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

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

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

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

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

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

Gorski claimed:

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

Data talks

BS walks

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

In fact, I think I’m being too kind

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

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

“antineoplastons are chemotherapy”

“They even have significant toxicity!”

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

NONE !!!

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

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

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

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

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Antineoplaston A-10 and AS2-1 LESS TOXIC THAN CONVENTIONAL CHEMOTHERAPIES and useful in maintenance therapy for cancer patients
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[15] 1996 Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which control neoplastic growth
——————————————————————
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
——————————————————————
Clinical experience of hepatocellular carcinoma (HCC) patient whose tumor, after incomplete trancathere arterial embolization (TAE) for a 7cm 7cm HCC, has been stable for more than 15 months during which time he has been taking Antineoplaston AS2-1 continuously WITHOUT ANY SERIOUS ADVERSE EFFECTS
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[16] 5/1996
——————————————————————
In pursuit of alternative treatments for chemoresistant tumor cells, tested response of multidrug-resistant (MDR) tumor cell lines to aromatic fatty acids phenylacetate (PA) and phenylbutyrate (PB), 2 differentiation inducers currently in clinical trials
——————————————————————
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 their parental counterparts
——————————————————————
PA and PB potentiated cytotoxic activity of doxorubicin against MDR cells
——————————————————————
Taken together, in vitro data indicate PA and PB, differentiation inducers of aromatic fatty acid class, may provide alternative approach to treatment of MDR tumors
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[17] 12/1996 PHENYLACETATE (PA) and related aromatic fatty acids constitute novel class of RELATIVELY NONTOXIC antineoplastic agents
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[18] 8/1997 aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB) are novel antitumor agents currently under clinical evaluation
————————————————————
ability to induce tumor differentiation in laboratory models and LOW CLINICAL TOXICITY PROFILE makes them promising candidates for COMBINATION WITH CONVENTIONAL THERAPIES
======================================
[19] 1997 PHENYLACETATE and analogs represent new class of pleiotropic growth regulators that alter tumor cell biology by affecting gene expression at both transcriptional and post transcriptional levels
————————————————————
Based on findings, NaPA and NaPB entered clinical trials at National Cancer Institute
————————————————————
Ongoing phase I studies with NaPA, involving adults with prostate and brain cancer, confirmed therapeutic levels can be achieved WITH NO SIGNIFICANT TOXICITIES, and provide preliminary evidence for benefit to patients with advanced disease (Thibault et al., submitted)
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[20] 10/1997 Sodium PHENYLACETATE (PA) and sodium PHENYLBUTYRATE (PB) are aromatic fatty acids that can effect differentiation in a variety of cell lines at doses that may be clinically attainable
——————————————————————
Pg. 1760
——————————————————————
PB has been successfully administered to patients with urea acid cycle disorders and sickle cell anemia for extended periods of time, and NO HEMATOLOGICAL TOXICITY has been reported
——————————————————————
Significant HEMATOLOGICAL TOXICITY was not reported in a Phase I trial of PA in patients with malignancy
——————————————————————
Pg. 1761
——————————————————————
Because of its ATTRACTIVE CLINICAL TOXICITY PROFILE, PB represents an excellent candidate for clinical trials in this group of disorders
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[21] 11..12/1997 Antineoplaston AS2-1 exhibits cytostatic growth inhibition of human hepatocellular carcinoma cells in vitro and SHOWED MINIMUM ADVERSE EFFECTS in phase I clinical trial
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[22] 6/1999 Burkitt’s lymphoma (BL) is readily treated malignancy, recurrences, as well as disease arising in immunosuppressed patients, are notoriously resistant to conventional therapeutic approaches
——————————————————————
Using in vitro models of EBV-transformed lymphoblastoid as well as BL cell lines, we demonstrate increased expression of genes coding for HLA class I and EBV latent proteins by differentiation inducer PHENYLBUTYRATE (PB)
——————————————————————
Aromatic fatty acid also caused cytostasis associated with sustained declines in c-myc expression, a direct antitumor effect that was independent of EBV status
——————————————————————
Findings may have clinical relevance because in vitro activity has been observed with PB concentrations that are
WELL TOLERATED
and nonimmunosuppressive in humans, a desirable feature for different patient populations afflicted with this disease
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[23] 8/2001 PHENYLBUTYRATE (PB) is aromatic fatty acid with multiple mechanisms of action including histone deacetylase inhibition
——————————————————————
Overall DRUG WELL TOLERATED with most common TOXICITIES being grade 1-2 DYSPEPSIA and FATIGUE
——————————————————————
Nonoverlapping dose-limiting TOXICITIES of NAUSEA/VOMITING and HYPOCALCEMIA were seen at 36 g/day
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PB (p.o.) IS WELL TOLERATED and achieves concentration in vivo shown to have biological activity in vitro
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[24] 10/2001 Sodium PHENYLBUTYRATE (PB) demonstrates potent differentiating capacity in multiple hematopoietic and solid tumor cell lines
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Pharmacokinetics performed during and after first infusion period using validated high-performance liquid chromatographic assay and single compartmental pharmacokinetic model for PB and principal metabolite, PHENYLACETATE
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24 patients with hormone refractory prostate cancer being predominant tumor type
——————————————————————
All evaluable for TOXICITY and response
——————————————————————
Dose escalated 150 to 515 mg/kg/day
——————————————————————
One patient at 515 mg/kg/day and one at 345 mg/kg/day experienced this DLT
——————————————————————
Maximum tolerated dose 410 mg/kg/day for 5 days
——————————————————————
Recommended Phase II dose 410 mg/kg/day for 120 h
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Dose-limiting TOXICITY (DLT) was neuro-cortical, exemplified by EXCESSIVE SOMNOLENCE and CONFUSION and accompanied by clinically significant HYPOKALEMIA, HYPONATREMIA, and HYPERURICEMIA
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Other TOXICITIES mild, including FATIGUE and NAUSEA
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DLT in Phase I study for infusional PB
given for 5 days every 21 days is neuro-cortical in nature
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TOXICITY resolved < or =12 h of discontinuing infusion
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[25] 2003 Case of survival for nearly 8 years after treatment of unresectable multiple liver metastases from colon cancer, using microwave ablation and NONTOXIC ANTITUMOR AGENT, ANTINEOPLASTONS
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72-year-old man diagnosed with adenocarcinoma of ascending colon and 14 bilateral liver metastases underwent right hemicolectomy combined with microwave ablation of 6 metastatic liver tumors
——————————————————————
Antineoplaston A10 given intravenously, followed by oral antineoplaston AS2-1
——————————————————————
Patient underwent 2nd and 3rd microwave ablation of recurrent tumors, and has survived for nearly 8 years WITHOUT SUFFERING ANY SERIOUS ADVERSE EFFECTS
——————————————————————
Currently FREE FROM CANCER
——————————————————————
Demonstrates potential effectiveness of NONTOXIC ANTITUMOR AGENT, ANTINEOPLASTONS, for controlling liver metastases from colon cancer
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[26] 4/2005 Determined maximum tolerated dose (MTD), TOXICITY profile of … oral sodium PHENYLBUTYRATE (PB) in patients with recurrent malignant gliomas
——————————————————————
All PB doses of 9, 18, and 27 g/day WELL TOLERATED
——————————————————————
At 36 g/day, 2 of 4 patients developed dose-limiting grade 3 FATIGUE and SOMNOLENCE
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At MTD of 27 g/day, one of 7 patients developed reversible grade 3 SOMNOLENCE
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[27] 4/2007 PHENYLBUTYRATE (PBA), and its metabolite PHENYLACETATE (PAA), induce growth inhibition and cellular differentiation in multiple tumor models
——————————————————————
Conversion of PBA to PAA and PHENYLACETYLGLUTAMINE (PAG) documented without catabolic saturation
——————————————————————
THERAPY WELL TOLERATED OVERALL
——————————————————————
Common ADVERSE EFFECTS included grade 1 NAUSEA/VOMITING, FATIGUE, and LIGHTHEADEDNESS
——————————————————————
Dose limiting TOXICITIES were SHORT-TERM MEMORY LOSS, SEDATION, CONFUSION, NAUSEA, and VOMITING
——————————————————————
Administration of PBA twice-daily infusion schedule is SAFE
======================================
None of the above publications indicate that antineoplastons are toxic as Gorski would have people believe

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

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

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

[14]Ba Primitive neuroectodermal tumor (13)

