Stanislaw Rajmund Burzynski, Stanislaw R. Burzynski, Stanislaw Burzynski, Stan R. Burzynski, Stan Burzynski, S. R. BURZYNSKI, S. Burzynski, Arthur Burzynski, Hippocrates Hypocrite Hypocrites Critic Critics Critical HipoCritical
Tag Archives: “Critiquing: Dr. David H. “Orac” Gorski and The Skeptics™”
====================================== [0] – “Our only goal is to promote high standards of science in medicine”
====================================== [1] – 12/12/2012 – “Burzynski lumps all responses together in an oncologically meaningless way”
====================================== [2] – .3/14/2013
—————————————————————— “Temodar and Avastin both had proper, completed, and published phase II trials before approval”
====================================== [3] – .3/30/2013
——————————————————————
For years, Gorski has been able to comment on Burzynski’s “personalized gene targeted therapy” with impunity
It’s about time he received some personal attention, leading to heapin’ helpings of not-so-Respectful Insolence
All of the below articles by Gorski were tagged as having to do with:
personalized gene targeted cancer therapy, or mention it
—————————————————————— http://scienceblogs.com/insolence/tag/personalized-gene-targeted-cancer-therapy/
—————————————————————— I AM ADDING TO THIS AS I GO ALONG
====================================== [1] – 6/5/2013 – ” … in January the Burzynski Clinic removed all references to antineoplaston therapy on its website … “
—————————————————————— [2] – 8/4/2013 – I proved Gorski wrong since Burzynski’s scientific publications regarding antineoplaston therapy are on the Burzynski website
====================================== [1] – 6/5/2013 – “Three years should be plenty of time to line up clinical sites for a phase III trial”
“Of course, given that after three years the clinical trial hasn’t been opened, more than likely no reputable institution wants to partner with the Burzynski Research Institute, and ResearchPoint collected its checks”
—————————————————————— [3] – 7/18/2013 – This statement by Gorski is disingenuous since 6/3/2013 he reviewed Burzynski: Cancer Is Serious Business, Part II where this issue was addressed, and he made NO COMMENT about it in his review
Gorski can distort, exaggerate, and even lie to the public
====================================== [1] – 6/5/2013 – “Another interesting tidbit in the SEC filing is Burzynski’s report of the results of several of his clinical trials”
“They aren’t really “results’ per se, in that the information presented really isn’t provided in a form that really allows other investigators to evaluate it and potentially replicate it”
“Basically it’s a big table listing Burzynski Research Institute clinical trials”
“Of course, I realize that this is an SEC filing, not a scientific paper in the peer-reviewed literature, but if Burzynski has all this data to produce this table it boggles the mind that, given at least a decade and a half since these trials began, he hasn’t been able to publish any meaningful data thus far”
“That he hasn’t been able to do so is also a big red flag”
—————————————————————— [5] – 8/21/2013 – That Gorski has NOT been able to prove that the 4 Burzynski publications I refer to are NOT “meaningful data” is a big red flag
====================================== [6] – 6/4/2013 – “It’s a theme that is repeated throughout the report but that ignores the astounding level of sheer deception that goes on at the Burzynski Clinic, the allegations of overfilling, and how Burzynski has abused the clinical trial process to keep treating patients with antineoplastons without actually having to do the science that any other doctor would be required to do to validate a new treatment”
—————————————————————— [7] – 6/23/2013 – This is the 1st time I’ve seen Gorski allege “overfilling,” and I sure have NOT seen him provide any proof of that or that Burzynski is NOT doing “the science that any other doctor would be required to do to validate a new treatment”
If anyone is being “deceptive,” it seems to be Gorski
====================================== [6] – 6/4/2013 – 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, … “
—————————————————————— [8] – 8/7/2013 – Gorski has NO response for where I list where Burzynski “explains which genes are targeted by antineoplastons”
====================================== [6] – 6/4/2013 – ” … what the preclinical evidence supporting their efficacy are … “
—————————————————————— [9] – 3/16/2013 – Gorski does NOT mention where he’s reviewed “the preclinical evidence supporting their efficacy”
====================================== [6] – 6/4/2013 – ” … or what the scientific rationale is to expect that they might have antitumor activity”
—————————————————————— [10] – 8/8/2013 – Gorski reviewed “Burzynski: Cancer Is Serious Business” (Part I), but acts as if Dvorit D. Samid was NOT mentioned, and that he is NOT aware that the BurzynskiMovie website contains supporting documentation
I can’t let such statements go unchallenged
It means NadaZeroZip
====================================== [6] – 6/4/2013 – “In science, all that matters is what you publish, and Burzynski hasn’t published anything other than case reports, tiny case series, and unconvincing studies, mostly (at least over the last decade or so) in crappy journals not even indexed on PubMed”
—————————————————————— [5] – 8/21/2013 – I remain unimpressed that Gorski has NOT written a review of Burzynski’s 2003-2010 phase II clinical trial preliminary reports
====================================== [6] – 6/4/2013 – “Without a doubt, the most effective part of the story is the segment in which Dr. Jeanine Graf of the Texas Children’s Hospital is introduced”
“Dr. Graf is the director of the pediatric intensive care unit there and has taken care of lots of Burzynski patients, as her hospital is “just down the road” from the Burzynski Clinic and these unfortunate children are brought to her hospital when they decompensate”
“Indeed, coupled with this segment is an interlude where Luna Petagine’s mother complains that the staff there know and recognize Burzynski patients (and, she notes, hate the Burzynski Clinic)”
“Particularly damning is how Ms. Petagine said that the Texas Children’s Hospital Staff “were always cleaning up Burzynski’s messes.””
“Luna was brought to the Texas Children’s Hospital during her time in Houston, and the staff there recognized right away that she was a Burzynski patient because they had seen so many similar patients suffering the same complications before”
“It was also clear how much contempt the staff there had for the Burzynski Clinic”
“If there’s one thing Panorama did right in this report, it’s showing how seeing so many already dying children show up in our ICU because of hypernatremia due to antineoplaston therapy will do that”
“Perhaps the most devastating part of this segment was seeing Dr. Graf stating, point blank, that she’s never seen a Burzynski patient survive”
“True, she does point out that patients don’t come to her until they are in extremis, but the fact remains that she’s never seen any of them live”
—————————————————————— [11] – 4/24/2013 – What is so ridiculous about this is that Richard Bilton wanted numbers from Burzynski, but then when it came to this part of the documentary, he somehow forgets how to ask how many patients this applies to, and Gorski compounds this by trying to blame hypernatremia on antineoplaston therapy, but he refuses to explain how it is that in this Division of Internal Medicine / Department of General Internal Medicine, University of Texas, MD Anderson Cancer Center, Houston, TX, USA, cancer study, over a 3 month period in 2006 re 3,446 patients, most of the HYPERNATREMIA (90 %) was acquired during hospital stay, and these patients were NOT on antineoplaston therapy
Arrogance, dismissiveness, and condescension make him his own worst enemy
====================================== [6] – 6/4/2013 – “Burzynski also pulls out the old trope that, if the FDA has been letting him use antineoplastons for 20 years in clinical trials if they weren’t safe and potentially effective, that the FDA wouldn’t let him “sell hope without evidence.””
