New England Journal of Medicine
Why ?
Because they say: “Sorry, but you didn’t receive enough priority to be published, and if you look in these journals and 1/2 of the, these journals, they are advertising for pharmaceutical companies
Obviously if this would come from a pharmaceutical company, this would be published on the 1st page

Mhmm

Ok
Because this, you don’t have objectivity with these guys
They are on the payrolls of the big cartels, ok, and again and if you try again to send, oh, oh, my manuscript to good journals, if they reject it, we go on Internet and you describe what are these guys
So then everybody will know, because I have very good evidence
that we tried many times to publish in 1st class journals, and we are always rejected

It’s just, persistent

And not, and not because of lack of scientific knowledge
No, because of lack of priority
And who has priority ?
The guys who are paying money for advertising
Ok
So that’s, unfortunately what I think will end sometime
—————————————————————
And we are now preparing publication, on some of these results
We have already published the results on the technique of very difficult variety of breast cancer, which is triple-negative breast cancer
Now we are preparing another article on the technique of
gynecological cancer, which is best series of over 100 patients treated with incurable ovarian cancer, uterine cancer, (?)
So this, has now been prepared for press
Eh, of course, I would like to, give everybody intravenous antineoplastonssee, if they qualified, but, this is limited by the government, because the government limits us to only the patients who are
have
brain tumors, but the other patients, they can be treated through this combination of medication which work on the genes
Antineoplastonswork on over 100 different genes
That’s why they give us, very good advantage
There are medications that also work on a number of different genes, and we can combine them together, and use them in the right way
So
that’s what we’ll continue to perfect, and that’s, uh, most of our patients
been treated with just combination of targeted medications
—————————————————————
The Future (9:00)
—————————————————————
Why do you continue to do this ?
Because you know the truth, and you want to get the truth out there ?

Absolutely, because we understand we on the right track
Somebody has to do it
I was lucky enough to, find out about it
We have evidence that we are right, and, uh, I don’t think, why should I stop if, people that don’t have sufficient knowledge, who are working, on behalf of some big business, would like to stop us
We are right, and we would like to continue to help people, and, uh, that is what is going to happen
Of course, probably the best reason to make a discovery, and let it stay as it is and ask the other people to publish after I die

Yeah

That’s what happened with the discovery of Nicolaus Copernicus, who was my countryman
Eh, his book was published, sss, when he died, and, uh, for good reason, because of such fears for execution of the people who followed him
like

Hmmm

Galileo, Giordano Bruno, that it took the church, uh, only until recently to agree that, uh, they made the error, in the case
Ok
So if you come up with some breakthrough, you have a choice
Keep it quite until the other guys who understand what you do
or try to use it
In my case, I decided to use it, because I would like to, help people, and now that we can save people, so why should I keep quiet, ok, but certainly if, my work won’t get published because it keeps getting rejected by some of the journals, then we wait until I die, and then we let the other guys publish it
So, ok
======================================

======================================

Pete Cohen chats with Dr. Stanislaw Burzynski

======================================
Pete talks with Dr. Stanislaw Burzynski
——————————————————————
December 2011 (1:02:30)
======================================
How did you kind of get into this, into this field in the 1st place ?

Uh well, it was a coincidence, ’cause obviously I made discovery of new chemicals, peptides which is in blood, and I noticed that they were deficient in patients with cancer, and there was a curiosity, why there was such deficiency, and I was interested what these peptides that I discovered, are doing in the body
So the connection with cancer was quite obvious
He, healthy people have abundance of these chemicals in blood
Cancer patients have varied to none
So could be that cancer is another deficiency disease
So

So when you found this out

Yes. Mhmm ?

how did you feel ?
I mean, did you not just want to shout from the rooftops, and could you believe that you’d actually discovered something ?

Not yet
Of course I was skeptical, and I found something that was interesting, but obviously, it was just the very beginning and when I shared this news uh with some other guys, who are obviously much older than me, who, other guys who were professors, who ever, so (laugh) they began to laugh so much they almost died from laughing
Ok ?
That (laughing)
Wow, this guy would like to kill cancer
Forget it
Ok ?

That’s just not going to happen

What are you doing ?
Yes sir (laugh)

Well how did that affect you ?

Well it didn’t affect me too much because I knew that uh the science uh requires uh some successes and uh setbacks and I felt, well I still would like to know, what these peptides can do, and I would like to know what they can do, not only regarding cancer but in various aspects of body function
For instance, the activity of the heart, the activity of the uh uh G.I. tract
Whatever
Ok
I needed to expand this knowledge
Suddenly I found some like 119 new peptide fractions
Nobody ever heard of them
So I wanted to know
What do they do ?
And when I was in Poland I couldn’t have really do any further testing, because I didn’t have such possibility to require different group of people who would do the testing, and simply by working in the biochemistry laboratory I did not have such capacity, and obviously the budget for doing uh research was extremely small
Besides, I was continuously harassed by the communists and they were sending me to, eh, the military, so I couldn’t do much
I still did whatever I could
Then I came to U.S.

Oh so you came to U.S.
What, what year was that ?

It was 1970

I heard you came with not very much money in your pocket

Uh well it was better than where I came first to the U.K., because when I came first to U.K., I came practically with nothing, and uh, when I went to British uh Medical Student Association, they were going to give me 7 pounds for one month stay in U.K. (laughing)
You were supposed to get this money in Poland

Yeah

(laughing) Sorry about that
So ultimately they decided to give me 7 pounds, and obviously at that time it was a lot of money, so with 7 pounds I was able to survive a month
(laughing) Good luck (laughing)
But in U.S., I was allowed by the communist government to $15, which again, was equivalent probably to 7 pounds, whatever (laughing)

So you came here with $15

I smuggled another 10

Yeah

So the proper balance was like

So what
So what did you do when you got here ?

Well, ehhh, when I arrived I was uh, uh, uh, trying to get ahold of my relatives
My uncle that lived in Bronx

Yeah

And uh I officially came to visit him and uh I was expecting him to see me at the airport, and surely enough he came to the airport but uh at the time he was an elderly man
He was close to 80, and eh, he probably went to a different part of Kennedy airport, so he couldn’t find me
So I was stuck in the airport
This was Holiday
This was 4th of uh September, which was a Labor Day, and so I couldn’t get uh uh to his apartment
So finally I spent most of this money for the cab, the taxi rides to his apartment
Some, like $13 worth

You had $2 left

Ye, Yeah

Plus the $10

Sure
Well, so then I stay uh I, I was obviously in the family’s, I couldn’t

Yeah

I, I don’t need to worry about it
So obviously I had a food and lodging, and uh, still I was trying to get hold of some of the people whom I knew were doing the research in the area, whi, which I was interested

Mhmm

which was peptide research, and uh trying to see if I can advance my research
And then I thought, well, if I go back to Poland, I didn’t expect to stay
And in the meantime uh my job at the university in Poland was terminated, and I wondered they needed my position for the woman who was the wife of the 3rd Secretary of the communist party
Finally when I was terminated from my job, uh, there was no need for me to go back, because I would not be able to find job anywhere in Poland, because obviously everything was controlled by communist
So that I decided to stay and to look for the possible, possibility for me to find a job in the U.S.

And wha, what job did you find ?

Um

So you were in New York ?

Yes, I was very active, of course since I was involved in the research
I knew the key people who were involved in peptide research
There were not many of them, but at least there was one good team in New York and Columbia
Um, there was another one at, uh, Cleveland Clinic, and there was another one in Houston, and so, uh, I check with all of them and, uh, the place in New York was unavailable because they hired, um, somebody, um, about a week before I came
Uh but uh, uh, I was invited to the interview to Houston
I was surprised but uh, prepared for my trip and I arrived to Houston and had interview with a professor at Baylor College of Medicine and he gave me the employment, and so it was relatively simple

And then what were you doing on like a day-to-day basis ?

Uh, well, uh, when I arrived to Houston I uh, obviously received a job
I received the job as “Research Associate,” and um, obviously this was associated with a reasonable salary, but the salary was paid once a month, so I had to think, what do I do for the 1st half of the month, because I came in the middle of the month, and didn’t have any money (laughing: both), but some good people loaned me some money so I, I have enough money to rent the apartment, and finally after I got my pay, I was able to do quite well, and I was able to advance, uh, in peptide research

So were you able to do your own research or

Absolutely. Absolutely

that they wanted you to do ?

Absolutely, and uh, I was quite lucky to join the team of the famous professor
Professor George H
er, uh, who was initially professor of Sorbonne in Paris
Then in World War II he emigrated to U.K. and he was professor at Oxford, and so finally he came to U.S., and, uh, he put together the peptide research team
He needed people who know how to do analysis of peptides, so that’s why he hired me
And uh I uh told him that I have my own project, which is peptides, and if you wouldn’t mind that I do some research of mind, and he agreed
So basically this was gentleman agreement that I will spend 50% of my time working for him, and spend 50% time, working in my area
Uh, the equipment and the instruments were the same, so it wasn’t too difficult

And then you, and then when you had something to show then, when. when you had even more of something to show them, how was that received, because you see, I’ve really got something here ?

Ah

I think I’ve got something here

Absolutely, it was received with great curiosity, and, um, and obviously he needed people who could use, the cutting edge, uh, methods for peptide analysis, and that’s what I knew about, but I couldn’t use this for him because I didn’t have funds to do it, but I knew exactly what needs to be done, and on the other hand, uh, this was great surrounding because just across the corridor, another team receive a Nobel Prize for working on peptides
The only problem is, uh, one of these researchers uh was of Polish origin who received Nobel Prize for peptides (laughing)

Yeah

began, uh, fighting with the other one and finally his job was terminated because he punched (laughing)

Punched him ?

the other guy in the nose (laughing)

Yeah
Huh

So, but the good thing about it is that ultimately I inherited uh, their equipment

Yeah

for peptide research, so

Wow. So that must have been like a, like, a, a child in a sweet shop

Absolutely, so was a great coincidence so

So then you were really able to, to, to, to look at it in more detail, and ?