A10/AS2-1

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

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

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

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

When science based medicine keeps saying the following:
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[9] 9/1994 increasing incidence of melanoma and POOR RESPONSIVENESS OF DISSEMINATED DISEASE TO CONVENTIONAL TREATMENT CALL FOR DEVELOPMENT OF NEW THERAPEUTIC APPROACHES
======================================
[29] 9/27/1995 (7/17/2006) Alterations in expression of ras oncogenes are characteristic of wide variety of human neoplasms
——————————————————————
Accumulating evidence has linked elevated ras expression with disease progression and FAILURE OF TUMORS TO RESPOND TO CONVENTIONAL THERAPIES, INCLUDING RADIOTHERAPY AND CERTAIN CHEMOTHERAPIES
——————————————————————
observations led us to investigate response of ras-transformed cells to differentiation-inducer PHENYLACETATE (PA)
——————————————————————
Interestingly, IN CONTRAST TO THEIR RELATIVE RESISTANCE TO RADIATION and doxorubicin, ras-transformed cells were significantly more sensitive to PA than their parental cells
======================================
[30] 5/1996 CYOTOXIC CHEMOTHERAPIES OFTEN GIVE RISE TO MULTIDRUG RESISTANCE, WHICH REMAINS MAJOR PROBLEM IN CANCER MANAGEMENT
————————————————————
IN PURSUIT OF ALTERNATIVE TREATMENTS FOR CHEMORESISTANT TUMOR CELLS, we tested response of multidrug-resistant (MDR) tumor cell lines to aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB), 2 differentiation inducers currently in clinical trials
======================================
[15] 1996 Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which control neoplastic growth
——————————————————————
reported cytostatic inhibitory effect of A10 on human hepatocellular carcinoma cells and differentiation inducing effect of AS2-1 on various tumor cells suggest potential benefit for treatment of human hepatocellular carcinoma since TUMOR RECURS FREQUENTLY DESPITE INITIAL SUCCESSFUL TREATMENT
======================================
[31] 7/1997 Children with malignant GLIOMAS THAT PROGRESSED AFTER CONVENTIONAL THERAPY
——————————————————————
0 / 0% – EXHIBITED CLEAR-CUT TUMOR regression
======================================
[32] 2000 treatment combination PRODUCED NO SIGNIFICANT CHANGE in overall POOR prognosis of patients
——————————————————————
Most tumors responded initially to treatment but RECCURED as study progressed
——————————————————————
Based on POOR RESULTS, recommend ALTERNATIVE TREATMENTS be tested in patients with this type of tumor
======================================
[33] At time of approval, NO RESULTS were available from randomized controlled trials in refractory ANAPLASTIC ASTROCYTOMA that show clinical benefit such as improvement in disease-related symptoms or prolonged survival
======================================
[34] 12/2000 NO CLEAR PROOF OF EFFICACY
——————————————————————
NO BETTER THAN SURVIVAL BEFORE THE INTRODUCTION OF temozolomide
======================================
[35] 2002 p53 tumor suppressor gene plays important role in protecting cells from developing undesirable proliferation
——————————————————————
Mutant p53 gene or malfunctioning p53 protein found in more than 50% of cancer cells impedes DNA repair or apoptosis induction
——————————————————————
MAY BE WHY SOME CANCERS GAIN RESISTANCE TO CHEMOTHERAPY AND RADIATION AND BECOME MORE RESISTANT AFTER FREQUENT CANCER TREATMENTS
======================================
[36] 2004 outcome for patients with either type of tumor is POOR when STANDARD multimodality THERAPY IS USED
——————————————————————
children are ideal candidates for INNOVATIVE TREATMENT approaches
——————————————————————
33 / 100% – DIED OF DISEASE PROGRESSION
——————————————————————
administration of temozolomide after RT DIDN’T ALTER POOR PROGNOSIS associated with newly diagnosed diffuse BRAINSTEM GLIOMA in children
======================================
[37] 2/2008 addition of vincristine and oral VP-16 to standard external beam radiation causes moderate toxicity and DOESN’T IMPROVE SURVIVAL OF CHILDREN WITH DIFFUSE INTRINSIC BRAIN STEM GLIOMA
======================================
[38] 5/6/2009 Currently, NO DATA available from randomized controlled trials demonstrating improvement in disease-related symptoms or increased survival with Avastin in GLIOBLASTOMA
======================================
[39] 10/12/2011 Afinitor (ubependymal giant cell ASTROCYTOMA (SEGA) brain tumor)
——————————————————————
none of their tumors went away completely
======================================
[18] 8/1997 aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB) are novel antitumor agents currently under clinical evaluation
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ability to induce tumor differentiation in laboratory models and LOW CLINICALTOXICITY PROFILE makes them promising candidates for COMBINATION WITH CONVENTIONAL THERAPIES
======================================
So what does Gorski think is going to fill the void?

His clinical trial drug ?