“(Those of us following Burzynski for a while know, unfortunately, that that isn’t necessarily true.)”
—————————————————————— [12] – 4/25/2013 – “The FDA’s Drug Review Process: Ensuring Drugs Are Safe and Effective” advises:
“[T]he emphasis in Phase 2 is on EFFECTIVENESS”
“Phase 3 studies begin if EVIDENCE of EFFECTIVENESS is shown in Phase 2″
The FDA has approved Burzynski’s phase 3 clinical trials, which means that antineoplastons have shown evidence of effectiveness, whether Gorski likes it or NOT
====================================== [6] – 6/4/2013 – ” … he goes on to repeat the same refrain he’s been repeating for the last decade or so about how he’s on the verge of publishing all the results that will convince everyone”
“One notes that we’re still waiting”
—————————————————————— [13] – 7/25/2013 – Gorski provides NO citation to support his statement, and, he did a review of “Burzynski: Cancer Is Serious Business, Part II,” but conveniently does NOT comment in his review about the refusal e-mail shown in the film, and its suspect content
====================================== [6] – 6/4/2013 – “Burzynski needs to publish, but I highly doubt that he will, at least not in a form that is informative to real oncologists”
—————————————————————— [5] – 8/21/2013 – I’m waiting for Gorski to prove that the 4 Burzynski publications I refer to are “NOT in a form that is informative to real oncologists”
Why don’t YOU cite a phase 2 clinical trial final publication that has substantially more data fields than the 4 publications I mention ?
====================================== [4] – 6/3/2013 – “I refer you to the link for my discussion of many of the problems with the movie”
“Here I will concentrate mainly on issues that I haven’t discussed before, because actually seeing Burzynski II was a revelation”
“(Yes, I put that sentence there on purpose, Eric Merola; quote mine it if you have the cojones)”
—————————————————————— [3] – 7/18/2013 – Gorski, don’t wait for Eric Merola to quote you
I’ve quoted you
Now let’s see if YOU have the cajones
MY review of your “review” should be a revelation to YOU
====================================== [4] – 6/3/2013 – “I’m referring to Chris Onuekwusi, a man who was diagnosed with stage I colon cancer”
“Instead of undergoing straightforward surgery that we know to have a high probability of success (which, I’ll also point out, can be done these days through minimally invasive laparoscopic techniques), Onuekwusi balked, as described in more detail than in the movie in this article on the Burzynski Patient Group website”
“He had even gone for a second opinion at one of the leading cancer centers in the world, the University of Texas M.D. Anderson Cancer Center, where the surgeon told him the same thing”
“He needed surgery first”
—————————————————————— [3] – 7/18/2013 – Mr. Onuekwusi did NOT want surgery
====================================== [4] – 6/3/2013 – “So what did Burzynski recommend instead of surgery?”
“He recommended a cocktail of three drugs given off-label:”
“Zolinza, Xeloda, and Avastin”
“Zolinza is vorinostat, a histone deacetylase inhibitor; Xeloda is capecitabine, which is a prodrug for 5-fluorouracil (5-FU), a pyrimidine analog that inhibits the enzyme thymidylate synthetase and thereby inhibits DNA synthesis to toxic effect in rapidly dividing cells; and Avastin is bevacizumab, a humanized monoclonal antibody directed against vascular endothelial growth factor-A (VEGF-A)”
“As I described in a previous post about Burzynski’s “personalized, gene-targeted cancer therapy,” apparently Burzynski sent Onuekwusi’s tumor to Caris for testing”
====================================== [14] – 3/2010 – Burzynski advised that a blood or pathology specimen can be used for testing, and that results from a blood test can be obtained within 2 days, and used and refined by a pathology specimen within 2 to 3 weeks
====================================== [4] – 6/3/2013 – “Caris generated a report, as it always does, and Burzynski came up with a witches’ brew of new expensive targeted agents, all said to be “off-label.””
====================================== [15] – 5/17/2011 – Well, not exactly
Burzynski made it clear in part 2 of this interview that there is constant searches of medical literature (phase 2 and phase 3 publications) to research the medications to be used based on the cancer genes involved, and that they have worked on software so oncologists can use it to choose the best medications instead of reinventing the wheel and having to review the medical literature again
So, he does NOT come up with a “witches’ brew”
====================================== [4] – 6/3/2013 – “One of these drugs is just an old chemotherapy drug in a new form”
“Xeloda is, in essence, 5-FU, a chemotherapeutic drug that has been used to treat colorectal cancer, both as adjuvant chemotherapy and first-line therapy for metastatic disease, for over 40 years”
“There’s nothing really “targeted” about the drug except that it inhibits an enzyme, the way that many drugs do and have been known to do for decades”
“The advantage of Xeloda is that it can be administered orally, which is a good thing”
====================================== [16] – What Gorski fails to mention is that Xeloda (Capecitabine) is approved to be used alone or with other drugs to treat:
Stage III colon cancer in patients who have had surgery to remove cancer
May also apply to unapproved uses being studied
—————————————————————— [17] – fluoropyrimidine carbamate belonging to class of antineoplastic agents called antimetabolites
As prodrug, capecitabine is selectively activated by tumor cells to cytotoxic moiety, 5-fluorouracil (5-FU); subsequently, 5-FU is metabolized to 2 active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP) by tumor cells and normal cells
FdUMP inhibits DNA synthesis and cell division by reducing normal thymidine production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate for incorporation into RNA strand
====================================== [4] – 6/3/2013 – “Similarly, Avastin, although relatively new, is also commonly used for colorectal cancer, albeit usually for metastatic disease and not as adjuvant chemotherapy”
====================================== [18] – What Gorski fails to mention is that Avastin (Bevacizumab) is approved to be used alone or with other drugs to treat:
Colorectal cancer that has metastasized (spread to other parts of body)
May also apply to unapproved uses being studied
—————————————————————— [19] – A recombinant humanized monoclonal antibody directed against the vascular endothelial growth factor (VEGF), a pro-angiogenic cytokine
Bevacizumab binds to VEGF and inhibits VEGF receptor binding, thereby preventing the growth and maintenance of tumor blood vessels
====================================== [4] – 6/3/2013 – “That leaves Zolinza, which is an HDAC inhibitor used to treat cutaneous T cell lymphoma”
====================================== [20] – What Gorski fails to mention is that Zolinza (Vorinostat) is a histone deacetylase inhibitor, approved for treatment of cutaneous manifestations of cutaneous T-cell lymphoma (CTCL) in patients with progressive, persistent, or recurrent disease
May also apply to unapproved uses being studied
—————————————————————— [21] – A synthetic hydroxamic acid derivative with antineoplastic activity
Vorinostat, a 2nd generation polar-planar compound, binds to catalytic domain of histone deacetylases (HDACs)
Allows hydroxamic moiety to chelate zinc ion located in catalytic pockets of HDAC, thereby inhibiting deacetylation and leading to accumulation of both hyperacetylated histones and transcription factors
Hyperacetylation of histone proteins results in upregulation of cyclin-dependant kinase p21, followed by G1 arrest
Hyperacetylation of non-histone proteins such as tumor suppressor p53, alpha tubulin, and heat-shock protein 90 produces additional anti-proliferative effects
Agent induces apoptosis and sensitizes tumor cells to cell death processes
Vorinostat crosses blood-brain barrier
====================================== [4] – 6/3/2013 – “One wonders if Burzynski included a second HDAC inhibitor, his second favorite drug after antineoplastons, sodium phenylbutyrate”
====================================== [22] – 11/19/2012 – Gorski, if you had done “exhaustive research” on Burzynski and “Gene-Targeted Cancer Therapy,” you would have viewed this @youtube video:
Texas Med. Bd. v. Dr. Burzynski – Gene-Targeted Cancer Therapy – Case Dismissed 11/19/2012
BurzynskiMovie
and you would have heard Mr. Onuekwusi say at 3:45, that he took phenylbutyrate (PB)
====================================== [4] – 6/3/2013 – “So, by Merola’s own description, what Burzynski did was to administer a toxic form of treatment that was probably not needed (chemotherapy) using drugs that were not approved for that indication, and apparently didn’t insist that the patient needed surgery”
====================================== [23] – 12/13/2012 – Gorski publishes so much garbage that he may have forgotten his article where he posted:
“Then, there is also this video, produced by the Burzynski clinic itself:”
“At around the three minute mark, the announcer states:”
“We combine gene-targeting drugs and low dose chemo, if needed”
====================================== [4] – 6/3/2013 – “Now, it’s possible that the combination of drugs did eliminate the tumor”
====================================== Gorski, do you think that’s because as mentioned in [15], above, Burzynski would review publications like this ?