Absolutely, so then of course I was really out of work uh, and the team of Dr. Unger, and also, uh, I was spending a lot of time, uh, progressing in my research, which was very important uh, of course it means long hours uh, ’cause of, uh, 8 hours I would spending working for Dr. Unger and probably not 8 hours until midnight working on my uh, project, but uh, I enjoy it
In the meantime I need to prepare for exams because I wanted to have a license
So I was lucky because uh, within 3 months I was able to pass exams to uh, to naturalize my diploma, and then uh, just, uh, the day, on the eve of my birthday, on January 22nd, President Nixon had a speech in which he promised American people that by 200th anniversary of America, they would have a cancer cure, and no limits would be set on the funding
So then I thought, well, if that’s the case, perhaps I should apply for the grant also, and I did
It was crazy idea because I could barely understand when the people were talking to me (laughing: both)
Well I decided to put together grant application, in to the National Cancer Institute, and include the project on the peptides which I discovered, and I was surprised when this was approved
So then in uh 1971 I get approved as Principle Investigator, to do the project, which included eh, the top people from M.D. Anderson Cancer Center, and from Baylor College of Medicine, um, and I was supervising this
I was at that time 28 years old, but I was supervising the guys who were famous, and who were some like 60 years old (laughing)

Wow

and so the money was coming to me from the National Cancer Institute, and I was uh daily uh, running the project, sharing, obviously with the guys from M.D. Anderson, so, and going ahead with the research, so
and of course at that time I was disappointed to have to (work ?) with M.D. Anderson and Baylor, and then I could move independently what I was doing

So at what point were you actually, able to start testing on people

Mmm
It took a long time because

I mean you couldn’t wait, right ?

Yeah it took a long time because obviously um, initially you have to go through a lot of pre-clinical testing
The 1st time it was uh, around the beginning of ’77, yeah
So then we began phase I clinical trials, and this phase I clinical trials were approved by one of the very good hospitals in Houston, which is part of the hospital chain American Medical International, and they interviewed my project and their Institutional Review Board approved it for clinical trials
Well then I did my 1st clinical trials, phase I clinical trial, with a medication that I am not using at this moment because we made further progress of course, at a hospital, and this hospital at that time was called Twelve Oaks Hospital
At this time it’s called River Oak Hospital

Yep

Yes

And then, at what, at what, was there a time where you realized: This is actually working ?

Well, now this was in 1977, and (laughing) surprisingly, uh, uh, perhaps one of the 1st successful case where you can really, document a clear-cut improvement by doing the scan before and after
It shows tremendous decrease of uh, uh, tumors which corresponded to colon cancer which spread to the liver
(This guy was ?)
(laughing)

(?)

(laughing)
And uh, his case was so interesting, that when I sent it for press, the editors decided to put us on the cover, of the journal, the scan

Yeah

They decided to put on the cover of Science, showing the tumor before, and, after the treatment
Eh, so this was uh , obviously

And then what happened ?
Didn’t that m kinda, didn’t word spread like wildfire and people, more and more people want to come and see you ?

Ah, Absolutely, well the 1st excitement occurred, basically what the President Nixon promised ok

That he would deliver

Yeah

cancer cure uh, by ’70, uh 6, 1976, and we did, ok, and we did deliver cancer cure

Yeah

by 1976, 1977 ok, and um, the um, main uh event was the presentation of uh our theory on our research, on perhaps one of the largest uh scientific (congress ? conference ?) in America, involved 19,000 uh, researchers attended
Eh this was annual meeting of the Federation of the Societies of Experimental Medicine and Biology
It happened that at that time it was in Anaheim, California
Uh, I sent uh, uh, the abstract of my presentation, and I was simply, patiently waiting until this would be shown, which was in ’76
In June ’76 right before 4th of July, and uh, I was surprised when they notified me that um, my abstract was selected out of one of few, which was in great interest of the news media, like Associated Press, for instance, and then when I did my presentation, then Associated Press decided to make a release of this, and then you can read about it in newspapers all over the world
In uh, (laughing) distant places like Buenos Aries, receiving CBS newspaper clips from all corners of the world

And what was that like for you ?
I mean, how did that feel, just to see that your name was, all over the world ?

This was the 2nd time, what (?) this happened to me, because 1st time it made such news, by working on brain peptides with Professor Unger; this was around ’72, and suddenly, this wasn’t so much of my

Yeah, but still it was your (interest ?)

involvement, but I was working together with Professor Unger, and we made a great news, by discovery of, certain peptide in the brain, and then it spread all over the world, and then again, uh, uh, CBS

What was that like ?
I mean, how did you feel when you saw ?

Well, uh, it was surprising because uh suddenly we got uh news people coming, and the TVs from various countries, especially from Europe, for instance, from variety of corners, like from Europe, from New Zealand, from Brazil
You name it ok ?
Eh, so there was a great excitement about it, but 1st time that this excitement happened was, is around ’72, uh, really, eh, is typically what happened after such excitement, is the ? iation ?)
ok

Yeah (laugh)

Well, uh, (laughing) the uh, establishment is and this um will attack you and will try to destroy you

Did you know that was going to happen before ?

I knew it would because in Poland, uh, my father’s, uh, gave me the book of um MIT Professor, uh, Thomas Kuhn
(here’s a guy ? try to translate to (?)
(laughing)

(?) yeah
Yeah, probably

(laughing) sure
and then uh, this was uh, the book which was titled eh, Structures of Scientific Revolutions
It happens that this book was translated to Polish language as couple of years after it was printed, in U.S.; which was around uh, I think 19 uh, 64 probably, ok
So then I read the book, and the book shows uh, how, eh, the paradigm shift occurs, ok, and the, it never fails
It always goes through the same stages
1st it’s short period of excitement, and the a long time of harassment and persecution, and then finally the brief period when uh, uh, if you survive, then uh, the other people say
well it’s obvious
We always knew (laughing) that this

Yeah

was going to happen, ok ?
So I knew what was going to happen, uh, but uh, it was hard for me to believe it uh that, uh, in the 20th century, 21st century it could happen, ok, but then uh, when uh, I began going through this, it was like going to some uh, unpleasant disease
You read about it in the books and

Yeah (?)

then uh, you finding one symptom after another, and it affects you

Yeah

and you know that it could be deadly,
(?) survive

Well you could have ended up in prison, right ?

Yeah

(?)

You may die before uh, you be able to do anything

Mhmm

So the advice of the author of the book, was that you have to start early to make some medical discovery, because you probably have years of harassment in front of you, and probably the best chance that uh, you get accepted if you live longer than your opponent, because some guys will never accept you (laughing)

Yeah

until they die
So that’s what happened
Well then, of course, I witnessed what happened with Professor Unger
Yeah, he made the great news, and obviously I contributed to what he had, but he was uh, my boss, and then obviously I did not much, suffer much from retaliation, but he did, ok
So there was retaliation, and uh, they accused him of everything possible, uh, finally causing for him to move from Houston to Memphis, Tennessee, eh, zzz, about year later he died
So unfortunately his research was never brought to the time when it was accepted, ok
It was great research, ok, and if had really to more resource and time I can bring this to be accepted, because this isn’t a completely different field
This is brain function, memory, and peptides working in the brain
But at that time unfortunately the project was killed, which is great loss for humanity, eh, ’cause the discoverer passed away, and the product was gone together with him
It can be still resurrected, and I think it will be
Eh, so then, for me, eh, it meant only advancement, unfortunately, because, uh, when uh, uh, he was stripped from the funds, I received funding from the National Cancer agency funding from the university, and I was able to support him, because he was stripped of his grants and funds
So he was able to move forward with his research, but finally when he moved, I inherited very large laboratories
My laboratory was located in 3 buildings
So the lab space and uh, uh, some prime location, in the medical school
So then I did very well, then, of course, the publicity occurred, and this publicity was centered around me, not around both of us

Yeah

at that time, in ’76, and then again there was about 1/2 a year when there was a great enthusiasm, uh, good wishes, whatever, and after that, a retaliation occurred, ok
So then obviously

Mhmm
And what was, what, what was at the heart of the retaliation ?

Uh, well,

The fact that their people didn’t want this to come to the fore ?

Initially there was some overtures to take away the discovery from me, and uh, for instance, uh, uh, uh, Baylor College congratulated me
I received diploma, so suddenly became superstar, ok (laughing)

Yeah

and then, of course, uh, the wise people, the business people from the university said: “Look, probably we should talk now about patents, we should talk about pharmaceutical companies, we should try to, somehow, put this to motion,” ok, and that’s what we did
So then uh, we talked to some of the best lawyers in the country
Of course, uh, the university uh, are in control of this
There were visits of uh, pharmaceutical companies
I remember one of them came from the research center in U.K., from High uh, Wycombe , and this was so (encouraging that ?) was very interested, what we do
But then uh, the intention was just to take uh, my, uh, in, invention away from me, and obviously

Mhmm

I would have very little to, to, do to promote this, to develop this any further
So I thought about it and I felt that I’m not going to do it
There then uh, I was offered to join the mainstream cancer research at Baylor cancer medicine, and obviously uh, I would receive much better title, of professor

Yeah

and obviously there would be much better equipped laboratory, but again eh, they wanted me to, completely quit private practice of medicine, ’cause at the same time I was practicing medicine, which many researchers were doing
I was working at Baylor College and then I was practicing medicine uh, outside Baylor College, in the group of the other doctors
So in this way I had some independence, because obviously, I could always practice medicine (laughing)

And did you always want to keep your independence,

Yes

and did you know that was always a good thing ?

That’s right, that’s right
Because I, I did not want to be uh, at the mercy of the university or the government
Uh, but I still wanted to stay in academic surrounding, because obviously I came from a family which has great tradition of academic careers
So that’s something which obviously my father was always telling me that I should be really staying in the university, ok
Eh, uh, uh, but finally I decided that I was not going to accept this offer because uh, why should I resign from my private practice

Mmm

It didn’t hurt my research in any way
So I decided to continue, and uh, then that’s when the retaliation occurred, and uh, I was (crazy ?), harassed, and attacked, and finally

And how were you harassed ?
I mean, letters or (peop ?)