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

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

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

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

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

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References:
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Dvorit D. Samid learned about antineoplastons from Burzynski
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[1] 4/1/1992
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SAMID, D., Shack, S., and Sherman, l.. T.
http://www.ncbi.nlm.nih.gov/pubmed/1372534/
Cancer Res., 52: 1988-1992, 1992
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Cancer Res April 1, 1992 52; 1988v I
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Cancer Res 52:1988,1992
http://m.cancerres.aacrjournals.org/content/52/7/1988.full.pdf#page=1
SAMID D, Shack S, Ti-Sherman L
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
PHENYLACETATE-A novel nontoxic inducer of TUMOR CELL differentiation
↵1 Supported by Elan Pharmaceutical Corporation Grant G174ED
Reference: 12 (SAMID, D.)
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[2] .8/20/1992
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Dover GJ, Brusilow S, SAMID D. Increased fetal hemoglobin in patients receiving sodium 4-PHENYLBUTYRATE. N Engl J Med. 1992 Aug 20;327(8):569–570
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August 20, 1992
N Engl J Med 1992; 327:569-570
http://www.nejm.org/doi/full/10.1056/NEJM199208203270818
N Engl J Med 327569, 1992
Dvorit Samid, Ph.D
National Cancer Institute
, Bethesda, MD
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[3] 9/15/1992
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SAMID D, Yeh A, Prasanna P. Induction of erythroid differentiation and fetal hemoglobin production in human leukemic cells treated with phenylacetate. Blood. 1992 Sep 15;80(6):1576–1581
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Blood September 15, 1992 vol. 80 no. 6 1576-1581
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Blood 80:1576, 1992
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.abstract
Blood 80(6):1576–1581
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.full.pdf
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD
SAMID D References: 15, 20-21 and 34
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[4] 5/1993
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SAMID D, Shack S , Myers CE . Selective growth arrest and phenotypic reversion of prostate cancer cells in vitro by NONTOXIC pharmacological concentrations of PHENYLACETATE . J. Clin. Invest . 1993;91:2288
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J Clin Invest. 1993 May;91(5):2288-95
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J Clin Invest. 1993 May; 91(5): 2288–2295
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Published in Volume 91, Issue 5 (May 1993)
http://m.jci.org/articles/view/116457
J Clin Invest. 1993;91(5):2288–2295
1993, The American Society for Clinical Investigation
http://m.jci.org/articles/view/116457/pdf.mobile
J Clin Invest 91:2288, 1993
PMCID: PMC288233
doi:10.1172/JCI116457
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
SAMID D References: 9, 13-14, 17 and 33
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[5] .10/1/1993
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Enhanced fetal
hemoglobin production by PHENYLACETATE and 4-PHENYLBUTYRATE in erythroid precursors derived from normal blood donors and patients with sickle cell anemia and P-thalassemia
http://www.ncbi.nlm.nih.gov/pubmed/7691251/
Blood. 1993 Oct 1;82(7):2203-9
http://www.ncbi.nlm.nih.gov/m/pubmed/7691251/
Blood 822203, 1993
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Blood October 1, 1993 vol. 82 no. 7 2203-2209
http://m.bloodjournal.hematologylibrary.org/content/82/7/2203.abstract
1993 82: 2203-2209
http://m.bloodjournal.hematologylibrary.org/content/82/7/2203.full.pdf
Blood 82(7):2203–2209
Department of Hematology, Hadassah University Hospital, Jerusalem, Israel
Fibach E, Prasanna P, Rodgers GP, SAMID D
SAMID D References: 15, 19-21 and 32
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[6] 2/15/1994
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SAMID, D., Ram, Z., Hudgins, W. R., Shack, S., Liu, L., Waibridge, S., Oldfield, E. H., and Myers, C. E. Selective activity of PHENYLACETATE against malignant gliomas: resemblance to fetal brain damage in phenylketonuria. Cancer Res., 54: 891-895, 1993
http://www.ncbi.nlm.nih.gov/pubmed/8313377/
Cancer Res. 1994 Feb 15;54(4):891-5
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Cancer Res February 15, 1994 54; 891
http://cancerres.aacrjournals.org/content/54/4/891/
Cancer Res 1994;54:891-895
Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
Work supported by funds from Elan Pharmaceutical Research Corporation through Cooperative Research and Development Agreement (CACR-0139)
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[7] 4/1/1994
� � � � � � � � � � � � � � � � �
A phase I and pharmacokinetic study of intravenous PHENYLACETATE in patients with cancer
http://www.ncbi.nlm.nih.gov/pubmed/8137283
Cancer Res. 1994 Apr 1;54(7):1690-4
http://www.ncbi.nlm.nih.gov/m/pubmed/8137283
Cancer Res 54(7):1690-4 (1994), PMID.8137283
http://m.cancerres.aacrjournals.org/content/54/7/1690.abstract
Clinical Pharmacology Branch, National Cancer Institute, NIH, Bethesda, Maryland
http://m.cancerres.aacrjournals.org/content/54/7/1690.full.pdf
Thibault A, Cooper MR, Figg WD, Venzon DJ, Sartor AO, Tompkins AC, Weinberger MS, Headlee DJ, McCall NA, SAMID D, et al.
http://cancerres.aacrjournals.org/content/54/7/1690
Study supported in part by grant from Elan Pharmaceutical Research Co
SAMID D
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BURZYNSKI
Reference: 13
13. BURZYNSKI, S. R., Kubove E., Burzynski, B. Treatment of hormonally refractory cancer of the prostate with antineoplaston AS2-1. Drugs Exp. Clin. Res., 16: 361-369, 1990
http://www.ncbi.nlm.nih.gov/pubmed/2152694/
Drugs Exp Clin Res. 1990;16(7):361-9
http://www.ncbi.nlm.nih.gov/m/pubmed/2152694/
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[8] 6/1/1994
� � � � � � � � � � � � � � � � �
Growth inhibition, tumor maturation, and extended survival in experimental brain tumors in rats treated with PHENYLACETATE.
http://www.ncbi.nlm.nih.gov/pubmed/8187079/
Cancer Res 54:2934-2927, 1994
http://www.ncbi.nlm.nih.gov/m/pubmed/8187079/
Cancer Res. 1994 Jun 1;54(11):2923-7
http://m.cancerres.aacrjournals.org/content/54/11/2934.abstract?ijkey=03bc67e581ef77536842806b949046916458d548&keytype2=tf_ipsecsha
Cancer Res 54(11):2923–2927
http://m.cancerres.aacrjournals.org/content/54/11/2923.abstract
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland
http://m.cancerres.aacrjournals.org/content/54/11/2923.full.pdf
Ram Z, SAMID D, Walbridge S, et al:
http://cancerres.aacrjournals.org/content/54/11/2923
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[9] 1994
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Liu L , Shack S , Stetler-Stevenson WG , Hudgins WR , SAMID D . Differentiation of cultured human melanoma cells induced by the aromatic fatty acids PHENYLACETATE and PHENYLBUTYRATE . J. Invest. Dermatol . 1994;103:335
http://www.ncbi.nlm.nih.gov/pubmed/8077698/
J Invest Dermatol. 1994 Sep;103(3):335-40
http://www.ncbi.nlm.nih.gov/m/pubmed/8077698/
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
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[10] 4/1995
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Disposition of PHENYLBUTYRATE and its metabolites, PHENYLACETATE and PHENYLACETYLGLUTAMINE.
J Clin Pharmacol 35:368-373, 1995 Abstract
http://www.ncbi.nlm.nih.gov/pubmed/7650225/
J Clin Pharmacol 35:368-373, 1995 Abstract
http://www.ncbi.nlm.nih.gov/m/pubmed/7650225/
The Journal of Clinical Pharmacology
Volume 35, Issue 4, pages 368–373, April 1995
http://m.jcp.sagepub.com/content/35/4/368.abstract?ijkey=74bff0d86ce76b404728762fe2a1bfde1641fa41&keytype2=tf_ipsecsha
J Clin Pharmacol. 1995 Apr;35(4):368-73
http://onlinelibrary.wiley.com/doi/10.1002/j.1552-4604.1995.tb04075.x/abstract;jsessionid=DFDEF1599D764E2845EC2897269C198B.d01t01
Article first published online: 8 MAR 2013
http://onlinelibrary.wiley.com/doi/10.1002/j.1552-4604.1995.tb04075.x/abstract;jsessionid=43600D49608A093971D675F3DB5FF13D.d01t03
Piscitelli SC, Thibault A, Figg WD, et al: (SAMID D)
http://jcp.sagepub.com/content/35/4/368
Pharmacy Department, National Institutes of Health, Bethesda, Maryland, USA
DOI: 10.1002/j.1552-4604.1995.tb04075.x
http://m.jcp.sagepub.com/content/35/4/368.abstract?ijkey=74bff0d86ce76b404728762fe2a1bfde1641fa41&keytype2=tf_ipsecsha
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[11] 6/15/1995
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Phase I study of PHENYLACETATE administered twice daily to patients with cancer
http://www.ncbi.nlm.nih.gov/pubmed/7773944/
Cancer. 1995 Jun 15;75(12):2932-8
http://www.ncbi.nlm.nih.gov/m/pubmed/7773944/
Cancer 75(12):2932–2938
Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
Thibault A, SAMID D, Cooper MR, Figg WD, Tompkins AC, Patronas N, et al
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[12] 10/12/1995
� � � � � � � � � � � � � � � � �
Cytostatic activity of PHENYLACETATE and derivatives against tumor cells:
Correlation with lipophilicity and inhibition of protein prenylation.
http://www.ncbi.nlm.nih.gov/pubmed/7488244/
Biochem Pharmacol. 1995 Oct 12;50(8):1273-9
http://www.ncbi.nlm.nih.gov/m/pubmed/7488244/
Biochem Pharmacol 50:1273-1279, 1995
http://www.sciencedirect.com/science/article/pii/0006295295020133
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD, USA
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[13] 10/1995
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Stockhammer G, Manley GT, Johnson R, et al: (SAMID D) Inhibition of proliferation and induction of differentiation in medulloblastoma and astrocytoma-derived cell lines with PHENYLACETATE. J Neurosurg 83:672-681, 1995
http://www.ncbi.nlm.nih.gov/pubmed/7674018/
J Neurosurg. 1995 Oct;83(4):672-81
http://www.ncbi.nlm.nih.gov/m/pubmed/7674018/
Cotzias Laboratory of Neuro-Oncology, Memorial Sloan-Kettering Cancer Center, New York, New York, USA
http://thejns.org/doi/abs/10.3171/jns.1995.83.4.0672?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed&#038;
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[14] 1995
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Toxicological study on antineoplastons A-10 and AS2-1 in cancer patients
http://www.ncbi.nlm.nih.gov/pubmed/8667595
Kurume Med J. 1995;42(4):241-9
http://www.ncbi.nlm.nih.gov/m/pubmed/8667595
The Kurume Medical Journal
Vol. 42 (1995) No. 4 P 241-249
https://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_article
JST.Journalarchive/kurumemedj1954/42.241
https://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_pdf
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://dx.doi.org/10.2739/kurumemedj.42.241
Tsuda H, Hara H, Eriguchi N, Nishida H, Yoshida H, Kumabe T, Sugita Y
https://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_article/references
Burzynski References: 1 – 3 and 5
Nishida et al. (Japan) A-10 Reference: 4 and 7
Muldoon et al. A-10 Reference: 6
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[15] 1996
� � � � � � � � � � � � � � � � �
Inhibitory effect of antineoplaston A10 and AS2-1 on human hepatocellular carcinoma
Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/pubmed/8755117
Kurume Med J. 1996;43(2):137-47
http://www.ncbi.nlm.nih.gov/m/pubmed/8755117
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article
Burzynski References: 1 – 3, 5 and 7
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article/references
SAMID Reference: 13 (who learned from Burzynski re PHENYLACETATE)
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_pdf
Nishida et al. (Japan) A10 Reference: 4 and 10
Muldoon et al. A10 Reference: 8
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[16] 5/1996
� � � � � � � � � � � � � � � �
Vulnerability of multidrug-resistant tumor cells to the aromatic fatty acids phenylacetate and PHENYLBUTYRATE
http://www.ncbi.nlm.nih.gov/pubmed/9816242/
Clin Cancer Res. 1996 May;2(5):865-72
http://www.ncbi.nlm.nih.gov/m/pubmed/9816242/
Clin Cancer Res 2(5):865–872
http://m.clincancerres.aacrjournals.org/content/2/5/865.abstract
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland, USA
http://m.clincancerres.aacrjournals.org/content/2/5/865.full.pdf
Shack S, Miller A, Liu L, Prasanna P, Thibault A, SAMID D
http://clincancerres.aacrjournals.org/content/2/5/865
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[17] 12/1996
� � � � � � � � � � � � � � � � �
Gorospe M, Shack S, Guyton KZ, et al: (SAMID D)
Up-regulation and functional role of p21Waf1/Cip1 during growth arrest of human breast carcinoma MCF-7 cells by PHENYLACETATE. Cell Growth Differ 7:1609-1615, 1996
http://www.ncbi.nlm.nih.gov/pubmed/8959328/
Cell Growth Differ. 1996 Dec;7(12):1609-15
http://www.ncbi.nlm.nih.gov/m/pubmed/8959328/
Cell Growth Differ 7(12):1609–1615
http://cgd.aacrjournals.org/cgi/reprint/7/12/1609.pdf
Laboratory of Cellular and Molecular Biology, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, Maryland, USA
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[18] 8/1997
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Miller AC, Whittaker T, Thibault A, et al: (SAMID D)
Modulation of radiation response of human tumor cells by the differentiation inducers, PHENYLACETATE and PHENYLBUTYRATE. Int J Radiat Biol 72:211-218, 1997
http://www.ncbi.nlm.nih.gov/pubmed/9269314/
Int J Radiat Biol. 1997 Aug;72(2):211-8
http://www.ncbi.nlm.nih.gov/m/pubmed/9269314/
Armed Forces Radiobiology, Research Institute, Bethesda, MD, USA
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[19] 1997
� � � � � � � � � � � � � � � � �
PHENYLACETATE and PHENYLBUTYRATE as novel, NONTOXIC differentiation inducers
http://www.ncbi.nlm.nih.gov/pubmed/9547596
Adv Exp Med Biol (1997), PMID.9547596
http://www.ncbi.nlm.nih.gov/m/pubmed/9547596
Adv Exp Med Biol. 1997;400A:501-5
http://link.springer.com/chapter/10.1007%2F978-1-4615-5325-0_67
DOI
10.1007/978-1-4615-5325-0_67
http://link.springer.com/content/pdf/10.1007%2F978-1-4615-5325-0_67.pdf
Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury 2
Advances in Experimental Medicine and Biology Volume 400, 1997, pp 501-505
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD USA
D D SAMID, W R WR Hudgins, … C E CE Myers
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[20] 10/1997
� � � � � � � � � � � � � � � �
Impact of the putative differentiating agents sodium PHENYLBUTYRATE and sodium PHENYLACETATE on proliferation, differentiation, and apoptosis of primary neoplastic myeloid cells
http://www.ncbi.nlm.nih.gov/pubmed/9815560/
Clin Cancer Res. 1997 Oct;3(10):1755-62
http://www.ncbi.nlm.nih.gov/m/pubmed/9815560/
Clin Cancer Res October 1997 3; 1755
http://m.clincancerres.aacrjournals.org/content/3/10/1755.full.pd
Clin Cancer Res. 1997a;3:1755–1762
http://m.clincancerres.aacrjournals.org/content/3/10/1755.abstract
The Johns Hopkins Oncology Center, Baltimore, Maryland, USA
http://m.clincancerres.aacrjournals.org/content/3/10/1755.full.pdf
Gore SD, SAMID D, Weng LJ
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[21] 11..12/1997
� � � � � � � � � � � � � � � � �
Antineoplaston AS2-1 for maintenance therapy in liver cancer
H Tsuda phase I clinical trial
http://www.ncbi.nlm.nih.gov/pubmed/21590224
Oncol Rep. 1997; 4:1213- 1216
http://www.ncbi.nlm.nih.gov/m/pubmed/21590224
Oncol Rep. 1997 Nov-Dec;4(6):1213-6
http://www.spandidos-publications.com/or/4/6/1213
Oncol Rep 4 (6):1213-6 (1997)
Oncology Reports
4 (6):1213-6
KURUME UNIV,SCH MED,DEPT SURG,KURUME,FUKUOKA,JAPAN. KURUME UNIV,SCH MED,DEPT INTERNAL MED,KURUME,FUKUOKA,JAPAN. KURUME UNIV,SCH MED,DEPT RADIOL,KURUME,FUKUOKA,JAPAN
� � � � � � � � � � � � � � � �
[22] 6/1999
� � � � � � � � � � � � � � � �
PHENYLBUTYRATE induces cell differentiation and modulates Epstein-Barr virus gene expression in Burkitt’s lymphoma cells
http://www.ncbi.nlm.nih.gov/pubmed/10389940/
Clin Cancer Res. 1999 Jun;5(6):1509-16
http://www.ncbi.nlm.nih.gov/m/pubmed/10389940/
Clin Cancer Res 5(6):1509–1516
http://m.clincancerres.aacrjournals.org/content/5/6/1509.abstract
Clin Cancer Res June 1999 5; 1509
http://m.clincancerres.aacrjournals.org/content/5/6/1509.long
Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA
http://clincancerres.aacrjournals.org/content/5/6/1509
Bar-Ner M, Thibault A, Tsokos M, Magrath IT, SAMID D
Supported in part by funds from Elan Pharmaceutical Research Corporation
� � � � � � � � � � � � � � � � �
[23] 8/2001
� � � � � � � � � � � � � � � � �
A phase Idose escalation and bioavailability study of oral sodium PHENYLBUTYRATE in patients with refractory solid tumor malignancies
http://www.ncbi.nlm.nih.gov/pubmed/11489804
Clin Cancer Res. 2001 Aug;7(8):2292-.300
http://www.ncbi.nlm.nih.gov/m/pubmed/11489804
Clin Cancer Res 7(8):2292-.300 (2001), PMID.11489804
http://m.clincancerres.aacrjournals.org/content/7/8/2292.long
Division of Medical Oncology, Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, USA
J Gilbert, S D Baker, … M A Carducci
SAMID D References: 2-3, 5-6, 15 and 20
� � � � � � � � � � � � � � � � �
[24] 10/2001
� � � � � � � � � � � � � � � � �
A Phase I clinical and pharmacological evaluation of sodium PHENYLBUTYRATE on an 120-h infusion schedule
http://www.ncbi.nlm.nih.gov/pubmed/11595694
Clin Cancer Res. 2001 Oct;7(10):3047-55
http://www.ncbi.nlm.nih.gov/m/pubmed/11595694
Clin Cancer Res 7(10):3047-55 (2001), PMID.11595694
http://m.clincancerres.aacrjournals.org/content/7/10/3047.long
Division of Medical Oncology, The Johns Hopkins Oncology Center, Bunting-Blaustein Cancer Research Building, Baltimore, MD, USA
M A Carducci, J Gilbert, … R C Donehower
SAMID D References: 10-11, 13-14, 17-18, 23-24, 27, 33, 40-41 and 47
� � � � � � � � � � � � � � � � �
[25] 2003
� � � � � � � � � � � � � � � � �
Long-term survival following treatment with antineoplastons for colon cancer with unresectable multiple liver metastases: report of a case
http://www.ncbi.nlm.nih.gov/pubmed/12768372
Long-Term Survival Following Treatment with Antineoplastonsfor Colon Cancer with Unresectable Multiple Liver Metastases:
Report of a Case
A10 and AS2-1 – Phase II Clinical Trial
Hideaki Tsuda
http://www.springerlink.com/content/b48ch3ha165nbrqp
Surg Today. 2003;33(6):448-53
http://link.springer.com/article/10.1007%2Fs10595-002-2503-2
Surg Today 2003; 33:448–53
http://link.springer.com/content/pdf/10.1007%2Fs10595-002-2503-2
Surg Today. 2003; 33:448-453
http://link.springer.com/article/10.1007%2Fs10595-002-2503-2?LI=true
33 (6):448-53
http://link.springer.com/content/pdf/10.1007%2Fs10595-002-2503-2
Surgery Today, Springer
http://sciencelinks.jp/j-east/article/200313/000020031303A0389449.php
Surg Today 2003
http://sciencelinks.jp/j-east/article/200313/000020031303A0389449.php
DOI: 10.1007/s10595-002-2503-2
http://ci.nii.ac.jp/naid/10015483373
Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan
http://ci.nii.ac.jp/naid/10015483373
� � � � � � � � � � � � � � � �
[26] 4/2005
� � � � � � � � � � � � � � � �
Oral sodium PHENYLBUTYRATE in patients with recurrent malignant gliomas:

A dose escalation and pharmacologic study
http://www.ncbi.nlm.nih.gov/pubmed/15831235/
Neuro Oncol. 2005 Apr;7(2):177-82
http://www.ncbi.nlm.nih.gov/m/pubmed/15831235/
Neuro-oncol. 2005 April; 7(2): 177–182 PMCID: PMC1871887
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1871887/pdf/neu0702p177.pdf
The New Approaches to Brain Tumor Therapy CNS Consortium, Winship Cancer Institute, Emory University, Atlanta, GA, USA
Buckner Reference: 3
SAMID D References: 12, 17 and 19-21
� � � � � � � � � � � � � � � � �
[27] 4/2007
� � � � � � � � � � � � � � � � �
Phase I dose escalation clinical trial of PHENYLBUTYRATE sodium administered twice daily to patients with advanced solid tumors
http://www.ncbi.nlm.nih.gov/pubmed/17053987
Invest New Drugs. 2007 Apr;25(2):131-8. Epub 2006 Oct 20
http://www.ncbi.nlm.nih.gov/m/pubmed/17053987
Investigational New Drugs
April 2007, Volume 25, Issue 2, pp 131-138
http://link.springer.com/article/10.1007%2Fs10637-006-9017-4
Invest New Drugs 25(2):131-8 (2007), PMID.17053987
Department of Medicine, Memorial Sloan-Kettering Cancer Center, Joan and Sanford I. Weill Medical College of Cornell Medical Center, New York, New York, USA
Luis H LH Camacho, Jon J Olson, … Mark G MG Malkin
SAMID D References: 4-5, 7, 20, 24, 30 and 32-38
� � � � � � � � � � � � � � � � �
[28] 2005
� � � � � � � � � � � � � � � � �
14. Burzynski SR, Weaver RA, Janicki T, et al.: Long-term survival of high-risk pediatric patients with primitive neuroectodermal tumors treated with antineoplastons A10 and AS2-1. Integr Cancer Ther 4 (2): 168-77, 2005
http://www.ncbi.nlm.nih.gov/pubmed/15911929/
Integr Cancer Ther. 2005 Jun;4(2):168-77
http://www.ncbi.nlm.nih.gov/m/pubmed/15911929/
� � � � � � � � � � � � � � � � �
[29] 9/27/1995
� � � � � � � � � � � � � � � � �
Increased susceptibility of ras-transformed cells to PHENYLACETATE is associated with inhibition of p21ras isoprenylation and phenotypic reversion. Int J Cancer 63:124-129, 1995
http://www.ncbi.nlm.nih.gov/pubmed/7558439/
Int J Cancer. 1995 Sep 27;63(1):124-9
http://www.ncbi.nlm.nih.gov/m/pubmed/7558439/
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD, USA
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910630122/abstract
Int J Cancer 63:124-129, 1995
Int J Cancer. 1995 Sep 27;63(1):124-9.
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910630122/references
International Journal of Cancer
Volume 63, Issue 1, Article first published online: 17 JUL 2006
DOI: 10.1002/ijc.2910630122
Shack S, Chen L-C, Miller AC, et al: (SAMID D)
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910630122/abstract
Shack, S., Chen, L-C., Miller, A. C., Danesi, A., and SAMID, D. Int. J. Cancer, 63: 124-129, 1995
� � � � � � � � � � � � � � � � �
[30] 5/1996
� � � � � � � � � � � � � � � � �
Shack, S., Miller, A., Liu, L., Prasanna, P., Thibault, A., and SAMID, D.. Vulnerability of MULTIDRUG-RESISTANT TUMOR CELLS to the aromatic fatty acids PHENYLACETATE and PHENYLBUTYRATE. Clin. Cancer Res., 2: 865-872, 1996
http://www.ncbi.nlm.nih.gov/pubmed/9816242/
Clin Cancer Res. 1996 May;2(5):865-72
http://www.ncbi.nlm.nih.gov/m/pubmed/9816242/
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892, USA
http://m.clincancerres.aacrjournals.org/content/2/5/865.abstract