[24] – 8/23/2011 – A randomized, phase III trial of capecitabine [Xeloda] plus bevacizumab [Avastin] (Cape-Bev) versus capecitabine plus irinotecan plus bevacizumab (CAPIRI-Bev) in first-line treatment of metastatic colorectal cancer: the AIO KRK 0110 trial/ML22011 trial [1st-line treatment of patients with unresectable metastatic colorectal cancer (mCRC)]
—————————————————————— [25] – 11/2/2010 – Vorinostat [Zolinza] synergises with capecitabine [Xeloda] through upregulation of thymidine phosphorylase
—————————————————————— [26] – 4/2012 – Phase I–II study of vorinostat [Zolinza] plus paclitaxel and bevacizumab [Avastin] in metastatic breast cancer: evidence for vorinostat-induced tubulin acetylation and Hsp90 inhibition in vivo
—————————————————————— [4] – 6/3/2013 – “In my opinion, Burzynski deserves to have his medical license taken away on the basis of how he treated Chris Onuekwusi alone, not even considering all the other dubious things he’s done”
====================================== [27] – 8/27/2013 – In my opinion, Gorski deserves to have his medical license taken away on the basis of how he has misinformed, disinformed, and lied about Burzynski, not even considering all the other dubious things he’s done
====================================== [4] – 6/3/2013 – “All I can say is that Merola and Burzynski must not have searched very hard, because I quickly found a few … “
“Truly, Merola’s “exhaustive” research skills need some upgrading”
“It took me two minutes to find those articles”
====================================== [22] – 11/19/2012 – All I can say is that Gorski must NOT have searched very hard, because I quickly found this @youtube video about Dr. Burzynski – Gene-Targeted Cancer Therapy, which includes a segment on Burzynski’s cancer gene testing at 2:45
Truly, Gorski’s “exhaustive” research skills need some upgrading, since nowhere does it indicate that Burzynski was involved with doing Merola’s research
It took me 2 minutes to find this out
Seeing is believing?
To me seeing is knowing just how intellectually dishonest David Gorski is
====================================== [4] – 6/3/2013 – Seeing The Skeptics
“Particularly seemingly damning are a series of Tweets flashed on the screen saying things like the Hope for Laura fund (the fund set up by Laura Hymas to pay for her treatment at the Burzynski Clinic) “appears to be just a money laundry for a lying quack fraud” and “when Laura dies #Burzynski will just move on to his next mark if she doesn’t run out of money first.””
“I think I know whose Tweets these were”
“In fact, I’m sure I know whose Tweets these were, and all I can say to that person is this:”
“Zip it”
“Stop it”
“Put a sock in it”
“In fact, if I’m correct about whose Tweets these are I think I have already done so on Twitter when I’ve seen this person getting too close to attacking cancer patients”
“Still, as utterly insensitive and “dickish” as those Tweets were, they do not represent the majority of skeptics, but rather a few jerks”
“However, we as skeptics need to remember that a few jerks perceived (or painted) as attacking cancer patients can do immeasurable damage to the cause of science-based medicine”
“So if you’re one of those skeptics making comments like that, knock it off”
“If I see you doing it again, next time I will call you out publicly”
====================================== [28] – 2/19/2013 – Like this ?
——————————————————————
Of course it's always possible that the money launderers are appearing as themselves in the #Burzynski advertisement.
——————————————————————
And this ?
——————————————————————
BurzynskiSaves (@BurzynskiSaves) tweeted at 7:42pm – 25 Dec 11:
“@RatbagsDotCom:They will be even more vulnerable when Laura dies and #Burzynski forgets her and moves on to the next mark” #unconscionable https://twitter.com/BurzynskiSaves/status/151115741888909312
—————————————————————— [29] – 8/1/2013 – And like you called this guy out ?
——————————————————————
David James (@StortSkeptic) tweeted at 7:08pm – 1 Aug 13:
The new Doctor Who will be Stanislaw #Burzynski. He manages to continually avoid getting cornered and he gets away with murder.
The new Doctor Who will be Stanislaw #Burzynski. He manages to continually avoid getting cornered and he gets away with murder.
====================================== [4] – 6/3/2013 – “Then, there was the kicker”
“Eric Merola and Laura Hymas’ fiancé Ben Hymas called me a liar”
“Ben Hymas is quite mistaken in saying about me,”
““He’s lying to them.””
“Moreover, if I had screwed up, I would have admitted it”
“Indeed, part of the reason I looked into this so closely was because I wondered if somehow Merola had actually found a mistake I had made”
“You know the saying about the proverbial blind squirrel occasionally managing to find a nut?”
“It’s possible, albeit unlikely, and in fact there was no mistake”
“There is nothing in deceptive to change my assessment of what happened in the case of or my opinion of Eric Merola”
====================================== [3] – 7/18/2013 – As I said before, Gorski’s research skills leave much to be desired
Gorski is a hack and is only funny by accident because he has no filters
If anything, having seen his “review” of Burzynski II, my opinion of Gorski has plummeted even further, something I had thought possible
Gorski, so you got lucky like a blind squirrel and found an error
However, this does NOT change the fact that you’ve been proven to be a liar
Do you want me to subtract one of your lies from the tally ?