Mmm, well, as I could do the research for such a long time, because really, this was some like 7 years at the university, because uh, very few people in the university knew what I was doing, because I was only responding to the National Cancer Institute, and uh, I was not part of the mainstream cancer research center
What happened is that uh, (laugh) I was employed by the Department of Anesthesiology, which obviously, on the surface has nothing to do with cancer, but, who cares ?
I was receiving grants from the National Cancer Institute, and so Anethesiology was a very wealthy department, and they had a lot of space, but they were doing very little research
So they wanted to do some type of research, and uh, the chairman of the department was supportive of my doing cancer research
So basically I conducted uh, Anethesiology
laboratory into cancer, into cancer research laboratory, and very few people knew about it
They learn about it
when uh, the Associated Press (laughing) broke the news
So then uh, the retaliation happened

Mhmm

and then they wanted me to join the mainstream, but obviously I was enjoying very much (laughing) working, in peace and tranquility, and responding only to the National Cancer Institute
So then uh, what happened at that time was that uh, obviously Dr. Unger, moved to another university, and um, uh, the chairman of the department uh, his uh, uh, employment was terminated, because it uh, he was involved in uh, the war between 2 superstars of (the ?)
One of Dr. DeBakey
and the other one was Dr. Cooley
They were 2 famous, eh, eh, cardiovascular surgeons, who were competing with each other
Ehhh, Dr., eh, the chairman of the department, was on the side of Dr. Cooley, but the boss of, uh, Baylor College was Dr. DeBakey
So after Dr., Dr. DeBakey
learned that, uh, the sympathy of Chairman of the Department; which was Dr. Cooley, his job was terminated
So then they, took another man; very old, professor, who was already retired, to be the chairman of the department
They, he knew nothing about, any type of research (laugh), especially cancer research, and, uh, once I decided to not join the mainstream, Baylor Research Center, eh, the people who are in charge of Baylor Research Center, they put a pressure, on the new chairman of the department, and they frightened him, saying look, you are, uh, in a charge of anesthesiology, but here’s a guy doing cancer research, eh, and see this was a great, uh, like liability to you, and pretty soon he may be sued, uh, without knowing what he’s doing
Ok
So then, uh, they, they, um, brainwashed the old man, and he decided to strip me, slowly from my laboratories, eh, and, and, harass me
Ok, uh, ultimately, he sent me the letter that, uh, in which he informed me that he does not see any connection between, uh, my research and anesthesiology; which was obvious, eh, but obviously I was doing the research which made the university famous, more or less

Yeah

So then one thing to another, and I decided, no, I am not going to work with, in this environment anymore, and I decided to do, try to do on my own, to start my own laboratory
So that’s what happened
Ok

And then you did that ?
You had your own, laboratory ?

Yes, and then I decided, this was just the beginning of 1977, and, uh, e, we put together a laboratory; of course I already had private practice, and, uh, I was still working

In your private practice

Yes

you were still seeing patients ?

Absolutely, absolutely

Seeing any results ?

Yeah, seeing patients, getting results
I began phase I clinical trials

Mhmm

in the hospital where I was seeing patients
I had patients at that time, in about 2 or 3 different hospitals, uh, but the hospital, where I get permission to do clinical trials, was a most supportive, and that’s why I did it this way, and, uh, obviously it was necessary for me to build from scratch, the laboratory, the research laboratory
I decided that I just, uh, I just, uh, make some funds in, our private practice, and at that time, of course, this was just, um, general (?) private practice, internal medicine private practice, em, and, uh, the funds which I produced in private practice I can use to, put together the laboratory, and that’s what we did
Ok
Step by step we build the laboratory, and we expanded our private practice
So basically, I switch from the government and then I found it best to fund the research, just privately funded research, which nothing unusual, thhh, some like 50 years before everyone was doing it

Everyone is doing this

Yes, and there’s still some people, especially in the U.K., who are doing this
Ok

Yeah

Um, the most of the discoveries were made through the, sss, through the research that was funded, by the researchers

Mhmm

There are also some, wealthy people who donated the money to do it
So only after World War II, this was, um, the system was created where, the researchers became, um, really became the slaves so, the government

Mhmm

and pharmaceutical companies, and new companies, and if they do not receive the money, they couldn’t do anything
This way I could have independence, and, uh, do whatever I want
Yes

So at what point did it get to where, action was taken against you, and you knew that you were going to have to go to court ?

The action, um, um, started very soon, and the, and began at the lowest level, which is like, county level, and then you go obviously

Mhmm

higher as you move along, and when, uh, I was leaving, uh, the university, the chairman promised me that (laugh) when I leave, uh, the obviously, quote, unquote, “They will bust my ass”
Ok ?

Yeah

(laughing)

When leaving the university

When I was leaving the university ?

Yeah

Yes
And, uh, he promised me that, uh, they will trigger the action from Harris County’s Medical Society; which is probably the lowest level of harassment and just, the somewhat prestigious society if you are are a good doctor practicing medicine, in Harris County, where Houston is, then you should be a member of the Harris County Medical Society
Uh, if you are not a member of Harris County Medical Socity they won’t grant you privileges to see patients in hospital
So this was important to be a member of the Harris County Medical Society because I was practicing medicine

Why do you think
Why do you think they wanted to stop you ?

Why did’d they wanted me to stop ?

Yeah

Well, probably just for the heck of it
I don’t know

(Laughing: both)

Ok

Well do you think they were threatened by you ?

Well, I doubt it
Their probably some type of revenge
Ehhh, since I didn’t yield to their harassment, and I decided to do whatever I was doing, and decide to do it on my own

Mhmm

and they felt, well, let’s try to kick his behind if we can
Ok

Yeah

Well I don’t think I was, uh, causing any threat to them at all, because this was really, large institution

So it escalated ?

Yes
Just starting at the lowest level
It was, eh, unpleasant because they were dragging me to like, holy inquisition proceeding, explain what I was doing, and basically they’re trying to force me to stop what I was doing by using various ways
Obviously they didn’t have any, uh, reason to do it because, uh, my clinical research; which I was doing in the most, done under the supervision of, Institutional Review Board, and before I started anything I asked, uh, I retained medical lawyers, and I asked them to check, if I can, uh, for instance, do the research to use medicine, and use it, in a patient, and they
checked with this, State authorities, Federal authorities, and at that time it was perfectly alright
So I was doing, everything, legally
So, they really couldn’t do much, but, they were harassing me, asking for me to give them a lot of documents, whatever, and suddenly, all of it stopped
It stopped because they were exposed by news media

Yeah

So, when the article was written about it, they disappeared from, the horizon, and then they never, harass me since then (laugh)

Yeah

I think it’s, lasted probably for, 2 or 3 years, and then it was gone, so

And then, and then how did that end up ?
How did you end up going to court for the 1st time then ?

Oh well, so obviously there was no, uh, issue of going to court at that time, it was only the issue that, I might not be a member of, uh

But you might not have been able to practice medicine

the medical society, and then I would not be able to see patients in the hospital
Ok
So this was deliberate, ok, and at that time, m, most of my patients were treated in the hospital, because I didn’t have yet the system to use treatment outside the hospital, like for instance the pumps that we are using now
They did not exist at that time
So it was necessary to use I.V. posts

Mhmm

and, uh, and heavy pump, heavy treatment
So then, uh, so this was, uh, it started around ’78, it continued for a couple of years, and then nothing happened after that
I was visited by, um, FDA people, but we have pretty constructive meeting
They didn’t bother me, and, uh, the next attack occurred in a 1983, and this was by, uh, Food and Drug Administration
So, suddenly I was sued, and, um, they really wanted to put me out of business
Ok

They didn’t just want to put you out of business
I mean, they wanted you, they wanted you to go to prison

No, in ni, 1983, they wanted me out of business

Right, just out of business

Yeah

Don’t want you practicing

Shut down, what I am doing, and they did it, secretly (laugh)
Most of this actions occurred around, uh, just before say Passover, and Easter
Ok

Yeah

Every year
It never failed
Ok (laughing), a, and a usually they were attacking, uh, uh

Someone

No, no
For instance it happened for instance I was away, and, uh, they were filing papers in court, like, um, around 5 p.m. on Thursday, ok, and Friday was day off, because was big Friday, Good Friday
Ok
So then, obviously, um, they then
realized I’d be away because I participated in some T.V. program, and they want to do it while I was away, but, uh, it so happens that
a one of the friendly lawyers was in court at the time, and he overheard whatever they were doing, ok (laughing),they were going for injunction, ok, and so then, uh, I would be stopped immediately
I wouldn’t be able to do much, ok, until the judge would reverse it, but, uh, he read about it and he prepared immediately temporary restraining order, and filed at the same time (laughs)

Yeah

So then, uh, I could practice without any interruptions, but, uh, then, of course,

So do you think of all the people that were trying to stop you

Yeah

Do you think any of those people actually, really, genuinely believed that you were causing harm to people

Hmmm

or do you think that they were just stopping you because ?

I think some stupid people,was at the lower level, like, uh, uh, some lower level FDA agents, they didn’t know what they were doing
They were manipulated, ok, but the guys who above, they knew very well (laughs) that, I was right

They knew what they were doing

Absolutely

They knew you were doing something

Absolutely, yes

groundbreaking

They knew very well, and that’s the reason why they attack me
Ok
Yeah
It’s obvious
So this 1st encounter, was relatively brief
Uh, we went to court, which was Federal court, and the judge, uh, would rule in our favor, and the judge, uh, uh, in the verdict, uh, cleared me from any, of the charges, and, uh, I found that I could, uh, I could treat anybody, by using my methods, but I cannot really, uh, sell medications outside the State of Texas, and that’s what I was not doing anyway
So really,
the judge
affirmed what I was doing

Right

That I’m free to use my invention, and treat people in the State of Texas, which made, of course, the government, uh, people furious, and they threatened the judge
They send the judge a letter saying that, if the judge will not rule their way, then they will go after me with criminal investigation, uh, with seizures, uh, eh, grand jury investigation
That’s what they did as the next step

When was the next step ?
How many years later was that ?