http://m.clincancerres.aacrjournals.org/content/2/5/865.full.pdf
� � � � � � � � � � � � � � � � �
[31] 7/1997
� � � � � � � � � � � � � � � � �
A phase I study of high-dose tamoxifen for the treatment of refractory malignant gliomas of childhood
http://www.ncbi.nlm.nih.gov/pubmed/9815790/
Clin Cancer Res. 1997 Jul;3(7):1109-15
http://www.ncbi.nlm.nih.gov/m/pubmed/9815790/
Clin Cancer Res July 1997 3; 1109
http://m.clincancerres.aacrjournals.org/content/3/7/1109.full.pd
Department of Neurosurgery, Children’s Hospital of Pittsburgh, Pittsburgh, Pennsylvania, USA
http://clincancerres.aacrjournals.org/content/3/7/1109
� � � � � � � � � � � � � � � � �
[32] 2000
� � � � � � � � � � � � � � � � �
Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse BRAINSTEM GLIOMAS:

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

new indication
http://www.ncbi.nlm.nih.gov/pubmed/11475493/
Prescrire Int. 2000 Dec;9(50):170-1.
http://www.ncbi.nlm.nih.gov/m/pubmed/11475493/
� � � � � � � � � � � � � � � � �
[35] 2002
� � � � � � � � � � � � � � � � �
A novel strategy for remission induction and maintenance in cancer therapy
A10 and AS2-1
H Tsuda
http://www.ncbi.nlm.nih.gov/pubmed/11748457
Oncol Rep 2002;9:65–8
http://www.ncbi.nlm.nih.gov/m/pubmed/11748457
Oncol. Rep. 2002;9:65-68
http://www.spandidos-publications.com/or/9/1/65
Oncol Rep 9(1):65-8 (2002)
Oncology Reports, Spandidos Publications
Department of Anesthesiology, Kurume University, School of Medicine, Fukuoka-ken, Japan
� � � � � � � � � � � � � � � � �
[36] 2004
� � � � � � � � � � � � � � � � �
Supratentorial high-grade ASTROCYTOMA and DIFFUSE BRAINSTEM GLIOMA:

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

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

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

Burzynski: Oh, RATS!!!

After again showing how questionable the “research” of #ScienceBasedMedicine Dr. David H. “Orac” Gorski is:
https://stanislawrajmundburzynski.wordpress.com/2013/07/23/is-dr-david-h-orac-gorski-down-and-out-in-detroit-and-an-ethically-bankrupt-researcher-2/
and he is involved in the “War on Cancer,”(!!!) I decided to provide this more in-depth listing of Burzynski related scientific publications regarding animal, mice, and rat studies re: antineoplastons
——————————————————————
1983 – Burzynski SR, Hendry LB, Mohabbat MO, et al. Purification of structure determination, synthesis and animal toxicity studies of antineoplaston A10. In: Proceedings of the 13th International Congress of Chemotherapy. Vienna, Austria; 1983:17, PS. 12.4 11-4.
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1984 – Burzynski, S.R., Mohabbat MO, Burzynski B.
Animal toxicology studies on oral formulation of antineoplaston A10
Drugs Exptl Clin Res 1984;10:113-118
——————————————————————
1984 – Lee, S.S., Mohabbat, M.O., Burzynski, S.R.
Tissue culture and animal toxicity studies of antineoplaston A2
Drugs Exptl Clin Res 1984;10:607-610
——————————————————————
1985 – Lee, S.S., Mohabbat, M.O., Burzynski, S.R.
Tissue culture and acute animal toxicity studies of antineoplaston A2
Future Trends in Chemotherapy 1985;6:481-484
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1986 – Burzynski, S., Mohabbat. M., Lee, S.
Preclinical studies of antineoplaston AS2-1 in mice with oral administration
Drugs Exptl Clin Res 1986;132
——————————————————————
1986 – Burzynski, S. R., Mohabbat, M. O. , Le e, S. S. Pre clinical studies of antineoplaston AS2-1 and antineoplaston AS2-5
Drugs Exptl Clin Res 1986;12 (suppl1):11-16
http://www.ncbi.nlm.nih.gov/pubmed/3743376/
Drugs Exp Clin Res. 1986;12 Suppl 1:11-6.
http://www.ncbi.nlm.nih.gov/m/pubmed/3743376/
——————————————————————
1986 – Ashraf, AQ., Liau, M.C., Mohabbat, M.O., Burzynski, S.R.
Preclinical studies of antineoplaston A10 injections.
Drugs Exptl Clin Res 1986;12 (suppl 1):37-45.
http://www.ncbi.nlm.nih.gov/pubmed/3743379/
Drugs Exp Clin Res. 1986;12 Suppl 1:37-45.
http://www.ncbi.nlm.nih.gov/m/pubmed/3743379/
——————————————————————
1986 – Burzynski, S.R., Mohabbat M.O.
Chronic animal toxicity studies on antineoplaston A2.
Drugs Exptl Clin Res 1986;12 (suppl 1):73-75.
http://www.ncbi.nlm.nih.gov/pubmed/3743382/
Drugs Exp Clin Res. 1986;12 Suppl 1:73-5.
http://www.ncbi.nlm.nih.gov/m/pubmed/3743382/
——————————————————————
1987 – Lee, S.S., Mohabbat, M.O., Burzynski, SR
In vitro cancer growth inhibition and animal toxicity studies of antineoplaston A3
Drugs Exptl Clin Res 1987;13 (suppl1):13-16
http://www.ncbi.nlm.nih.gov/pubmed/3569011/
Drugs Exp Clin Res. 1987;13 Suppl 1:13-6.
http://www.ncbi.nlm.nih.gov/m/pubmed/3569011/
——————————————————————
1987 – Lee, S.S., Burzynski, S.R
Tissue culture and animal toxicity studies of antineoplaston A5
Drugs Exptl Clin Res 1987;13 (suppl 1):31-5.
http://www.ncbi.nlm.nih.gov/pubmed/3569013/
Drugs Exp Clin Res. 1987;13 Suppl 1:31-5.
http://www.ncbi.nlm.nih.gov/m/pubmed/3569013/
——————————————————————
1987 – Ashraf AQ, Liau MC, Kampalath BN, et al. Pharmacokinetic study of radioactive antineoplaston A10 following oral administration in rats. Drugs Exptl Clin Res. 1987;13(suppl 1):45-50.
http://www.ncbi.nlm.nih.gov/pubmed/3569015/