====================================== [30] – 5/9/2013 – “On what basis is he “targeting” his therapy?”
“As I’ve recounted before, Burzynski usually sends off blood and tissue samples to Caris for testing”
“The Caris Target Now™ test, which since my discussion of Burzynski’s “personalized therapy” appears to have been renamed Caris Molecular Intelligence and is now available at more levels of service (although its reports look much the same to me), is nothing unique to the Burzynski Clinic”
“Anyone who is willing to pay for it can have it, and the report will be the same”
“In any event, there is as yet no convincing evidence that the Caris tests (or any of the other competing tests) result in better outcomes”
====================================== [31] – 5/28/2013 – A key pillar of Gorski’s position on Burzynski’s “personalized gene-targeted cancer therapy” is that he alleges that he is “someone relatively knowledgeable about the state of personalized cancer therapy”
I can’t help but wonder why it is that he did NOT know the above information
Maybe he isn’t as knowledgeable about personalized cancer therapy and targeted therapies as he claims
(Oh, wait. He isn’t!)
That’s why when he wrote his “review” on Sheila Herron, he did NOT even refer to Burzynski’s publication:
—————————————————————— [32] – 8/2011 – Successful Treatment of Recurrent Triple-Negative Breast Cancer with Combination of Targeted Therapies
When it comes to Gorski’s “story writing” pal Robert J. “Bob” Blaskiewicz, I might allow for some leeway since he’s only a “Perfessor,” but with Gorski on the other hand, I’m not nearly so benevolent
In my ever-Insolent opinion, he and his propagandist are cynically using patients like human shields to deflect criticism
Activities I cannot countenance
====================================== [33] – 4/19/2013 – “I now think I probably know with around 95% certainty) and Didymus Judas Thomas (whose identity I’m probably about 75% sure of … also obsessively read anything posted about Eric Merola or Stanislaw Burzynski on any social media”
====================================== [34] – 4/19/2013 – Gorski has had over 4 months to say who he thinks I supposedly am, and so far he’s been a failure
But then again, as could be expected, he was wrong about his 2nd theory as well
Finally, I believe that people like Gorski are hypocrites, feeling free to paint Burzynski to their heart’s content (from what I’ve read about Burzynski on blogs, Twitterarticles, and elsewhere, posted by biased, disingenuous, “holier than thou” Skeptics, in them Burzynski is all but portrayed as Satan Incarnate) but running like whipped puppies to the Coward section when either they or Gorski are criticized, no matter how civil, reasonable, or science-based that criticism is (and my blog is all of the above)
The reason is, of course, clear
Having no convincing science, no convincing medicine, and no convincing evidence to support their hero’s antineoplastons hackery or “personalized MUD-targeted therapy for dummies,” they resort to Twitter thuggery
Same as it ever was
One more thing:
If Gorski and his crew of sycophants, toadies, and lackeys are offended by my opinion, my characterization of them that I have based on analyses of claims and observation of the behavior of them and their propagandist, they should try something different to shut me up
I have just the thing, too
Publishing the results of some of the responses to my blog for the scientific community comes to mind first
If Gorski really has the goods, as he and “The Skeptics” claim, then he can best shut me up by bringing the science—solid, convincing science, that is
I’ve said it before many times, and I’ll say it again:
I can be convinced by strong truthful and factual evidence
I have yet to see anything resembling strong evidence from Gorski
At least, if he has such evidence he hasn’t published it yet, preferring to publish a mixture of whiny blog articles where he takes a swipe at Burzynski, tiny-mind series, unimpressive basic science, and the like in bottom-feeding blog articles, some of which aren’t even indexed in PubMed
Nor is a conspiracy of cowardice—excuse me, “The Skeptics”—the reason why trying to ignore criticism will boomerang on “The Skeptics”
It’s all because of their own behavior and willingness to distort, misinform, and slime Burzynski
====================================== [35] – 1/14/2013 – “As you might recall, antineoplastons are chemicals that Burzynski found in the urine of cancer patients and that (or so he claims)”
====================================== [36] – 2/19/2013 – Seriously, Gorski ?
Where did you come up with that ?
After comparing the blood of healthy people to the blood of people with cancer, Dr. Burzynski found that people with cancer have lower amounts of a certain group of chemicals
====================================== [35] – 1/14/2013 – “None of this would have been too bad if only he had actually bothered to do the proper science and clinical trials to demonstrate that antineoplastons (1) have significant anti-cancer activity and (2) have acceptable levels of toxicity”
====================================== [10] – 8/8/2013 – Here’s (1)
—————————————————————— [37] – 2/19/2013 – And (2)
====================================== [35] – 1/14/2013 – “Oh, sure, he has a bunch of clinical trials listed on ClinicalTrials.gov, but virtually all of them are listed as having “unknown” status, and it’s unclear whether most, if any, of them are actually accruing”
====================================== [38] – 5/21/2011 – Cancer Breakthrough: 50-60% Success Rate, Cures the Incurable
May 21, 2011
12 phase 2 clinical trials have been successfully completed under supervision of FDA, and now conducting 3 phase 3 clinical trials
Or I can cite from Burzynski’s Securities and Exchange Commission (SEC) filings re his phase 2 clinical trials like you did [1] – 6/5/2013
====================================== [35] – 1/14/2013 – “In any case, Merola named the sequel what he named it … along with a website full of a “sourced transcript” to be used by Burzynski minions and shills everywhere to attack any skeptic who dares to speak out”
====================================== [39] – Gorski, you should have used the “sourced transcript” so you didn’t end up embarrassing yourself as much as you have
Actually, no one who is an apologist for Dr. Gorski, a.k.a. “Orac,” who over years ago unleashed MUD-targeted therapy on unsuspecting cancer patients, much likes Burzynski
It’s not surprising
Basically, Gorski’s a hack
—————————————————————— [40] – Or, you can use this – Burzynski: The Movie — Illustrated Screenplay and Screencap Gallery (Nader Library):
====================================== [35] – 1/14/2013 – “Part of the reason that Eric Merola doesn’t like me, aside from the fact that I am willing to help publicize Bob Blaskiewicz’s present to Dr. Burzynski for his 70th birthday on January 23, is that I think that every so often I happen to run into stories about the bad science and unethical nature of Burzynski’s work, and I blog about it”
====================================== [41] – 3/26/2013 – Maybe Eric does NOT like you because part of that “present” was your “pal” saying:
“The Burzynski clinic is a place you go to die”
—————————————————————— [42] – 8/24/2013 – Gorski, where were you when these 374 children died of brain cancer in #ScienceBasedMedicine clinical trials ?