Well again, there was some like couple of years when it was relative quiet
Of course, in order to be, eh, in, eh, in order to do what I was doing, it was necessary for me to have inspection, by the inspectors, approved by the FDA, who
check our manufacturing facility, and, ah, certify that what ever we do, we do right, and there are no discrepancies
So this was obviously something, very difficult, because obviously we knew that the FDA inspectors
will always find something wrong, you know

Yeah

So these agents are trained to always find something wrong, but anyway, at inspection, uh, found we are doing everything perfect
Ok (laughs)
So we were able to pass the inspection
Uh, we are in full compliance with what is called good manufacturing practices, and then everything was quite until about 3 years later when, uh, there was a raid on our clinic by the FDA, and seizure of, ah, medical records, and then there was another, uh, obviously, ah, another, uh, part of the war began, and then, uh, we file a lawsuit against FDA, and, uh, as a result the judge forced the FDA to give back some, of the documents, and permit us to, uh, be able to copy the rest of the documents, and so then, uh, FDA began a grand jury process, and, uh, there was some, like 4 different grand juries, uh, ah, which did not find me, guilty of anything, and then finally 5th grand jury was able to indict me, which was in ’95
Ok

So when you were, when you were going to court; because I remember seeing in the

Yeah

Burzynski, the movie

Yes

I remember seeing in the photographs

Yeah

around here

Sure

there were lots and lots of people outside there (?)

Yeah

What was that like to see that ?

Oh well, ah, this was, uh, going for ever, going to court, and obviously I was going before this grand jury investigation, whatever, but ultimately, their lawsuit, uh, the trial began, in, ah, January of ’96, and, uh, it took a number of months
Ok
So I was going to court almost every day, and the people realized what was going on, and they were giving us a lot of support
So then you can see people outside the court

What was that like to see your patients ?

Well it was, ah, it was, ah, very good, uh, uh, show of (laughs)

Yeah

patient solidarity
They wanted obviously, to help us, and they knew that, uh, they have the power, and, uh, they knew that they were fighting for their lives
Ok ?
So they, uh, were dedicated people
It wasn’t easy because this was winter, and it was raining, and so it was cold weather, but obviously

Were you prepared to, to face what you could have faced, you know, that you actually could have gone to prison ?

Sure, yes
I, I knew, but I was, convinced that I am going to win
So, should I, obviously, statistically it was, uh, highly unlikely, but, uh (laugh)

Do you think that this will stop one day ?

That people will just get off your back, and (laugh)

(laughs)

you know

(?)

and can see what you’ve done

(?)

and, and see that there’s really something there

Absolutely

This is just the (?)

Absolutely, absolutely
I
That’s what I was convinced was going, to happen, and, uh, I was convinced that we are going to win, with FDA

Good, ’cause I mean, anyone does any research

Yeah

you know
I had this on here

Yeah, sure

which I’m sure you’ve seen, like on Wikipedia

Yeah

and what it says
That there’s no convincing evidence

Yeah, sure

that a randomized controlled trial has, you know
That your work, that, that there’s nothing there

Yeah

What’s that like when you come across that stuff
Do you just not read it, and just

So (laughs)
Simply don’t pay attention to it, because it, it’s not true
Ok

Yeah

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

They’re against you, but you’ve been working with them for, for

Yes, so since 1997
Yes, but you see

Yeah

Obviously they didn’t have any sympathy to us because they lost
So they would love to find something which is wrong with what we are doing
They would love to prove that the treatment doesn’t

Yeah

So this is, very difficult
Ah, so the fact that they’ve, um, agreed that what we have has value, and they allow us to do phase 3 clinical trials, it means that we are right
Ok ?

Yeah

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

Yeah

So whatever Wikipedia says, well, I don’t care for them (laughing)

Ok, so, we, we talked a little bit about, what you, where you’ve come from, and what you’ve been through
As far as your treatment, um, to cancer, and this I’m very interested in, and why you don’t think high doses of chemotherapy is, is particularly helpful for the body, and what

Well it is generally wrong approach
It can help, some patients, wi, with a rare form of cancer, but only, eh, in limited capacity
Those who, are quote, unquote “cured”, usually die later on from adverse reactions, of chronic adverse reactions from chemotherapy or radiation, or they develop secondary cancer
So certainly, there is, this is not such a cure which you have in mind, that, use the treatment, patient recovers and lives normal life
Such cure does not exist for patients who are taking chemotherapy or radiation
They will always suffer, some problems
Either from cancer, or radiation, chemotherapy, and there is only small minority of patients who have advanced cancer who can, have long term responses
So obviously, this is unacceptable treatment
Of course, it was important at certain stage of development, but now, of course, uh, when we know more about cancer, it’s becoming, uh, unacceptable, and I think it will disappear, from the surface of the earth, in another 10 years, or 15 years, and, uh, in the medical textbook, this will be described as strange period of time, when people were using some barbaric treatment
Ok

Mmm
You have a number of different ways of treating cancer
So, one of them is the antineoplastons

Yes

This, this, this is the peptides

Mhmm

The, the this is the thing that my partner is on at the moment

Sure

in the clinical trial, and, uh, you’ve had some real great success

Mhmm

using that
Right ?

Yes

But you also have

Mhmm

another way, of, of, of treating, which is, using, it’s using some sort of chemotherapy, but in low doses

Well, um, um, whatever we are using we are using treatment which works on the genes

Antineoplastonswork on the genes, and they work on about 100 different genes

So what are they doing to the genes ?

Well, they work as molecular switches
They turn off the genes which are causing cancer, and turn on the genes which are fighting cancer
So, that’s what they do, and they produce this in about 100 different genes
It’s not enough, to control all cancer
Actually you can control some cancers, but not all of them, because you may have, numerous genes involved, in cancer
Well, for instance, in average case of breast cancer may have 50 abnormal genes involved
Uh, in, uh, like grade 3 brain tumors, for instance, anaplastic astrocytoma you might 80, or might be 100, but if, uh, you go to highly malignant tumors like, glioblastoma, you have, probably about 550
Eh, if you don’t cover such a spectrum of genes, you won’t, you’re not going to have good results
So that’s why, we know from the very beginning that we have some limitations
We can help some patients but not all of them, because, they have involvement of different genes which are causing, their cancer
So then you can still have these patients who are combining the treatmentof antineoplastons,with different medications which are in existence, which work on different genes, and this includes also some chemotherapy drugs, which are available
Eh, so this means that, um, for the patients for whom we, cannot use antineoplastons, because they are not in clinical trials, then we are using combination treatment, which consists of medication which already, approved as prescription medications, and, uh, by using the right combination by knowing which genes we need to attack, we get much better results
Now this also includes chemotherapy, but we never use, high-dose chemotherapy
If necessary, we use low-dose chemotherapy, and when you use low-dose chemotherapy you don’t have, uh, toxicity, which is, bad
We use this for
patients continuously, without much problem

So, so one of the main reasons of using low-dose chemotherapy is to try and keep your immune system strong, as well ?

No, to try to quickly decrease the size of the tumor, in combination with the other medications
We can use, for instance, low-dose chemotherapy and another medication which will increase activity,of chemotherapy, and as a result, you can have, as good, uh, uh, decrease of the tumor, with the low-doses

when you use heavy-dose
Well, there’s nothing unusual about it
For instance, uh, many doctors are using medications which are quite toxic

Mmm

And they, if they use the dosages, it’s helpful to the patient
The question is, what dosage will you use ?
If you use the dosages which are not toxic, it may still help the results, for instance, eh, the medication which was introduced, in mid, uh, 18th century for a particle for heart failure, in U.K. by
Dr. Withering, which was digitalis extract
Obviously it was highly toxic medication
It can kill people, in dosages much smaller than chemotherapy, but if you use the right dosage, it can help people
It was helping people for over 200 years
So those are the question
What kind of dosage do you use, and what combination do you use, and then, it can be useful

How did work that out then ?
I mean, how did you work out

Mhmm

that using small dosages of chemotherapy, could be effective ?

Uh, well, uh, it’s not only based on, uh, our research, it’s based on the research of the other, doctors
There are numerous publications on the subject, and in many cases the low-dosages can be used more effective than high-dosages, and, uh, on the other hand, by doing genetic testing, we can identify, which, uh, medications are the best for the patient

‘Cause you use

(?)

’cause you use a lab, in Phoenix
Right ?

Correct, yes

And, and how did you find out about them ?
Um, how did you ?
Yeah

Well, uh, uh, frankly speaking (laughs), 1st time I find about it by, treating patients who’s referred to us by one of the best oncologists in the country
He was usually treating some movie stars (laughs)

Yeah

and I found that this patient had, uh, genetic testing done, and I got interested in this, and I found about this laboratory
It was some time ago, but anyway, while we were doing genetic testing before, but, uh, we didn’t use this laboratory yet, we did it, through some other laboratories, and such testing was much, much simpler
So, we are using such testing, for a number of years, but in the capacity we are using now, this is really the last 2 to 3 years

So what happens is someone’s, bit of their tissue gets sent off to this lab ?

Yeah, the tissue is sent to the laboratory, and, uh, they do, testing on the entire genome of 24,000 genes
They identify the abnormal genes, and they go in-depth, by studying what happened to these genes?
Are they mutated ?
Are they amplified ?
And then from this, we have, a lot of information, and ultimately we like to know, which medications we can use to treat genes
What we are doing, we are treating genes, rather than, the tumor, as such

Mhmm

And, uh, if you identify all the genes that are involved, and find out which medications we can use, we can have very good results

And that’s what you found ?