http://www.ncbi.nlm.nih.gov/m/pubmed/3569015/
——————————————————————
1988 – Ashraf, AQ., Kampalath, B.N., Burzynski, S.R
Pharmacokinetic analysis of antineoplaston A10 injections following intravenous administration in rats
Adv Exptl Clin Chemother 1988;6:33-39
http://www.encognitive.com/node/2449
——————————————————————
7/20/1988 – Chemopreventive effect of antineoplaston A-10 on urethane-induced pulmonary neoplasm in mice
http://www.ncbi.nlm.nih.gov/pubmed/3183462
Nihon Gan Chiryo Gakkai Shi. 1988 Jul.20; 23 (7):1560-5
http://www.ncbi.nlm.nih.gov/m/pubmed/3183462
23(7):1560-5 (1988)
Tsuda
N E
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1/20/1990 – A-10 Injection – The anticancer effect of antineoplaston A-10 on human breast cancer serially transplanted to athymic mice
http://www.ncbi.nlm.nih.gov/pubmed/2157780
Nihon Gan Chiryo Gakkai Shi. 1990 Jan 20;25(1):1-5
http://www.ncbi.nlm.nih.gov/m/pubmed/2157780
1st Department of Surgery, Kurume University School of Medicine
The Anticancer Effect of Antineoplaston A-10 on Human Breast Cancer Serially Transplanted to Athymic Mice, Journal of the Japan Society for Cancer Therapy 25(1):1-5 (1990)
Hashimoto K, Koga T, Shintomi Y, Tanaka M, Kakegawa T, Tsuda H, Hara H.
http://www.abstractboard.com/abstract/2157780/The-anticancer-effect-of-antineoplaston-A-10-on-human-breast-cancer-serially-transplanted-to-athymic.html
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1990 – Inhibitory effect of antineoplaston A-10 on breast cancer transplanted to athymic mice and human hepatocellular carcinoma cell lines. The members of Antineoplaston Study Group
Tsuda H (Japan) et al
http://www.ncbi.nlm.nih.gov/pubmed/2175003
Kurume Med J. 1990;37(2):97-104
http://www.ncbi.nlm.nih.gov/m/pubmed/2175003
Kurume Med J 37 (2):97-104 (1990)
http://www.jstage.jst.go.jp/article/kurumemedj1954/37/2/37_2_97/_article
Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/37/2/37_2_97/_article/references
Burzynski References: 1 – 8 and 11 – 14
http://www.jstage.jst.go.jp/article/kurumemedj1954/37/2/37_2_97/_pdf
The Kurume Medical Journal
http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.1992.tb01960.x/abstract
J-STAGE, Japan Science and Technology Information Aggregator, Electronic
http://ci.nii.ac.jp/naid/130000888719
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1991 – Inhibitory effect of orally administered antineoplaston A10 on the growth curve of human breast cancer transplanted to athymic mice
http://jglobal.jst.go.jp/public/20090422/200902015871267390
J Jpn Soc Cancer Ther 26:595-601, 1991
26:3:595-601:1991 03
Kurume Univ. School of Medicine
NISHIDA H, YOSHIDA H, KUBOTA H
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5/1992 – The inhibitory effect of the combination of antineoplaston A-10 injection with a small dose of cis-diamminedichloroplatinum on cell and tumor growth of human hepatocellular carcinoma
H TSUDA, et al (Japan)
http://www.ncbi.nlm.nih.gov/pubmed/1377669
The Inhibitory Effect of the Combination of Antineoplaston A-10 Injection with a Small Dose of cis-Diamminedichloroplatinum on Cell and Tumor Growth of Human Hepatocellular Carcinoma
http://www.ncbi.nlm.nih.gov/m/pubmed/1377669
Jpn J Cancer Res. 1992 May;83(5):527-31
http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.1992.tb01960.x/abstract
Jpn. J. Cancer Res. 83, 527-531
http://onlinelibrary.wiley.com/store/10.1111/j.1349-7006.1992.tb01960.x/asset/j.1349-7006.1992.tb01960.x.pdf?v=1&t=hd97ht7z&s=3481466c7830e5f8e2bb925a698de6f8155da747
Jpn J Cancer Res. 1992 May;83 (5):527-31
http://onlinelibrary.wiley.com/store/10.1111/j.1349-7006.1992.tb01960.x/asset/j.1349-7006.1992.tb01960.x.pdf;jsessionid=4ECD3F595A3971B5AB87763862867844.d03t02?v=1&t=hbmd55gj&s=a14b626a37db3ecd558109cee30dfe26c71827763862867844
Jpn J Cancer Res 83 (5):527-31 (1992)
http://onlinelibrary.wiley.com/store/10.1111/j.1349-7006.1992.tb01960.x/asset/j.1349-7006.1992.tb01960.x.pdf?v=1&t=hkfile3i&s=2756f110cf2202084cfc90a3715d8f1f9df7774c
Department of Anesthesiology, Kurume University, School of Medicine, Fukuoka-ken
http://onlinelibrary.wiley.com/store/10.1111/j.1349-7006.1992.tb01960.x/asset/j.1349-7006.1992.tb01960.x.pdf?v=1&t=hdcl29bl&s=dd78f02b92e0f5544c136e7b897a7d65bcf5dc71&systemMessage=Wiley+Online+Library+will+be+disrupted+on+23+February+from+10%3A00-12%3A00+BST+%2805%3A00-07%3A00+EDT%29+for+essential+maintenance
Article first published online: 26 AUG 2005
DOI: 10.1111/j.1349-7006.1992.tb01960.x
Japan Journal Cancer Research
Cancer Science, Wiley Online Library
Volume 83, Issue 5, pages 527–531, May 1992
Burzynski References: 1, 4 – 7 and 9
http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.1992.tb01960.x/references
Nishida (Japan) A-10 Reference: 2
——————————————————————
11/15/1995 – Sodium PHENYLACETATE Induces Growth Inhibition and Bcl-2 Down-Regulation and Apoptosis in MCF7ras Cells in Vitro and in nude mice
http://cancerres.aacrjournals.org/content/55/22/5156.abstract?sid=29b3d08f-4e59-473c-a804-10c68ed99112
Cancer Res. 1995 Nov 15;55(22):5156-60.
http://cancerres.aacrjournals.org/content/55/22/5156.full.pdf
Institut d’Oncologie Moléculaire et Cellulaire Humaine, Bobigny, France.
http://m.cancerres.aacrjournals.org/content/55/22/5156.full.pdf#page=1
References:
http://m.cancerres.aacrjournals.org/content/55/22/5156
1. SAMID, D., Shac, S., and Sherman, L. T. Phenylacetate: a novel nontoxic inducer of tumor cell differentiation. Cancer Res., 52: 1988-1992, 1992
http://www.naderlibrary.com/burzynski.screen3.htm
——————————————————————
9/2001 – Sodium PHENYLACETATE enhances the inhibitory effect of dextran derivative on breast cancer cell growth in vitro and in nude mice
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2375080
Br J Cancer. 2001 September; 85(6): 917–923.
doi: 10.1054/bjoc.2001.1993
PMCID: PMC2375080
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3/2005 Effects of antineoplaston AS2-1 against post-operative lung metastasis in orthotopically implanted colon cancer in nude rat
Hideaki TSUDA
http://www.ncbi.nlm.nih.gov/pubmed/15706406
Oncol Rep. 2005 Mar; 13 (3):389-95
http://www.ncbi.nlm.nih.gov/m/pubmed/15706406
Oncol Rep 13 (3): 389-95 (2005)
http://www.spandidos-publications.com/or/13/3/389
Oncology Reports, 3/2005, Volume 13 Number 3
Pages: 389-395 Oncology Reports, Spandidos Publications
Department of Surgery, Kurume University School of Medicine, Kurume City, Fukuoka, Japan
——————————————————————
7 – 8/27/2007 Induction of apoptosis in human hepatocellular carcinoma cells by synthetic antineoplaston A10
http://www.ncbi.nlm.nih.gov/pubmed/17695534
Induction of Apoptosis in Human Hepatocellular Carcinoma Cells by Synthetic Antineoplaston A10
http://www.ncbi.nlm.nih.gov/m/pubmed/17695534
Anticancer Res. 2007 Jul-Aug;27(4B):2427-31
http://ar.iiarjournals.org/content/27/4B/2427.short
Anticancer Res 27(4B):2427-31 (2007)
http://ar.iiarjournals.org/content/27/4B/2427.long
Anticancer Res. 7 – 8/2007; 27(4B):2427-31
http://ar.iiarjournals.org/content/27/4B/2427.full.pdf
Anticancer Research, Vol. 27, No. 4B, 2007, pp. 2427-2431
http://www.iiar-anticancer.org/main.php?pid=3398&id=2&ch=52&gch=&volume=27&issue=4B&show=details&page=2
Anticancer Research
HighWire Press
School of Pharmaceutical Sciences, Shandong University, Jinan, Japan
International Journal of Cancer Treatment
Burzynski References: 1, 3, 5, 13 and 15
Badria (Egypt) A-10 References: 2 and 20
Wang A10 Reference: 4