====================================== [35] – 1/14/2013 – “I also run into patient stories”
“Although I don’t cover them as systematically as Bob does, I like to think that what I lack in comprehensiveness of coverage I make up for with my in-depth knowledge of cancer science and treatment”
====================================== [43] – 8/31/2013 – Your “in-depth knowledge of cancer science and treatment” ?
You sure have NOT presented a very strong case for that
Is your “man-crush”, Robert J. “Bob” Blaskiewicz still adding false statements to his “stories” ?
====================================== [35] – 1/14/2013 – “There are a number of things about this documentary that one can learn if one is involved in caner care and knowledgeable about Stanislaw Burzynski”
“Indeed, he’s even taken credit for pioneering the concept of personalized cancer therapy based on genes and the concept that cancer is a genetic disease, claiming to have published a journal article about it 20 years ago, allegedly long before conventional scientists and oncologists even thought of it”
“The problem, of course, is that, as far as I can tell, he published no such paper and personalized therapy is a concept older than 20 years”
====================================== [44] – 7/26/2013 – Indeed, from my perspective Gorski’s an egomaniac, full of the arrogance of ignorance about things like Burzynski’s “personalized cancer therapy”, prone to contemptuously dismissing anyone who has the temerity to question the Great and Powerful “Orac” is god
Because I was able to find the publication with NO problem
“Orac’s” Oracolytes remind me of the “believer” who said:
“god said it, and I believe it, so that settles it”
Of course, “Orac” is Oz tends to clam up when questioned by people who are NOT likely to be sycophants, toadies, and lackeys
====================================== [35] – 1/14/2013 – “Given that these are all phase II studies, it’s hard to believe that the FDA would allow Burzynski to keep them open over 13 years, but apparently it has”
====================================== [45] – 7/26/2013 – Gorski, why don’t you ask the FDA?
3/29/1996 Then United States Food and Drug Administration Commissioner, David Kessler told the American people:
“The … FDA’s initiatives … will allow …the agency … to rely on smaller trials … fewer patients … if there is evidence … of partial response in clinical trials”
—————————————————————— [46] – 6/7/2013 – Then you could be like Blatherskitewicz and do this:
Bob Blaskiewicz (@rjblaskiewicz)
6/3/13, 3:49 PM
@FauxSkeptic @bbc5live I believe he said, “Put up or shut up, you little bitch.” Something like that.
rjblaskiewicz: @bbc5live “I believe he said
“Put up or shut up
you little bitch”
BB: why not check with the @US_FDA
#Burzynski
BBC Panorama
====================================== [35] – 1/14/2013 – “Finally, why doesn’t Burzynski offer Seán his “personalized gene-targeted cancer therapy.””
“It probably wouldn’t be that big a deal to get the blocks of tissue from Seán’s biopsy and have them analyzed”
“Yes, inquiring minds do want to know”
====================================== [35] – 1/14/2013 – Gorski, why don’t you cite the applicable phase 2 and / or phase 3 clinical trial publications of FDA approved drugs for “inoperable brainstem glioma” ?
And while your at it, is the “girl from England” referred to in your article, the same one that is referred to in Burzynski 2 ?
====================================== [47] – 1/7/2013 – “That’s why I’m joining P.Z. Myers in asking you to help make Stanislaw Burzynski pay cold hard cash to a worthy cause
====================================== [41] – 3/26/2013 – Yes Gorski, your “pal” E.Z. P.Z. who wrote:
“The Burzynski clinic is a place you go to die”
He has no shame
But at least ya’ll raised money for a worthy cause while at the same time bringing attention to yourself and what I consider to be your incredibly unethical behavior
====================================== [23] – 12/13/2012 – “In fact, from my perspective, it appears to me as though over the last few years Dr. Burzynski has pivoted”
“No longer are antineoplastons the center of attention at his clinic”
“Rather, these days, he appears to be selling something that he calls “personalized gene-targeted cancer therapy.””
====================================== [48] – 4/26/2013 – Gorski it’s great to see you’ve been paying attention
” … in 1997, his medical practice was expanded to include traditional cancer treatment options such as
chemotherapy,
gene targeted therapy,
immunotherapy and
hormonal therapy
in response to FDA requirements that cancer patients utilize more traditional cancer treatment options in order to be eligible to participate in the Company’s antineoplaston clinical trials”
====================================== [23] – 12/13/2012 – “Finally, around the 4:30 mark, we see Dr. Gregory Burzynski, Dr. Burzynski’s son, talking about genomic profiling of cancers and biomarkers in the blood and in circulating tumor cells. … plus a claim that surgery will no longer be necessary for surgery, what’s left over doesn’t sound too different from what quite a few “conventional” cancer researchers say about “personalized medicine.””
====================================== [23] – 12/13/2012 – Gorski, “surgery will no longer be necessary for surgery” ?
Is this “attention to detail”” related to:
“because of the positions I hold at an NCI-designated comprehensive cancer center” ?
====================================== [23] – 12/13/2012 – “Clearly, the producer went to great lengths to make Burzynski’s lab look like any other molecular and cell biology lab–even like my lab”
====================================== [23] – 12/13/2012 – Gorski, are you trying to suggest that the producer rented or bought equipment to produce this look ?
Do you know how ridiculous that sounds ?
====================================== [23] – 12/13/2012 – “When we do this we have a very good chance to have positive results in most patients”
“SS: How many respond?”
“SB: About 85 per cent for whom we have the proper gene signature; about 15 percent do not respond”
“In our responders many of them have tumors which disappear completely and in others the tumors remain small”
“The problem is finding the genetic signature because for many of these different genetic signatures we don’t have blood tests…yet”
“Note that at the time this book was published, Dr. Burzynski was claiming that he could identify who would benefit from specific targeted therapies simply from blood tests”
“If he could do this for real, Burzynski could easily publish in high impact journals like Clinical Cancer Research, the Journal of Clinical Oncology, or another high impact clinical cancer journal”
“Heck, a result like that could probably make it into general medical journals, such as the New England Journal of Medicine or The Lancet, which have an even higher impact factor”
“If he were able to demonstrate that his method of testing tumors and picking targeted therapy could result in a complete response rate anywhere near 85% for breast cancer, even more so”
“If, as he claims later in the chapter, Dr. Burzynski has patients with pancreatic cancer and advanced liver cancer whose tumors have disappeared within two months after he began treatment, the same would be true”
“If, as Burzynski claims, he achieves a 50% complete response rate in advanced brain tumors, again, the same would be true”
“He doesn’t submit his results to these journals”
“Why not?”
====================================== [3] – 7/18/2013 – Gorski, why would Burzynski want to publish in The Lancet when you saw the lame excuse they gave in Burzynski 2 for NOT publishing Burzynski’s results; which YOU have refused to address ?