That’s right

So in some case you’re treating people that might have a certain type of cancer

Yes, mhmm

with a drug that was designed for a different type of cancer

Uh, that’s right, because we are treating the genes, and, uh, if you find out that, this particular patient has, uh, an abnormal gene, which is not typical for this cancer but we have medication

Hmmm

that works on this gene, that’s what we use

So I would imagine that to treat, uh, that to treat people, this way, is obviously the future
Everyone’s different
Everyone’s genetics are d, d, different

That’s right

genetic markers, but to treat them that way, would require a bit more work

That’s, uh, obviously (laughs) (a life’s ?) work
Uh, uh, we’ll, like, uh, not just simply for, eh, uh, 4 different types of lung cancer

Yeah

Maybe 100,000 different types of lung cancer, each with, different, uh, genetic signature, ok, and once you identify this, then you can treat, such patients logically, and have good results, and if you do it on the scale of, uh, the entire country, this would, uh, give you much better results, and, uh, great savings, because

Mmm

you won’t use expensive medications for everybody, but perhaps for 10% of the population, and then for this 10% of population is going to work

Yeah

Which means that these people will avoid disability
They won’t spend time in the hospital
Uh, they will have short course of treatment, and then they go back to work
So the government would understand, uh, that’s something that can give them a lot of savings
I think they will go for it
Eh, gene testing, eh, at this time is still, uh, relatively expensive
It’s covered by, uh, the insurance of the United States, but for people outside, may cost 5500 euros, for instance, but I think it will be substantially less expensive in the near future
I think it will be below $1,000 for complete testing
So for running the test, uh, uh, eh, and, uh, finding out which treatment, has the best chance, you can save, 100’s of 1,000’s of dollars for individual patients

Yeah, but obviously pharmaceutical companies probably wouldn’t be too happy about that

No, no

People aren’t going to be taking their medications anymore

Well obviously be mostly happy that they can sell a lot of medications, but some of them are beginning to pay the attention, because they have to, because if they don’t, their competitors, will pay the attention

Mmm

Obviously, they would like to have, possibly, the best possible results, in clinical trials, so now they begin to screen population of patients for clinical trials, and do some limited, genetic testing, but, so, of course, they do it, uh, for the better of clinical trials so have best results

Yeah

Doesn’t mean that they’ll do, do it when they sell medicine, to millions of people commercially
They may forget about mentioning this medicine works the best for

Yes

this population of patient (laughs)

So what’s your, your vision ?
Wha, wha, what do you, striving to achieve ?

Well what I am trying to achieve is to introduce the way we treat patients, in, in various countries in the world, and, uh, what this would accomplish is, 1st of all, much better results of the treatment, much simpler treatment where perhaps only 1% of patient would need hospitalization, which would, uh, result in great savings
Uh, the treatment, uh, will be done for shorter period of time
For instance, few months to get rid of the tumors, then, uh, perhaps a year, to stabilize the results, and then go back, working and living, ok, without cancer
This, uh, genetic, genomic testing would be absolutely done for every patient who will come for treatment, to identify, what is the best treatment combination indication
So that’s what I would like to foresee, and then, of course, um, immediately, you substantially reduce, the expenditures for medical
For instance, if, you assume that in the mid, medium-sized country, will spend, for instance, a billion dollar, for, socialized medical treatment which will coincide with hospitalization
Ok
Uh, then, uh, most of the cost is for hospitalization, and services necessary for keeping the patient in hospital, then treating adverse reactions, which are, occurring because of the poor selection of medications
Eh, then if you switch to the outpatient treatment because you use medications which are not going to give such bad, side-effects, because you select this medication based on genomic testing, ok, and then immediately instead of a billion dollars a year, you cut down your expenditures to about $100,000

Yeah

100 million dollars
Ok ?
Probably slash it 10 times
Ok ?
And then people will be happy because, ah, the don’t need to stay in the hospital for a long time
They have less adverse reactions
They can go to back to work, much sooner
Ok
So that’s what I, can foresee as, the treatmentin the future
Not really hospital-based treatment

Mhmm

for patients, and most hospitalization is required because of adverse reactions from chemotherapy, radiation, but outpatient treatment, much easier treatment, also
medication given in tablet forms, for instince

And that’s what you’re doing here, right ?
I mean

Correct, yes correct
Usually in hospital, only, perhaps, for, one or two percent of patients, and, we would like to avoid it because when the patient goes to the hospital, he can pick up, some in-opportunistic infection, and then we are talking about more problem
Of course, I believe detection of cancer will be very important, because you don’t want to, uh, have a patient who is so advanced that he is fighting for, life, and he needs to be in the hospital
Ok

Yeah

If you had diagnosis in the early stages, then the patient does not need hospitalization
He can be treated very easily, then go back to work
So that’s the issue
And of course prevention is another important issue to us
To identify, changes in the body, which may indicate that the patient has already, early stages of cancer, also based on genetic tests, and get rid of this by using, behavior modification, by using proper diet, by using supplements, whatever, even without any medications

So, you’re obviously very passionate about what you do
Right ?
That, that’s my question about that

Well, I think it can help s, people in a great way, and, uh,

Well it can, I mean

Yeah

You have had so many su

Yes

I mean, I was talking to my girlfriend

Yeah

the other day,

Yeah

I mean, people, you know, you hear people say, this is a scam, and I was thinking, well the, if it is a scam

Yeah

it has to be one of the biggest scams ever

(laughing)

because all you’ve gotta do, is look on the walls

Yeah

and you look at those photographs

Yeah

Perhaps, this won’t surprise you
I’ve spoken to some oncologists just in the U.K., and they say, all of these people that you have helped, they either ever had cancer in the 1st place

Mhmm

or they were misdiagnosed

Yeah

or, uh, they went into spontaneous remission

Yeah, well

or they, it was the chemotherapy or radiation

These people, they don’t know what they do
They never, have never seen our results, and obviously they can’t believe that something like this could happen, but suddenly (laughs), in this room we are in now, we have some of
the top experts in the country, like people from FDA, who are expert oncologists, specialists

They’re working with you

Oh, they came here to inspect what we have

Yeah

They look at every scan of the people who are in clinical trials, and they decided that we have very good results

And is that stuff going to be published at some point ?

Ah, yes, we are publi, we are preparing this for publication, but, uh, obviously, in order to have the right results, you need, time, and most of our clinical trials began, approximately 10 years ago
So then we, if you would like to know what happen after, 10 years with these people

Mhmm

then you need to have a little time
So now we are preparing a number of, uh, publications, uh, and so this year we should have a number of publications, which will show final results
So far we didn’t have, final results, so were only interim reports, during the course of clinical trials

And with, uh, with brain tumors; because obviously, that’s an area that you’ve had

Yeah

huge suc, success rate

Yeah

What, why has that, do you think, as opposed to the other, types ?

Because that’s where we selected

Mhmm

We wanted to have something difficult
Ok (laughs)

Yeah

Because, uh, for the same reason that you mentioned
If you’d had something easier then, the doctors could say: “Well, this cancer usually disappears in its own”
And they are right
Some cancers may disappear on its own, in some higher percent than the others

Mhmm

But you know, brain tumors, you read, they never disappear on their own

Yeah

So that’s why we, decided to select such type of malignancies which are the most difficult

So what’s that been like when you’ve seen, I mean, I’ve seen obviously Jodi Fenton’s story

Yeah

Whe, whe, when you see these people’s

Yes

uh, scans

Yeah

and you see that that tumor has shrunk

Yeah

or broken down

Yeah

wha, what does that feel like ? (laughing)

Well, we see this all the time
(?) it just happens almost every day
Even today that we saw the patient, uh, who has pancreatic cancer, and after a few months of treatment it’s practically gone, and she is the wife of a doctor (laughs)
They came together, and that’s, that’s what we see practically every day
Ok

That must give you great strength to

Absolutely

continue

Absolutely, yes
So that’s something which is gratifying (laughs)

Yeah
What do you think the future is as far as drugs for cancer are concerned ?

I believe that, we are still at a very early stages of development in this area, but the future will be, with medications which are, highly specific, they will work on the genes that are involved in cancer
So, they will not harm normal part of the body, and, du, du, how to combine this medications will be established by, the special software, which will guide the doctors how to use proper medication for individual patient
I think this will be the, um, treatment that will be designed for, individual patient, and such design, it is not necessary to be done by the doctor
I think it should be, uh, certain computerized system which will put together, the best possible treatment plan, for a patient; which obviously needs to be checked and approved by the doctor
So I believe that this will be the future of medicine for the next, say, 40, and 50 years, coming up with better and better medications, which will be genomic switches, which will turn off, the cancerous process by regulating the genes which are involved; they simply will bring, the activity of these genes to normal levels, and finally, the new generation of medication which should work on cancerous stem cells, and, the medications which can kill cancerous stem cells without, uh, producing any harm to normal stem cells
So this will be the clue for, long-term control of cancer, because if you don’t eliminate, cancerous stem cells then the cancer will come back

Yeah

And that’s why chemotherapy, usually is unable to control cancer for a long time because, it’s pretty much powerless, ah, uh, regarding action on cancerous stem cells
But then after that, I think that we will make another, jump, and there will be, uh, procedures that will based on biophysics

Mmm

and by trying to get rid of, uh, the cancer and some of the diseases by effecting the body by using various, uh, wipes, which will be like magnetic wipes, it will be some other types of wipes, but using proper frequencies to, normalize all the cells in the body to normalize the activity of the genes
I think this will be a

Mmm

probably the next, uh, say 50 years of, uh, the end of this century when such (?)

So no one’s getting funding really, unless they’re doing it privately to,
being able to, isn’t that being able to research these areas, because funding really comes from pharmaceutical companies ?

Ah, well, most of this funding is from pharmaceutical companies, and also it is coming from the National Cancer Institute but, I think it’s regulated behind the scenes by the pharmaceutical companies
Eh, but they are still some researchers who are trying to do it on their own
Very few of them
I think there’s articles, in the Science magazine, some time ago which was talking about, uh, few of these researchers who are still trying to do, research on their own, and, I think, uh, I think there were probably some 4 or 5 of them in U.K. (laugh)

Yeah

still involved in research on their own

So what ah, what about the role of the mind ?
Do you think that, if someone has cancer and they wanna be well, do you think the way that someone thinks is important ?

Absolutely, that’s very important because, this, uh, can be translated, ah, to various biochemicals which can influence cancer
So obviously this is very important but, the question is how to, ah, direct this in the proper way
Ok
How to quantify this
So that’s something that should be done in the future

And nutrition as well

Yes, absolutely, yes
Why all have a lot of important chemicals in nutrition which can effectuate cancer, but regarding the mind you have to translate, uh, for instance, biophysical factors, in the brain, into biochemical factors, and certainly, that’s what the body’s doing all the time, but how to mobilize it, that’s a different story
Yeah

So if someone wants, if someone came to the Burzynski Clinic, wh, wh, what could they expect, to happen here?