References:

Adam L, Crépin M, Savin C, Israël L. Sodium phenylacetate induces growth inhibition and Bcl-2 down-regulation and apoptosis in MCF7ras cells in vitro and in nude mice. Cancer Res. 1995 Nov 15;55(22):5156–5160.

Shack S, Miller A, Liu L, Prasanna P, Thibault A, SAMID D. Vulnerability of multidrug-resistant tumor cells to the aromatic fatty acids phenylacetate and phenylbutyrate. Clin Cancer Res. 1996 May;2(5):865–872.

SAMID D, Shack S, Myers CE. Selective growth arrest and phenotypic reversion of prostate cancer cells in vitro by nontoxic pharmacological concentrations of phenylacetate. J Clin Invest. 1993 May;91(5):2288–2295.

SAMID D, Hudgins WR, Shack S, Liu L, Prasanna P, Myers CE. Phenylacetate and Phenylbutyrate as novel, nontoxic differentiation inducers. Adv Exp Med Biol. 1997;400A:501–505.

SAMID D, Wells M, Greene ME, Shen W, Palmer CN, Thibault A. Peroxisome proliferator-activated receptor gamma as a novel target in cancer therapy: binding and activation by an aromatic fatty acid with clinical antitumor activity. Clin Cancer Res. 2000 Mar;6(3):933–941.

Thibault A, Cooper MR, Figg WD, Venzon DJ, Sartor AO, Tompkins AC, Weinberger MS, Headlee DJ, McCall NA, SAMID D, et al. A phase I and pharmacokinetic study of intravenous phenylacetate
in patients with cancer. Cancer Res. 1994 Apr 1;54(7):1690–1694.
——————————————————————
3/2005 – Effects of antineoplaston AS2-1 against post-operative lung metastasis in orthotopically implanted colon cancer in nude rat.
http://www.ncbi.nlm.nih.gov/pubmed/15706406
Matono K, Ogata Y, Tsuda H, Araki Y, Shirouzu K.
http://www.ncbi.nlm.nih.gov/m/pubmed/15706406
Oncol Rep. 2005 Mar;13(3):389-95
http://www.spandidos-publications.com/or/13/3/389
Oncology Reports
March 2005
Volume 13 Number 3
Department of Surgery, Kurume University School of Medicine, Kurume City, Fukuoka, Japan
——————————————————————
PUBLICATIONS BY STANISLAW RAJMUND BURZYNSKI AND ASSOCIATES
http://www.cancermed.com
——————————————————————
(former web-site screenshots)
http://www.circare.org/info/bri/burzynski_fdauntitled_promo_2012.pdf
——————————————————————
Stanislaw Rajmund Burzynski Publications:

https://stanislawrajmundburzynski.wordpress.com/2013/03/16/stanislaw-rajmund-burzynski-publications/

Burzynski – The Antineoplaston Randomized Japan Phase II Clinical Trial Study

Burzynski – The Antineoplaston Randomized Japan Phase II Clinical Trial Study

Randomized Phase II Study of Hepatic Arterial Infusion with or without Antineoplastons as Adjuvant Therapy after Hepatectomy for liver Metastases from Colorectal Cancer

Annals of Oncology 2010;21:viii221
http://www.burzynskiclinic.com/images/stories/Publications/8774.pdf

http://oncologypro.esmo.org/meeting-resources/meeting-abstracts/european-society-for-medical-oncology-esmo-2010/randomized-phase-ii-study-of-hepatic-ar-3558.aspx

http://abstracts.webges.com/viewing/view.php?congress=esmo2010&congress_id=296&publication_id=3558

11. Antineoplaston Therapy Doubles 5-Year Survival Rate Following Curative Resection of Hepatic Mets (May 27/09)
Positive results borne from PHASE II clinical study of ANTINEOPLASTON therapy (ANP therapy) in metastatic colon cancer following curative resection of liver mets

study performed in Japan

study consisted of 65 colon cancer patients who had undergone curative resection of liver mets and were randomized to one of following groups:

1. infusion of X

2. infusion of X plus IV ANP therapy

There was significant difference in overall survival between the 2 groups

5 year survival rate:
X plus ANP therapy arm – 63% vs.
X only arm – 32%

Recurrence rate differed for the 2 groups
34%
69%

Lead investigator claims ANP therapy may find application not only in treatment of brain tumors as reported previously, but also in more common colorectal cancer
http://finance.yahoo.com/news/Metastatic-Colon-Cancer-In-a-bw-15355368.html?.v=1

http://www.colorectal-cancer.ca/IMG/pdf/CCAC_Research_June_19_2009.pdf

ANTINEOPLASTON Therapy Doubles 5-Year Survival Rate Following Curative Resection of Hepatic Mets

Randomized Phase II Study of Hepatic Arterial Infusion with or without Antineoplastons as Adjuvant Therapy after Hepatectomy for Liver Metastases from Colorectal Cancer
http://oncologypro.esmo.org/meeting-resources/meeting-abstracts/european-society-for-medical-oncology-esmo-2010/randomized-phase-ii-study-of-hepatic-ar-3558.aspx

Publication date: May 17, 2010
Category: Colorectal cancer
Publisher: ESMO
Y. Ogata; K. Shirouzu; K. Matono; M. Ushijima; S. Uchida; H. Tsuda
http://abstracts.webges.com/viewing/view.php?congress=esmo2010&congress_id=296&publication_id=3558

Abstract: 3558
Congress: ESMO 2010
Type: Publication
Topic: Colorectal cancer
Authors: Y. Ogata, K. Shirouzu, K. Matono, M. Ushijima, S. Uchida, H. Tsuda; Kurume/JP
http://www.biomeddefine.com/sdx/t31/all/100/epithelial+neoplasm+glandular+piperidines+chemical+ingredient.html

http://www.biomeddefine.com/sdx/t31/all/100/ca+secondary+cancer+piperidines+chemical+ingredient.html

Antineoplaston Therapy Doubles Five-Year Survival Rate Following Curative Resection of Hepatic Mets

Metastatic Colon Cancer:

In a Randomized Phase II Clinical Study, Antineoplaston Therapy Doubled the 5-Year Survival Rate Following Curative Resection of Hepatic Metastases
http://www.drugs.com/clinical_trials/metastatic-colon-cancer-randomized-phase-ii-clinical-study-antineoplaston-therapy-doubled-5-year-7307.html

HOUSTON–(BUSINESS WIRE)–May 27, 2009 – The Burzynski Research Institute, Inc.