Maybe you could find out if you visited the Burzynski Clinic
Oh, wait
You’ve said that people do NOT need to go to the Clinic to learn things
====================================== [23] – 12/13/2012 – “Gene-targeted cancer therapy is currently in its infancy and, except in rare situations outside of the existing currently validated biomarkers (such as HER2, ER, c-kit, and other genes for which targeted therapies exist) for the response of specific cancers, is not to be undertaken outside of the context of a clinical trial“
====================================== [23] – 12/13/2012 – Gorski, that’s all well and good for you to write, but you provide NO citation, reference, or link in support of your statement, and you’ve proven that what you post can NOT be trusted
Try again
====================================== [23] – 12/13/2012 – “Before discussing how the Burzynski Clinic does personalized cancer therapy, I think it’s worth looking at how real scientists do it right now”
====================================== [23] – 12/13/2012 – Gorski, what are you implying ?
That Burzynski is NOT a “real scientist” ?
Because you stated:
“From the description above, it sounded very much to me as though Dr. Burzynski is combining various targeted agents with metronomic chemotherapy“
“I know a thing or two about metronomic chemotherapy, because I was involved in a project whose end result was to be the testing of metronomic chemotherapy against cancer and because the concept is a spinoff of the work of one of my scientific heros, the late Judah Folkman”
“Whether this is what Dr. Burzynski is doing or not with the chemotherapy part of his approach, I don’t know for sure, but it sure sounds like it“
====================================== [23] – 12/13/2012 – “Now let’s take a look at how the Burzynski Clinic does it, at least as far as I can figure out from my various sources and from Ms. Trimble”
“In response to my query about personalized gene-targeted therapy offered by the Burzynski Clinic, Ms. Trimble stated that a gene expression analysis is performed, as well as mutational analysis, FISH, immunohistochemistry for selected genes and that a blood test is also performed to measure the “concentration of proteins which are products of most important oncogenes.””
“In addition, drugs are supposedly selected based on the patient’s clinical information, standard of care, FDA indication, data from phase II and III clinical trials“
====================================== [4] – 6/3/2013 – Gee Gorski
In your 6/3/2013 article you act as if you did NOT know this
====================================== [23] – 12/13/2012 – “To support this claim, Ms. Trimble also sent me two papers from the Burzynski Clinic, both of which appeared in a journal I had never heard of before, the Journal of Cancer Therapy, which is clearly not indexed on PubMed because these papers never showed up when I searched PubMed for Burzynski”
“One described Burzynski’s approach for triple negative breast cancer (TNBC)”
====================================== [32] – 8/2011 – Gorski, why am I NOT surprised that you’re able to refer to this TNBC publication 12/13/2012, but when reviewing Sheila Herron’s TNBC case 5/28/2013, you completely ignored this publication, even though it specifically states:
“Here we report the successful treatment of metastatic TNBC with combination targeted therapy, and we discuss MDT for a group of 16 women including this patient, whose treatment was based on the same principle” (Pgs. 372-373)
How do you NOT provide a link to a previous article you wrote on the same subject, like you normally do ?
====================================== [23] – 12/13/2012 – “It turns out that perhaps the best description of what “personalized” treatment means in Dr. Burzynski’s hands comes from the Texas Medical Board’s complaint against him, which can be found in over at the Ministry of Truth or at Casewatch”
“This complaint is based on the cases of two patients”
“First, here’s Patient A, who is described in the complaint thusly:”
“1. Patient A:”
“a. In approximately May of 2008, Patient A presented to Respondent with breast cancer that had metastasized to her brain, lung, and liver”
“b. Respondent prescribed a combination of five immunotherapy agents – phenylbutyrate, erlotinib, dasatinib, vorinostat, and sorafenib-which are not approved by the Food and Drug Administration (“FDA”) for the treatment of breast cancer, and which do not meet the FDA’s regulations for the use of off-label drugs in breast cancer therapy”
“c. In combination with the five immunotherapy agents, Patient A was prescribed capecitabine, a chemotherapy agent”
“This is what’s known as “throwing everything but the kitchen sink” at the tumor without any thought of interactions, as most of these agents have no proven role in the treatment of breast cancer”
“For example, erlotinib (brand name: Tarceva) is used to treat pancreatic cancer and non-small cell lung cancer”
“It works by inhibiting the tyrosine kinase of the epidermal growth factor receptor (EGFR) and is not FDA-approved for breast cancer”
“However, it’s not unreasonable to think that it could work in breast cancer, as EGFR is believed to be important in some breast cancers, which is why this is an area of active research”
“Dasatinib (trade name: Sprycel) is also a kinase inhibitor”
“It inhibits the Src family tyrosine kinase”
“Vorinostat is a histone deacetylase inhibitor approved for use against cutaneous T-cell lymphoma”
“Finally, Sorafenib is another tyrosine kinase inhibitor that inhibits the tyrosine kinases of different receptors, as well as raf kinases”
“The big problem with this sort of approach is that the more drugs you add, no matter how “targeted” they are, the more chance for interactions that increase toxicity, and throwing all these kinase inhibitors together in a cocktail with chemotherapy is a recipe for disaster, particularly because such cocktails haven’t been tested in proper phase I clinical trials to evaluate toxicity”
====================================== Gorski, you make it sound like you reviewed the medical literature and found NO phase I clinical trials were conducted, or NO combinations of some of these drugs were tested
But you do NOT reveal your research
I’m guessing you reviewed these pre 5/2008 publications, right ?
—————————————————————— [49] – 4/20/2007 – Phase III study:erlotinib in combination with cisplatin and gemcitabine in advanced non-small-cell lung cancer
—————————————————————— [50] – 5/2007 – randomized phase II study: sorafenib/erlotinib – advanced non-small-cell lung cancer
—————————————————————— [51] – 4/20/2006 – Phase II study: capecitabine and erlotinib
—————————————————————— [52] – 1/2008 – Phase II Clinical Trial: Sorafenib
—————————————————————— [53] – 4/2007 – Antitumor Activity: Sorafenib – 4 Phase I Trials: Advanced Refractory Solid Tumors
—————————————————————— [54] – 6/20/2007 – phase I study: vorinostat (VOR) in combination with capecitabine (CAP) – advanced solid tumors
====================================== [23] – 12/13/2012 – “In any case, as we have seen, Dr. Burzynski does give chemotherapy”
“Lots of chemotherapy”
====================================== [23] – 12/13/2012 – Gorski, what was the date of the video you quoted above, about low-dose chemotherapy ?
====================================== [23] – 12/13/2012 – “Instead, skirting the line between science and pseudoscience, Dr. Burzynski gives every appearance of recklessly throwing together untested combinations of targeted agents willy-nilly to see if any of them stick but without having a systematic plan to determine when or if he has successfully matched therapy to genetic abnormality”
====================================== [15] – 5/17/2011 – That sure explains away the review of the medical literature (phase 2 and 3 clinical trials)
NOT
====================================== [55] – 12/12/2012 – “Note: Orac is away In the meantime, he is rerunning some of his favorite posts”
“Given that the blog seems to have been infiltrated with Burzynski trolls again now seems a perfect time to rerun a post of Orac’s from about a year ago”
====================================== [55] – 12/12/2012 – “Orac”, who’s the idiot who posted that “trolls” had taken over the blog, and who were these “alleged”“trolls” ?