Well 1st of all, we would like to give a selection, and we don’t want the people who we cannot treat to come
Uh, at this time we rather avoid, uh, patients in early stages of cancer, because with such patients, uh, what is used is standard of care treatment, and we prefer to refer them to, ah, different doctors
So we prefer to treat it once cancer patient, because, uh, they cannot be helped by the other doctors, and, uh, when they come to our clinic, we try to find out 1st, see if we can really help them or not, and, uh, once they come to the clinic, in most of the cases we can try to, help them, of course, and, uh, we put together, the personalized treatment plan, which is (?)

But all of those go through you
You look at every single one of those

Yes
I’m seeing every patient, who’s coming, if I’m

Yeah

if I’m around here, but, after that all the patients are really assigned to different senior physician and they’re responsible for daily care of patient here

How many people do you have, working here now ?

About 150 people here, yes

And you started with, well, just one (?)

Eh, I think really when we moved from Baylor College I had about 7 people at that time

Yeah

Yes, because, some of these doctors who are working together at Baylor College decided to leave together with me, including my wife, because she was also working at Baylor College

Yeah

Ok

Thank you

You’re welcome
My pleasure

Thank you so much

Thank you very much
Ok
======================================

======================================

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

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

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

“Burzynski … antineoplastons … “:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

� � � � � � � � � � � � � � � �
[25] 12/1996 PHENYLACETATE (PA) and related aromatic fatty acids constitute novel class of relatively nontoxic antineoplastic agents
————————————————————
Using human breast carcinoma MCF-7 cells as model, we show PA-induced growth arrest associated with enhanced expression of cyclin-dependent kinase inhibitor p21Waf1/Cip1 …
————————————————————
induction of p21WAF1/CIP1 mRNA by PA independent of cellular p53 status
————————————————————
PA effectively induced p21WAF1/CIP1 mRNA and growth inhibition of wild-type mouse embryonal fibroblasts
————————————————————
findings strongly support role for p21Waf1/Cip1 in PA-mediated inhibition of cell growth
� � � � � � � � � � � � � � � �
[26] 1996 Cytotoxic chemotherapies often give rise to multidrug resistance, which remains major problem in CANCER management
————————————————————
In pursuit of alternative treatments for chemoresistant TUMOR CELLS, we tested response of multidrug-resistant (MDR) TUMOR CELL lines to aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB), 2 differentiation inducers currently in clinical trials
————————————————————
Both compounds induced cytostasis and maturation of multidrug-resistant BREAST, OVARIAN, and COLON CARCINOMA CELLS with no significant effect on cell viability
————————————————————
MDR cells generally more sensitive to GROWTH ARREST by PA and PB than parental counterparts
————————————————————
PA and PB potentiated the cytotoxic activity of doxorubicin against MDR cells
————————————————————
Taken together, our in vitro data indicate PA and PB, differentiation inducers of aromatic fatty acid class, may provide alternative approach to treatment of MDR TUMORS
� � � � � � � � � � � � � � � �
[27] 8/1997 aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB) are novel ANTITUMOR AGENTS currently under clinical evaluation
————————————————————
ability to induce TUMOR differentiation in laboratory models and low clinical toxicity profile makes them promising candidates for COMBINATION with CONVENTIONAL THERAPIES
————————————————————
In present studies, we characterized interactions between aromatic fatty acids and radiation, using as a model cell lines derived from CANCERS of PROSTATE, BREAST, BRAIN and COLON
————————————————————
in vitro findings identify aromatic fatty acids PA and PB as new class of non-toxic modulators of radiation response, antagonistic effect of these compounds on radiation response needs further examination
————————————————————
data strongly suggest that for PA or PB to have role in clinical radiotherapy, appropriate scheduling of combination therapies must take into account time-dependent effects in order to achieve clinical radiosensitization
� � � � � � � � � � � � � � � �
[28] 11-12/1997 Antineoplaston AS2-1 EXHIBITS CYTOSTATIC GROWTH INHIBITION of human hepatocellular carcinoma cells in vitro and showed minimum adverse effects in phase I clinical trial
——————————————————————
2 clinical cases of liver cancer (hepatocellular carcinoma and multiple liver metastases from colon cancer) in whom we believe antineoplaston A2-1 useful as maintenance therapy after transcatheter arterial embolization (TAE) and microwave coagulation necrosis (MCN)
——————————————————————
2 patients have continued to be in good condition for more than 2 years without limitation of normal activities
——————————————————————
Antineoplaston AS2-1 may be effective and useful as maintenance agent after TAE and MCN in patients with liver cancer
� � � � � � � � � � � � � � � �
[29] 1997 PHENYLACETATE and analogs represent new class of pleiotropic growth regulators that alter TUMOR CELL biology by affecting GENE EXPRESSION at both transcriptional and post transcriptional levels
————————————————————
Based on findings, NaPA and NaPB entered clinical trials at NATIONAL CANCER INSTITUTE
————————————————————
Ongoing phase I studies with NaPA, involving adults with PROSTATE and BRAIN CANCER, confirmed therapeutic levels can be achieved with no significant toxicities, and provide preliminary evidence for benefit to patients with advanced disease (Thibault et al., submitted)
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[34] 8/31/2000 Antineoplastons are naturally occurring CYTODIFFERENTIATING AGENTS
—————————————————————
Findings confirm presence of immune defects among patients with breast cancer and results should stimulate development of new strategies to induce and augment immunity for treatment of breast cancer
—————————————————————
Antineoplaston A-10 may provide rational basis for designing trials to employ its immune modulatory potentials as adjuvant therapy in breast cancer patients
� � � � � � � � � � � � � � � �
[35] 12/2000 4 new piperidinedione A10 analogs synthesized and tested for antimitotic activity on human breast cancer cell line against prototype A10 and antibreast cancer drug tamoxifen
—————————————————————
“3B” and “3D” were several-fold more potent ANTIPROLIFERATIVE AGENTS than A10 and tamoxifen and had significantly higher capacity to bind DNA than A10
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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)
======================================
� � � � � � � � � � � � � � � �
======================================
[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
� � � � � � � � � � � � � � � �

� � � � � � � � � � � � � � � �
References:
� � � � � � � � � � � � � � � �
[1] 7/1971
� � � � � � � � � � � � � � � �
Neish, W. J. P. Phenylacetic acid as a potential therapeutic agent for the treatment of HUMAN CANCER. Experientia (Basel), 27: 860-861, 1971
http://www.ncbi.nlm.nih.gov/pubmed/5139518/
Experientia. 1971 Jul;27(7):860-1
http://www.ncbi.nlm.nih.gov/m/pubmed/5139518/
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[3] 1990
� � � � � � � � � � � � � � � �
BURZYNSKI, S. R., Kubove E., Burzynski, B. Treatment of hormonally refractory CANCER of the prostate with ANTINEOPLASTON AS2-1. Drugs Exp. Clin. Res., 16: 361-369, 1990
http://www.ncbi.nlm.nih.gov/pubmed/2152694/
Drugs Exp Clin Res. 1990;16(7):361-9
http://www.ncbi.nlm.nih.gov/m/pubmed/2152694/
� � � � � � � � � � � � � � � �
[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
http://www.ncbi.nlm.nih.gov/m/pubmed/1372534/
Cancer Res 1992;52:1988-1992
http://m.cancerres.aacrjournals.org/content/52/7/1988.abstract
Cancer Res April 1, 1992 52; 1988v I
http://cancerres.aacrjournals.org/content/52/7/1988
Cancer Res. 1992 Apr 1;52(7):1988-92
http://m.cancerres.aacrjournals.org/content/52/7/1988.full.pdf
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
http://m.cancerres.aacrjournals.org/content/52/7/1988.full.pdf#page=1
SAMID D, Shack S, Ti-Sherman L PHENYLACETATE-A novel nontoxic inducer of TUMOR CELL differentiation. Cancer Res 52:1988, 1992
� � � � � � � � � � � � � � � �
[5] 9/15/1992
� � � � � � � � � � � � � � � �
SAMID, D., Yeh, A., and Prasanna, P. Induction of erythroid differentiation and fetal
hemoglobin production in HUMAN leukemic cells treated with PHENYLACETATE. Blood, 80: 1576-81, 1992
http://www.ncbi.nlm.nih.gov/pubmed/1381630/
SAMID D, Yen A, Prasanna P . Induction of erythroid differentiation and fetal hemoglobin production in HUMAN leukemic cells treated with PHENYLACETATE . Blood. 1992;80:1576
http://www.ncbi.nlm.nih.gov/m/pubmed/1381630/
Blood, 80: 1576-1581, 1992
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.abstract
Blood. 1992 Sep 15;80(6):1576-81
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.full.pdf
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD
� � � � � � � � � � � � � � � �
[6] 5/1993
� � � � � � � � � � � � � � � �
SAMID D, Shack S , Myers CE . Selective growth arrest and phenotypic reversion of prostate CANCER CELLS in vitro by nontoxic pharmacological concentrations of PHENYLACETATE . J. Clin. Invest . 1993;91:2288
http://www.ncbi.nlm.nih.gov/pubmed/8486788/
J Clin Invest. 1993 May;91(5):2288-95
http://www.ncbi.nlm.nih.gov/m/pubmed/8486788/
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC288233/

http://m.jci.org/articles/view/116457
� � � � � � � � � � � � � � � �
[7] 2/15/1994
� � � � � � � � � � � � � � � �
SAMID, D., Ram, Z., Hudgins, W. R., Shack, S., Liu, L., Waibridge, S., Oldfield, E. H., and Myers, C. E. Selective activity of PHENYLACETATE against MALIGNANT GLIOMAS: resemblance to fetal brain damage in phenylketonuria. Cancer Res., 54: 891-895, 1993
http://www.ncbi.nlm.nih.gov/pubmed/8313377/
Cancer Res. 1994 Feb 15;54(4):891-5
http://www.ncbi.nlm.nih.gov/m/pubmed/8313377/
Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
� � � � � � � � � � � � � � � �
[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.
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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)
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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&
� � � � � � � � � � � � � � � �
[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
� � � � � � � � � � � � � � � �
[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