(BRI) is pleased to announce the results of a RANDOMIZED Phase II clinical study of ANTINEOPLASTON therapy (ANP therapy) in metastatic colon cancer following curative resection of hepatic metastases

study was performed at Kurume University School of Medicine (Japan) Department of Surgery

A report of the study results is currently in press
http://oncologypro.esmo.org/meeting-resources/meeting-abstracts/european-society-for-medical-oncology-esmo-2010/randomized-phase-ii-study-of-hepatic-ar-3558.aspx

http://abstracts.webges.com/viewing/view.php?congress=esmo2010&congress_id=296&publication_id=3558

3 – 4/2003 – ANTINEOPLASTON AS2-1 – Japan
http://www.ncbi.nlm.nih.gov/m/pubmed/12579278
The preventive effect of ANTINEOPLASTON AS2-1 on HCC recurrence

We designed a PHASE II clinical trail to clarify whether ANTINEOPLASTON AS2-1 … prolongs the 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

10 patients experienced 35 recurrence-free intervals

Recurrence-free intervals during ANTINEOPLASTON AS2-1 administration were significantly longer than those without ANTINEOPLASTON AS2-1 …

Patients who experienced recurrence-free intervals with and without ANTINEOPLASTON AS2-1 showed longer intervals during ANTINEOPLASTON AS2-1 administration than those before and after ANTINEOPLASTON AS2-1 administration …

2 patients in stage I showed longer recurrence-free intervals than those in more advanced stages

… ANTINEOPLASTON AS2-1 … prolonged the recurrence-free interval between regional treatments and improved survival rate of these patients

Tsuda H, Sata M, Kumabe T, Uchida M, Hara H

Department of Anesthesiology, Kurume Daiichi Social Insurance Hospital, Kushihara Kurumeshi, Fukuoka, Japan

Oncol Rep. 2003 Mar-Apr;10(2):391-7
http://www.spandidos-publications.com/or/10/2/391

http://www.burzynskiclinic.com/images/stories/Publications/964.pdf
References:

3. 1976 – BURZYNSKI – ANTINEOPLASTONS
BURZYNSKI SR
ANTINEOPLASTONS;
Biochemical defense against cancer
Physiol Chem Phys 8: 275-279, 1976

4. 1996 – ANTINEOPLASTON A10 and AS2-1 – Japan
Tsuda H, Hara H, Eriguchi N, et al
Toxicology study on ANTINEOPLASTON A10 and AS2-1 in cancer patients
Kurume Med J 42: 241-246, 1996

12. 1987 – BURZYNSKI – ANTINEOPLASTON A10
Hendry LB, Muldoon TG, BURZYNSKI SR, et al
Stereochemical modelling studies of the interaction of ANTINEOPLASTON A10 with DNA
Drugs Exp Clin Res 1: 77-81, 1987

14. 1992 – SAMID (learned from BURZYNSKI)
Samid D, Shack S, and Sherman LT
Phenylacetate:
A novel nontoxic inducer of tumor cell differentiation
Cancer Res 52: 1988-1992, 1992

15. 1989 – BURZYNSKI

16. 1992 – ANTINEOPLASTON A10 – Japan

17. 1996 – ANTINEOPLASTON A10 and AS2-1 – Japan
Tsuda H, Iemura A, Sata M, et al
Inhibitory effect of ANTINEOPLASTON A10 and AS2-1 on human hepatocellular carcinoma cells
Kurume Med J 43: 137-47, 1996

19. 1998 – ANTINEOPLASTONS – Japan

20. 2002 – Japan

PUBLICATIONS BY S.R. BURZYNSKI AND ASSOCIATES (NOT INCLUDING PUBLICATIONS BEFORE 2002)
http://www.burzynskiclinic.com/scientific-publications.html

1996 – ANTINEOPLASTON A10 and AS2-1 – Japan
http://www.ncbi.nlm.nih.gov/m/PubMed/8755117
Inhibitory effect of ANTINEOPLASTON A10 and AS2-1 on human hepatocellular carcinoma cells

ANTINEOPLASTONS, first described by Burzynski …

ANTINEOPLASTON A10 is the first chemically identified ANTINEOPLASTONS

These metabolites are water soluble and have ANTITUMOR effect …

The mixture of phenylacetylglutamine and phenylacetic acid in the ratio of 1 to 4 was also shown to have ANTITUMOR effect in tissue culture study, then formulated as ANTINEOPLASTON AS2-1

The 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 the treatment of human hepatocellular carcinoma since this tumor recurs frequently despite initial successful treatment

Tsuda H, Iemura A, Sata M, Uchida M, Yamana K, Hara H.

Kurume University School of Medicine, Japan

1) Departments of Anesthesiology
2) Departments of Pathology
3) Departments of Medicine
4) Departments of Radiology
5) Departments of Surgery

Released 2009/08/11

Kurume Med J. 1996;43(2):137-47

The Kurume Medical Journal
https://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article
PDF:
https://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_pdf
References:
https://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article/references
1. 1976 – BURZYNSKI – ANTINEOPLASTON
BURZYNSKI SR
ANTINEOPLASTON;
Biochemical defense against cancer
Physiol Chem Phys 1976; 8:275-279

2. 1985 – BURZYNSKI – ANTINEOPLASTON A10
BURZYNSKI SR, and Hai TT
ANTINEOPLASTON A10
Drugs of the Future 1985; 10:103-105

3. 1986 – BURZYNSKI – ANTINEOPLASTON AS2-1 and AS2-5
BURZYNSKI SR, Mohabbat MO, and Lee SS
Preclinical studies of ANTINEOPLASTON AS2-1 and ANTINEOPLASTON AS2-5
Drugs Exp Clin Res 1986 (Suppl); 1:25-28

4. 1988 – JAPAN – ANTINEOPLASTON A10
Eriguchi N, Hara H, Yoshida H, Nishida H, Nakayama T et al.
Chemopreventive effect of ANTINEOPLASTON A10 on Urethane-induced pulmonary neoplasia in mice
J Jpn Soc Cancer Ther 1988; 23 (7):1560-1565

5. 1987 – BURZYNSKI – ANTINEOPLASTON A10
Hendry LB, Muldoon TG, BURZYNSKI SR, Copland JA, and Lerner AF
Stereochemical modelling studies of the interaction of ANTINEOPLASTON A10 with DNA
Drugs Exp Clin Res 1987 (Suppl); 1:77-81

7. 1986 – BURZYNSKI
Liau MC, and BURZYNSKI SR
Altered methylation complex isozymes as selective targets for cancer chemotherapy
Drugs Exp Clin Res 1986 (Suppl); 1:77-86

8. 1988 – see 5. – ANTINEOPLASTON A10
Muldoon TG, Copland JA, and Hendry LB
Actions of ANTINEOPLASTON A10 on the genesis and maintenance of specific subpopulations of rodent mammary tumor cells
Advances in Experimental and Clinical Chemotherapy 1988; 1:15-18

10. 1991 – JAPAN – ANTINEOPLASTON A10
Nishida H, Yoshida H, Eriguchi N, Hoshino K, Kubota H et al.
Inhibitory effect of orally administered ANTINEOPLASTON A10 on the growth curve of human breast cancer transplanted to athymic mice
J Jpn Soc Cancer Ther 1991; 26:596-601

12. 1991 – SAMID (learned from BURZYNSKI)
Samid D, Yeh T-J and Shack S
Interferon in combination with antitumorigenic phenylderivatives; potentiation of INF alpha activity in vitro
Br J Haematol 1991; 79 (Suppl) 1:81-83

13. 1992 – SAMID (learned from BURZYNSKI)
Samid D, Shack S, and Sherman LT
Phenylacetate:
A novel nontoxic inducer of tumor cell differentiation
Cancer Research 1992; 52:1988-1992
http://europepmc.org/abstract/MED/8755117/reload=0;jsessionid=MhBwMcen2a7a9AibBaLc.2