Inquiring minds want to know
====================================== [55] – 12/12/2012 – “No one would ever confuse my reviews with those of Roger Ebert (mine tend to be a lot longer, for one thing, and concentrate on science much more than moviemaking), but I do sometimes subject myself to these movies when I can find a way to watch them online that doesn’t cost me any money”
====================================== [55] – 12/12/2012 – Gorski
“Concentrate on science” ?
really ?
Really ??
REALLY ???
Did you actually count how many characters and / or words you devoted to criticism instead of “science” ?
====================================== [55] – 12/12/2012 – “In the process, I might even look into a couple of Burzynski’s studies that I’ve read and found to be–well–lacking, to put it kindly”
====================================== [2] – 8/4/2013 – Gorski, why don’t you “look into” Burzynski’s 2003-2010 preliminary phase 2 clinical trial reports, and write a “review” ?
====================================== [55] – 12/12/2012 – “One part of the movie that truly insults the intelligence of anyone with a modicum of knowledge about drug therapy occurs near the beginning of the movie”
“It’s a part that, as a cancer surgeon who is interested in targeted therapies for breast cancer, I found particularly idiotic”
“First, there is a screen with this caption:”
“Antineoplastons target the specific genes that allow cancer to grow and flourish”
“A little later we see:”
“There are currently over 25 FDA-approved gene-targeted cancer drugs on the market today”
“Many of them can only target single genes”
“All of which is true but irrelevant if Burzynski is trying to sell antineoplastons as targeted therapy”
“Now here’s the kicker:”
“Antineoplastons work on close to one hundred different genes”
“You know what you call a drug that works on “close to 100 genes”?”
“I don’t know either, but you don’t call it a “targeted” therapy unless all those genes are genes affected by the single target being inhibited; i.e., are downstream targets of the gene targeted by antineoplastons”
====================================== [5] – 8/21/2013 – Gorski, how do you NOT know “the single target being inhibited … are downstream targets of the gene targeted by antineoplastons”, when you did NOT even know which of Burzynski’s publications discussed which genes are “targeted by antineoplastons” ?
====================================== [56] – 12/5/2012 – “In reality, oncologists shun Burzynski—and rightly so, given that he has yet to publish anything resembling a convincing result suggesting the efficacy of his antineoplastons against cancer”
“It’s painfully obvious from this paragraph that Burzynski doesn’t know academic oncologists”
“The reason oncologists don’t respect Burzynski is because of how he hasn’t show that his treatments work better than conventional treatments—or even that they work at all—and because of the way he abuses patients by charging them huge sums of money to participate in a clinical trial”
“Those are the reasons legitimate oncologists, at least those familiar with Burzynski, look askance at him”
“How could they do otherwise?”
“The ones who don’t take him seriously are the ones who know him best”
====================================== [57] – 4/24/2013 – Gorski, that certainly explains why this 2011 cancer study that references Burzynski:
Phase II trial of tipifarnib and radiation in children with newly diagnosed diffuse intrinsic pontine gliomas
University of California—San Francisco
Children’s Hospital Boston, Massachusetts
St Jude Children’s Research Hospital, Memphis, Tennessee
Seattle Children’s Hospital, Seattle, Washington
Children’s Hospital of Philadelphia, Pennsylvania
Children’s Hospital of Pittsburgh, Pennsylvania
Children’s National Medical Center, Washington, DC
Cincinnati Children’s Hospital Medical Center, Ohio
======================================
British Journal of Cancer (2010) 103, 1680–1691. doi:10.1038/sj.bjc.6605969
Published online 2 November 2010 http://www.nature.com/bjc/journal/v103/n11/full/6605969a.html
Experimental Pharmacology Unit, Department of Research, Istituto Nazionale Tumori, National Cancer Institute Fondazione G, Via.M Semmola, Pascale, Napoli, Italy
====================================== [26] – 4/2012
Phase I–II study of vorinostat plus paclitaxel and bevacizumab in metastatic breast cancer: evidence for vorinostat-induced tubulin acetylation and Hsp90 inhibition in vivo http://www.ncbi.nlm.nih.gov/pubmed/22200869/
Breast Cancer Res Treat. 2012 Apr;132(3):1063-72. doi: 10.1007/s10549-011-1928-x. Epub 2011 Dec 27 http://www.ncbi.nlm.nih.gov/m/pubmed/22200869/
Breast Cancer Res Treat. Author manuscript; available in PMC 2013 April.1 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3486521/
Published in final edited form as:
Breast Cancer Res Treat. 2012 April; 132(3): 1063–1072
[3]
—————————————————————— https://twitter.com/oracknows/status/366866619508596737
—————————————————————— Josephine Jones proves that she does NOT have a clue, and probably has NOT watched Burzynski: Cancer Is Serious Business, Part II (2), OR she was trying to pull a Gorski, and saw the film, but chooses to act like she did NOT see what she chooses NOT to comment on
—————————————————————— [4]
It’s strange that #Burzynski skeptics were asked to name journals and that’s where the study was submitted. http://t.co/VkCsUIENcC
——————————————————————
As you can see below, @BurzynskiMovie posed the question to Doctor B. Paul Morgan 12/20/2012 at 5:12 PM, and he responded at 5:28 PM
@drpaulmorgan @dianthusmed Pick a medical journal Paul…
Eric Merola revealed in Burzynski, Part 2 (1:29:53), that The Lancet Oncology Peer Review Team D-12-01519, in 2 hours 8 minutes and 51 seconds, refused to publish Burzynski’s 11/26/2012 phase 2 clinical trial Progression-Free Survival (PFS) and Overall Survival (OS) re patients 8 – 16 years after diagnosis, results
—————————————————————— 11/26/2012 came before 12/20/2012 last time I checked
—————————————————————— The Lancet Oncology Peer Review Team D-12-01519: #FAIL:
—————————————————————— https://stanislawrajmundburzynski.wordpress.com/2013/07/25/the-lancet-oncology-peer-review-team-d-12-01519-fail/
� � � � � � � � � � � � � � � � [5]
As far as I know, we only have Merola’s word that the ANPs study was submitted to Lancet Oncology. http://t.co/VkCsUIENcC#Burzynski
A study of antineoplastons fails to be published. Stanislaw Burzynski’s propagandist Eric Merola whines about it. News at 11.