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

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

� � � � � � � � � � � � � � � �
[36] 8/2001
� � � � � � � � � � � � � � � �
A phase Idose escalation and bioavailability study of oral sodium PHENYLBUTYRATE in patients with refractory solid tumor malignancies
http://www.ncbi.nlm.nih.gov/pubmed/11489804
Clin Cancer Res 7(8):2292-300 (2001), PMID.11489804
http://www.ncbi.nlm.nih.gov/pubmed/11489804
Clin Cancer Res. 2001 Aug;7(8):2292-300
http://m.clincancerres.aacrjournals.org/content/7/8/2292.long
J Gilbert, S D Baker, … M A Carducci
SAMID References: 2-3, 5-6, 15 and 22
� � � � � � � � � � � � � � � �
[37] 2002
� � � � � � � � � � � � � � � �
A novel strategy for remission induction and maintenance in cancer therapy
H Tsuda A10 and AS2-1
http://www.ncbi.nlm.nih.gov/pubmed/11748457
Oncol Rep 2002;9:65–8
http://www.ncbi.nlm.nih.gov/m/pubmed/11748457
Oncol. Rep. 2002;9:65-68
http://www.spandidos-publications.com/or/9/1/65
Oncol Rep 9(1):65-8 (2002)
Oncology Reports, Spandidos Publications
Department of Anesthesiology, Kurume University, School of Medicine, Fukuoka-ken, Japan
� � � � � � � � � � � � � � � �
[38] 3 – 4/2003
� � � � � � � � � � � � � � � �
The preventive effect of antineoplaston AS2-1 on HCC recurrence
Hideaki H TSUDA Phase II Clinical Trial
http://www.ncbi.nlm.nih.gov/pubmed/12579278
Oncol Rep. 2003 Mar-Apr;10(2):391-7
http://www.ncbi.nlm.nih.gov/m/pubmed/12579278
Oncol Rep. 2003;10:391-397
http://www.spandidos-publications.com/or/10/2/391
Spandidos Publications
http://www.burzynskiclinic.com/images/stories/Publications/964.pdf
Oncology Reports 10: 391-397, 2003
Oncol Rep 10 (2):391-7 (2003)
Oncol Rep 2003;10:391–7
Department of Anesthesiology, Kurume Daiichi Social Insurance Hospital, Kushihara Kurumeshi, Fukuoka, Japan
� � � � � � � � � � � � � � � �
[39] 2003
� � � � � � � � � � � � � � � �
Long-term survival following treatment with antineoplastons for colon cancer with unresectable multiple liver metastases: report of a case
http://www.ncbi.nlm.nih.gov/pubmed/12768372
Long-Term Survival Following Treatment with Antineoplastons for Colon Cancer with Unresectable Multiple Liver Metastases:
Report of a Case
Hideaki Tsuda A10 and AS2-1 – Phase II Clinical Trial
http://www.springerlink.com/content/b48ch3ha165nbrqp
Surg Today. 2003;33(6):448-53
http://link.springer.com/article/10.1007%2Fs10595-002-2503-2
Surg Today 2003; 33:448–53
http://link.springer.com/content/pdf/10.1007%2Fs10595-002-2503-2
Surg Today. 2003; 33:448-453
http://link.springer.com/article/10.1007%2Fs10595-002-2503-2?LI=true
33 (6):448-53
http://link.springer.com/content/pdf/10.1007%2Fs10595-002-2503-2
Surgery Today, Springer
http://sciencelinks.jp/j-east/article/200313/000020031303A0389449.php
Surg Today 2003
http://sciencelinks.jp/j-east/article/200313/000020031303A0389449.php
DOI: 10.1007/s10595-002-2503-2
http://ci.nii.ac.jp/naid/10015483373
Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan
http://ci.nii.ac.jp/naid/10015483373
� � � � � � � � � � � � � � � �
[40] 2003
� � � � � � � � � � � � � � � �
http://www.ncbi.nlm.nih.gov/pubmed/12718563
——————————————————————
Drugs in R and D
——————————————————————
http://www.ncbi.nlm.nih.gov/m/pubmed/12718563
——————————————————————
(Drugs in Research and Development)
——————————————————————
http://www.burzynskiclinic.com/images/stories/Publications/960.pdf
——————————————————————
Drugs R D. 2003;4(2):91-101
Drugs in R&D 2003;4:91-101
——————————————————————
Pg. 100
======================================
[22] Tsuda H, Hara H, Eriguchi N, et al. Inhibitory effect of antineoplaston A10 on breast cancer transplanted to athymic mice and human hepatocellular carcinoma cell lines. Kurume Med J 1990; 37: 97-104
——————————————————————
[23] Wood J, Copland JA, Muldoon TG, et al. 3-phenylacetylamino-2, 6-piperidinedione inhibition of rat Nb2 lymphoma cell mitogenesis. Proc Soc Exp Biol Med 1991; 197: 404-8
——————————————————————
[24] Xu-W, Yu R, Gao C, et al. The preliminary antitumor assay of antineoplaston A10 against the s180 and the effects of cAMP levels in tumor and liver tissues of mice. Adv Exp Clin Chemother 1988; 2: 41-4
——————————————————————
[25] Hashimoto K, Kogo T, Shintomi Y, et al. The anticancer effect of antineoplaston A10 on human breast cancer serially transplanted to athymic mice. Nippon Gan Chiryo Gakkai Shi 1990; 25: 1-5
======================================
Pg. 101
——————————————————————
[26] Burzynski SR. Purified antineoplaston fractions and methods of treating neoplastic disease. US patent 4,470,970. 1984
——————————————————————
[27] Burzynski SR. Phase I clinical studies of antineoplaston AS2-5 injections. In Ishigami J, editor. Recent advances in chemotherapy. Tokyo: University of Tokyo Press, 1985: 586-7
——————————————————————
[28] Burzynski SR. Potential of antineoplastons in diseases of old age. Drugs Aging 1995; 7: 157-67
======================================
[29] Chang SM, Kuhn JG, Robins HI, et al. Phase II study of phenylacetate in patients with recurrent malignant glioma: a North American Brain Tumor Consortium Report. J Clin Oncol 1999; 17: 984-90
======================================
[30] Buckner JD, Malkin MG, Reed E, et al. Phase II study of antineoplaston A10 (NSC 648539) and AS2-1 (NSC 6200261) in patients with recurrent glioma. Mayo Clin Proc 1999; 74: 137-45
——————————————————————
[31] Burzynski SR. Efficacy of antineoplastons A10 and AS2-1. Mayo Clin Proc 1999; 74: 641-2
� � � � � � � � � � � � � � � �
[41] 8/2005
� � � � � � � � � � � � � � � �
Antineoplaston induces G1 arrest by PKCα and MAPK pathway in SKBR-3 breast cancer cells
Hideaki H TSUDA Antineoplaston A10
http://www.ncbi.nlm.nih.gov/pubmed/16012735
Antineoplaston induces G1 arrest by PKCo and MAPK pathway in SKBR-3 breast cancer cells
http://www.ncbi.nlm.nih.gov/m/pubmed/16012735
Antineoplaston induces G(1) arrest by PKCalpha and MAPK pathway in SKBR-3 breast cancer cells
http://www.spandidos-publications.com/or/14/2/489
Oncol Rep. 8/2005; 14(2):489-94
http://gyouseki.kurume-u.ac.jp/PDF/ichiran_2005.pdf
Oncol Rep 14(2):489-94 (2005)
http://research.kurume-u.ac.jp/K90RES.php?scode=49485632873864
Oncol Rep. 2005; 14:489–94
http://onlinelibrary.wiley.com/doi/10.1002/iub.574/abstract
Oncol. Rep. 14, 489–494
http://onlinelibrary.wiley.com/doi/10.1002/iub.574/full
Oncology Reports, 8/2005, Volume 14 Number 2
Pages: 489-494
http://onlinelibrary.wiley.com/store/10.1002/iub.574/asset/574_ftp.pdf?v=1&t=hbr9z60q&s=0b1c1e8655db9c54b45dbf72062e8b11cb7895ac
Oncology Reports, Spandidos Publications
Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan
� � � � � � � � � � � � � � � �
[42] 2006
� � � � � � � � � � � � � � � �
Inhibitory Effect of Antineoplaston A10 and AS2-1 on Human Hepatocellular Carcinoma
Tsuda H, et al
http://www.ncbi.nlm.nih.gov/pubmed/8755117
Kurume Med J. 1996;43(2):137-47
http://www.ncbi.nlm.nih.gov/m/pubmed/8755117
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article
Kurume Medical Journal
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_pdf
� � � � � � � � � � � � � � � �
[43] 1/2008
� � � � � � � � � � � � � � � �
Preclinical studies of molecular-targeting diagnostic and therapeutic strategies against breast cancer
http://www.ncbi.nlm.nih.gov/pubmed/18224398
antineoplaston
http://www.ncbi.nlm.nih.gov/m/pubmed/18224398
Breast Cancer 15(1):73-8 (2008)
DOI: 10.1007/s12282-007-0015-y
http://link.springer.com/article/10.1007%2Fs12282-007-0015-y
Breast Cancer. 2008;15(1):73-8. doi: 10.1007/s12282-007-0015-y
http://www.springerlink.com/content/p724x34746l56v73
15(1):73-8
http://ci.nii.ac.jp/naid/10021288533
Breast Cancer: January 2008, Volume 15, Issue 1, pp 73-78
Department of Surgery, Kurume University, Fukuoka, Japan
Burzynski Reference: 12
Tsuda (Japan) Antineoplaston Reference: 13
� � � � � � � � � � � � � � � �
[44] 10/2010
� � � � � � � � � � � � � � � �
Antineoplaston A10 phenylacetyl glutamine (PG)
http://www.springerlink.com/content/tj0177485773007t
(S)-2-((S)-2-(4-(3-[18F]fluoropropyl)benzamido)-3-phenylpropanamido)pentanedioic acid labeled with 18F
http://link.springer.com/article/10.1007%2Fs10967-010-0633-2?LI=true
(S)-2-((S)-2-(4-(3-[18 F] fluoropropyl) benzamido)-3-phenylpropanamido) pentanedioic acid labeled with 18 F
http://www.springerlink.com/content/tj0177485773007t
Journal of Radioanalytical and Nuclear Chemistry, 2010, 286, 1, 135
http://link.springer.com/article/10.1007%2Fs10967-010-0633-2
October 2010, Volume 286, Issue 1, pp 135-140
http://link.springer.com/article/10.1007/s10967-010-0633-2/fulltext.html
DOI
10.1007/s10967-010-0633-2

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

Critiquing: Dr. David H. “Orac” Gorski, M.D., Ph.D, L.I.A.R.

L.I.A.R.

Lacking
Integrity
And
Respect

Respect is EARNED

Dr. David H. “Orac” Gorski has NOT earned respect

Neither does he deserve it

6/4/2013 Gorski made an amazing 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”

“how Burzynski never explains which genes are targeted by antineoplastons … “
——————————————————————
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/
======================================
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:
——————————————————————
Gorski, here’s

” … how Burzynski never explains which genes are targeted by antineoplastons … “
======================================
[1] Pg. 98
——————————————————————
ras oncogenes
tumor suppressor gene p53
ras oncogene protein p21ras
p21 gene

======================================
[2] Pg. 47
——————————————————————
oncogenes
tumor suppressor genes

——————————————————————
Pg. 48
——————————————————————
gene p53
WRN gene

——————————————————————
Mechanism of Action of Antineoplaston
——————————————————————
tumor suppressor genes
oncogenes
p21 protein
p53 gene

——————————————————————
Pg. 49
——————————————————————
tumor suppressor gene p53
tumor suppressor gene p21

======================================
[3] Pg. 257
——————————————————————
tumor suppressor genes
oncogenes

——————————————————————
Pg. 260 Discussion
——————————————————————
oncogene AKT2
oncogene RAS
oncogene MYCC
tumor suppressor p53
tumor suppressor p21
tumor suppressor PTEN
tumor suppressor INI1

======================================
[4] Pg. 385
——————————————————————
AKT2 pathway
TGFB1 pathway
RAS
TP53
p21

======================================
[5] Pg. 386
——————————————————————
RAS pathway
AKT2 pathway
TGFB1 pathway
p53 tumor suppressor gene
p21 tumor suppressor gene

======================================
[6] Pg. 323 Discussion
——————————————————————
TP53 gene
——————————————————————
Pgs. 323-324
——————————————————————
RAS oncogene
TP53 tumor suppressor gene
p21 tumor suppressor gene
NF1 tumor suppressor gene
p21 RAS protein
RNAi
dsRNA
siRNA
RAS oncogene pathway (GF-RTK-RAS)
oncogenes
oncogene AKT2

======================================
[7] Pg. 173 Discussion
——————————————————————
proto-oncogene MYCC, ERBB2
——————————————————————
Pg. 174
——————————————————————
sonic hedgehog (SHH) receptor patched (PTCH)
MYCC
MYC-MAX dimers
G1-S
gene CCD2 (encoding cyclin D2)
gene CDK4 (which encodes cyclin dependent kinase 4)
KIP1
(or p27)
CUL-1
CKS
MYC
cyclin E-CDK2
INK4B
(or p15)
p21
cyclin E/CDK2
MIZ1 (MYC-interacting zinc finger protein 1)
CDKN1A
CDKN2B
MAD protein
MEFD2D (MADS box transcription enhancer factor
17p
tumor-suppressor gene HIC-1 (hypermethylated in cancer-1)
RAS/MAPK
RAS pathway
RAS protein
AKT2
BCL2
BCL-X
BAX

——————————————————————
Pgs. 175-176 Charts
======================================
[8] Pg. 40
——————————————————————
RAS
AKT
TP53
PTEN
INI1
p21
MYCC
apoptosis pathway
DNA
p21 protein
RAS oncogene
INI1 protein
BCL-X

——————————————————————
Pg. 41 Targeted Therapy with Antineoplastons chart
——————————————————————
protein p21
RAS oncogene
RAS
BCL-2
tumor suppressor gene TP53
tumor suppressor gene p21
DNA
oncogene AKT2
oncogene MYCC
tumor suppressor gene PTEN
tumor suppressor gene MAD
INI1 protein
BCL-X protein

——————————————————————
Pg. 46 Discussion / Conclusion
——————————————————————
AKT/PTEN
RAS
p53
p21
MYCC
apoptosis pathways

======================================
[9] Pg. 384 E. Multitargeted therapy
——————————————————————
RAS pathway
AKT2 pathway
TP53 pathway
PTEN
INI1
p21 pathway
MYCC
apoptosis pathways
TGFB1 pathway
MAD

======================================
[10] Pg. 1068
——————————————————————
AKT2 pathway
MYCC pathway
TGFB1
PTEN tumor suppressor gene
MAD tumor suppressor gene
RANBP1
INI protein
RAS pathway
BCL2 pathway
tumor suppressor TP53
tumor suppressor p21

======================================
[11] Pg. 923
——————————————————————
AKT pathway
RAS pathway
TP53 pathway
p21 pathway
PTEN pathway

======================================
Burzynski, Hideaki Tsuda (Japan), and the p53 gene:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/03/04/burzynski-hitoshi-tsuda-japan-and-the-p53-gene/
� � � � � � � � � � � � � � � �
References:
� � � � � � � � � � � � � � � �
http://www.burzynskiclinic.com/scientific-publications.html
======================================
[1] 2003
——————————————————————
Interim Reports on Clinial Trials
16. 2003 (BT-11)
Phase II study of antineoplaston A10 and AS2-1 in patients with recurrent diffuse intrinsic brain stem glioma: a preliminary report
DRUGS IN R&D
——————————————————————
http://www.ncbi.nlm.nih.gov/pubmed/12718563
——————————————————————
Drugs in R and D
——————————————————————
http://www.ncbi.nlm.nih.gov/m/pubmed/12718563
——————————————————————
(Drugs in Research and Development)
——————————————————————
http://www.burzynskiclinic.com/images/stories/Publications/960.pdf
——————————————————————
Drugs R D. 2003;4(2):91-101
Drugs in R&D 2003;4:91-101
======================================
[2] 3/2004
——————————————————————
Review Articles on Clinical Trials:
1. 3/2004
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
Volume 3 Number 1 March 2004
======================================
[3] 9/2004
——————————————————————
Case Reports:
4. 9/2004 (Special Exception (SE) to BT-11 Study (ST))
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
DOI: 10.1177/1534735404267748
======================================
[4] 10/2004
——————————————————————
Interim Reports on Clinial Trials:
2. 10/2004
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
======================================
[5] 10/2004
——————————————————————
Interim Reports on Clinial Trials:
3. 10/2004 (Study (ST) and Special Exception (SE))
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
======================================
[6] 2004
——————————————————————
Interim Reports on Clinial Trials:
17. 2004 (BT-13 and BT-23)
Phase II study of antineoplaston A10 and AS2-1 in children with recurrent and progressive multicentric glioma :
a preliminary report
DRUGS IN R&D
——————————————————————
http://www.ncbi.nlm.nih.gov/pubmed/15563234
——————————————————————
Drugs in R and D
——————————————————————
http://www.ncbi.nlm.nih.gov/m/pubmed/15563234
——————————————————————
(Drugs in Research and Development)
——————————————————————
http://www.burzynskiclinic.com/images/stories/Publications/1194.pdf
——————————————————————
Drugs R D. 2004;5(6):315-26
Drugs R&D 2004;5(6):315-326.
======================================
[7] 6/2005
——————————————————————
Interim Reports on Clinial Trials:
18. 6/2005 (CAN-01 and BT-12)
Burzynski, S.R., Weaver, R.A., Janicki, T., Szymkowski, B., Jurida, G., Khan, M., Dolgopolov, V.
Long-term survival of high-risk pediatric patients with primitive neuroectodermal tumors treated with Antineoplastons A10 and AS2-1
——————————————————————
http://www.ncbi.nlm.nih.gov/pubmed/15911929
——————————————————————
Integr Cancer Ther. 2005 Jun;4(2):168-77
——————————————————————
http://www.ncbi.nlm.nih.gov/m/pubmed/15911929
——————————————————————
Integrative Cancer Therapies 2005;4(2):168-177
——————————————————————
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
======================================
[8] 3/2006
——————————————————————
Interim Reports on Clinial Trials:
19. 3/2006 (BT-03, BT-11, BT-18, and CAN-01)
Targeted therapy with Antineoplastons A10 and AS2-1 of high grade, recurrent, and progressive brainstem glioma.
——————————————————————
http://www.ncbi.nlm.nih.gov/pubmed/16484713
——————————————————————
Integr Cancer Ther. 2006 Mar;5(1):40-7
——————————————————————
http://www.ncbi.nlm.nih.gov/m/pubmed/16484713
——————————————————————
Integrative Cancer Therapies 2006;5(1):40-47
——————————————————————
http://www.burzynskiclinic.com/images/stories/Publications/5825.pdf
——————————————————————
DOI: 10.1177/1534735405285380
——————————————————————
http://m.ict.sagepub.com/content/5/1/40.long?view=long&pmid=16484713
======================================
[9] 12/2007
——————————————————————
Review Articles on Clinical Trials:
3. 12/2007
Recent clinical trials in diffuse intrinsic brainstem glioma. Cancer Therapy 2007; 5, 379-390.
——————————————————————
http://www.burzynskiclinic.com/images/stories/Publications/5692.pdf
——————————————————————
Review Article
Cancer Therapy Vol 5, 379-390, 2007
——————————————————————
http://www.cancer-therapy.org/CT/v5/B/HTML/42._Burzynski,_379-390.html
——————————————————————
Volume 5 Number 2 December, 2007
======================================
[10] 12/2008
——————————————————————
Interim Reports on Clinical Trials:
12. 12/2008
(BT-8 – PATIENTS WITH ANAPLASTIC ASTROCYTOMA)
(BT-15 – ADULT PATIENTS WITH ANAPLASTIC ASTROCYTOMA)
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
Abstracts for the Eighth Congress of the European Association for Neuro-Oncology (EANO), Sept. 12-14, 2008, Barcelona, Spain
======================================
[11] 12/2009
——————————————————————
Case Reports:
1. 12/2009 (BT-11 Special Exception (SE))
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
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
======================================