Gorski makes me laugh at his antics
He supposedly has a Ph.D, and supposedly is a “cancer researcher”, yet his “research” is horrendous when it comes to actual cancer science
Dr. Gorski, as you recall, prefers to misdirect his Oracolytes away from Science, and instead focus on the mundane
An excellent example of this is where he states:
“(Burzynski) hasn’t bothered to actually demonstrate in a sufficiently rigorous fashion that they (antineoplastons) do what he claims they do or that they have significant anticancer activity in actual human beings”
notwithstanding the claims of his lackeys, toadies, and sycophants
So, when further on in his article where Gorski posts his usual garbage:
“However, even though Burzynski has dozens of clinical trials of antineoplastons against cancer registered at ClinicalTrials.gov but has not managed to publish even a single completed trial …”
you know he is being disingenuous, so that it fits his narrative
Gorski then continues the whining that never ends:
“… there is another investigator who has been doing a randomized clinical trial”
“His name is Dr. Hidaeki Tsuda of the Kurume University Hospital in Japan”
“He’s an anesthesiologist, not a surgeon or oncologist; so I’m not sure why he’s doing clinical trials of a chemotherapy agent”
As usual, Gorski is unable to state what difference it makes that Burzynski and Tsuda are NOT oncologists
Nor does he state whether he reviewed any of their clinical study publications in order to determine if any of the co-authors just happen to be oncologists
Why is this ?
Because Gorski is disingenuous and exhibiting his poor research
In reference to the Tsuda study, Gorski deposits:
“Nor did I have any idea whether any progress had been made in getting the study published”
Yet this is the same Gorski who supposedly blogged a “review” of Burzynski, Part 2, but when it came to the part of the film (1:29:53) where it showed the 11/26/2012 The Lancet Oncology Peer Review Team D-12-01519 lame excuse for NOT publishing Burzynski’s phase 2 clinical trial Progression-Free Survival (PFS) and Overall Survival (OS) re patients 8 – 16 years after diagnosis, results, in 2 hours 8 minutes and 51 seconds, Gorski was Mr. NO COMMENT #FAIL
====================================== See point #13
—————————————————————— Critiquing: In which the latest movie about Stanislaw Burzynski “cancer cure” is reviewed…with Insolence:
—————————————————————— https://stanislawrajmundburzynski.wordpress.com/2013/07/18/critiquing-in-which-the-latest-movie-about-stanislaw-burzynski-cancer-cure-is-reviewed-with-insolence-2/
======================================
Now, all of a sudden, Gorski acts like he thinks we should accept that he’s NOT just continuing his disingenuous behavior
Gorski, Gorski, Gorski, Gorski, you are such a funny man
I really did laugh out loud when I read how you did NOT compare the lame excuse given by The Lancet Oncology Peer Review Team, with the reply they supplied regarding the Tsuda study
Gorski whines about the experience he suffered when he had difficulty getting something published, and comments;
“If the topic is not interesting or the data are crap, its being well-written and rigorously adherent to the journal’s format won’t save it”
I guess this means that Gorski’s journal submission fit his criteria:
“the topic is not interesting or the data are crap”
Gorski continues with his foaming of the mouth and gnashing of teeth:
“The Tweet linked to in the Tweet above was this one:”
@BurzynskiMovie @dianthusmed 1. Journal of Clinical Oncology. 2. The Lancet Oncology. 3. New England Journal of Medicine. (1/2)
— Paul Morgan (@drpaulmorgan) December 20, 2012
“So basically, it appears that Mr. Merola likely transmitted suggestions for journals listed on Twitter to Dr. Burzynski and/or Dr. Tsuda, and the advice was taken”
“It’s almost as though this particular Burzynski apologist thought that Dr. Paul Morgan meant that Dr. Tsuda’s manuscript would definitely be accepted”
Such naiveté is almost cute
Gorski exhibits that he did NOT make any effort whatsoever to click on the provided link and read the material associated with the tweet
Actually, it’s painful to behold such basic ignorance about how Twitter links work
Of course, there is a way for Dr. Gorski to demonstrate my educated guess about what really happened to be wrong
All he has to do is to answer a question and provide one bit of information
The question is, “Did you watch Burzynski, Part 2?” If the answer is yes, then all we need to see to determine if you are NOT being disingenuous is true, is one simple thing
Explain WHY you did NOT mention The Lancet Oncology Peer Review Team lame excuse for NOT publishing Burzynski’s results
It’s really that simple, Dr. Gorski
Put up or shut up
In the meantime it is obvious what “plan B” is
You will continue with your usual deception, misdirection, misinformation, disinformation, MisDisInformation, and lies
The reason is easy
Gorski and the Oracolytes are disingenuous
Gorski supporters really need a new schtick
This one’s getting really old
So is the schtick of The Skeptics
Surely they could come up with something better than this?
Apparently not
They are Cowards who refuse to debate the issues on-line or in person
======================================
[1] Josephine Jones (@_JosephineJones) tweeted at 3:31am – 12 Aug 13:
——————————————————————
Antineoplastons study rejected by Lancet Oncology. It’s a conspiracy! scienceblogs.com/insolence/2013… #Burzynski
======================================
[2] Orac (@oracknows) tweeted at 3:47am – 12 Aug 13:
——————————————————————
Yo! New insolence! A study of antineoplastons fails to be published. Stanislaw Burzynski’s propagandist Eric M… bit.ly/1csAfRB
======================================
[3] Orac (@oracknows) tweeted at 5:19am – 12 Aug 13:
——————————————————————
Oh, @BurzynskMovie, here’s what I think of whining that Dr. Tsuda’s paper was rejected by Lancet Oncology. scienceblogs.com/insolence/2013… #Burzynski
======================================
[4] Josephine Jones (@_JosephineJones) tweeted at 3:33am – 12 Aug 13:
——————————————————————
It’s strange that #Burzynski skeptics were asked to name journals and that’s where the study was submitted. scienceblogs.com/insolence/2013…
======================================
[5] Josephine Jones (@_JosephineJones) tweeted at 3:37am – 12 Aug 13:
——————————————————————
As far as I know, we only have Merola’s word that the ANPs study was submitted to Lancet Oncology. scienceblogs.com/insolence/2013… #Burzynski
======================================
[6] David Gorski (@gorskon) tweeted at 5:21am – 12 Aug 13:
——————————————————————
.@_JosephineJones I think Tsuda’s aiming too high. Lancet Oncology is a top tier cancer journal. He should aim much lower. #Burzynski
======================================
[7] FW (@frozenwarning) tweeted at 5:08am – 12 Aug 13:
——————————————————————
@_JosephineJones Look forward to it being published in some shit altmed journal then! *twiddles thumbs*
======================================
[8] Primum Non Nocere (@DrNescio) tweeted at 7:20am – 12 Aug 13:
——————————————————————
A study of antineoplastons fails to be published. Stanislaw Burzynski’s propagandist Eric Merola whines about it…. pulse.me/s/p1zrK
======================================
� � � � � � � � � � � � � � � �
—————————————————————— 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 AS2-1used 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 therapyincluded testing of separate ingredientsphenylacetate (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
� � � � � � � � � � � � � � � �
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
——————————————————————
Drugs R D. 2003;4(2):91-101
Drugs in R&D 2003;4:91-101
—————————————————————— Pg. 100
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[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
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[29] Chang SM, Kuhn JG, Robins HI, et al. Phase II study of phenylacetate in patients with recurrent malignant glioma: a North American Brain Tumor Consortium Report. J Clin Oncol 1999; 17: 984-90
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[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
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