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
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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
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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
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Possible these would be sufficiently transient so as not to produce CNS toxicity and troughs not prolonged as to abrogate antitumor activity of drug
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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
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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
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In Phase I trial of PHENYLACETATE … commonly resulted in drug accumulation and REVERSIBLE DOSE-LIMITING NEUROLOGIC TOXICITY
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18 patients
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DOSE-LIMITING TOXICITY, consisting of REVERSIBLE CENTRAL NERVOUS SYSTEM DEPRESSION, observed for 3 patients at 2nd dose level
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[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
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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
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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
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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
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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
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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
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Both compounds induced cytostasis and maturation of multidrug-resistant breast, ovarian, and colon carcinoma cells with no significant effect on cell viability
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MDR cells generally more sensitive to growth arrest by PA and PB than their parental counterparts
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PA and PB potentiated cytotoxic activity of doxorubicin against MDR cells
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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
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ability to induce tumor differentiation in laboratory models and LOW CLINICAL TOXICITY PROFILE makes them promising candidates for COMBINATION WITH CONVENTIONAL THERAPIES
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[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
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Based on findings, NaPA and NaPB entered clinical trials at National Cancer Institute
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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
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Pg. 1760
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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
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Significant HEMATOLOGICAL TOXICITY was not reported in a Phase I trial of PA in patients with malignancy
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Pg. 1761
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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
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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)
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Aromatic fatty acid also caused cytostasis associated with sustained declines in c-myc expression, a direct antitumor effect that was independent of EBV status
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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
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Overall DRUG WELL TOLERATED with most common TOXICITIES being grade 1-2 DYSPEPSIA and FATIGUE
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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
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All evaluable for TOXICITY and response
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Dose escalated 150 to 515 mg/kg/day
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One patient at 515 mg/kg/day and one at 345 mg/kg/day experienced this DLT
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Maximum tolerated dose 410 mg/kg/day for 5 days
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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
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Antineoplaston A10 given intravenously, followed by oral antineoplaston AS2-1
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Patient underwent 2nd and 3rd microwave ablation of recurrent tumors, and has survived for nearly 8 years WITHOUT SUFFERING ANY SERIOUS ADVERSE EFFECTS
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Currently FREE FROM CANCER
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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
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All PB doses of 9, 18, and 27 g/day WELL TOLERATED
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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
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Conversion of PBA to PAA and PHENYLACETYLGLUTAMINE (PAG) documented without catabolic saturation
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THERAPY WELL TOLERATED OVERALL
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Common ADVERSE EFFECTS included grade 1 NAUSEA/VOMITING, FATIGUE, and LIGHTHEADEDNESS
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Dose limiting TOXICITIES were SHORT-TERM MEMORY LOSS, SEDATION, CONFUSION, NAUSEA, and VOMITING
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Administration of PBA twice-daily infusion schedule is SAFE
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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
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What Dr. Stanislaw Burzynski doesn’t want you to know about antineoplastons
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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
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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”?
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[28] 2005
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5 years 7 months (1-11) median age
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13 / 100% – children with recurrent disease or high risk
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5 / 38% – weren’t treated earlier with radiation therapy or chemotherapy
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3 / 23% – Complete Response
1 / 8% – Partial Response
4 / 31% – Stable Disease
5 / 38% – Progressive Disease
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6 / 46% – Survived 5+ years from initiation of ANP
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Serious side effects:
1 – anemia
1 – fever
1 – granulocytopenia
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average dosage of A10 was 10.3 g/kg/d and of AS2-1 was 0.38 g/kg/d
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REDUCED TOXICITY MAKES ANP PROMISING for very young children, patients at high risk of complication of standard therapy, and patients with recurrent tumors
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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
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[29] 9/27/1995 (7/17/2006) Alterations in expression of ras oncogenes are characteristic of wide variety of human neoplasms
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Accumulating evidence has linked elevated ras expression with disease progression and FAILURE OF TUMORS TO RESPOND TO CONVENTIONAL THERAPIES, INCLUDING RADIOTHERAPY AND CERTAIN CHEMOTHERAPIES
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observations led us to investigate response of ras-transformed cells to differentiation-inducer PHENYLACETATE (PA)
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Interestingly, IN CONTRAST TO THEIR RELATIVE RESISTANCE TO RADIATION and doxorubicin, ras-transformed cells were significantly more sensitive to PA than their parental cells
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[30] 5/1996 CYOTOXIC CHEMOTHERAPIES OFTEN GIVE RISE TO MULTIDRUG RESISTANCE, WHICH REMAINS MAJOR PROBLEM IN CANCER MANAGEMENT
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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
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[15] 1996 Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which control neoplastic growth
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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
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[31] 7/1997 Children with malignant GLIOMAS THAT PROGRESSED AFTER CONVENTIONAL THERAPY
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0 / 0% – EXHIBITED CLEAR-CUT TUMOR regression
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[32] 2000 treatment combination PRODUCED NO SIGNIFICANT CHANGE in overall POOR prognosis of patients
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Most tumors responded initially to treatment but RECCURED as study progressed
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Based on POOR RESULTS, recommend ALTERNATIVE TREATMENTS be tested in patients with this type of tumor
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[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
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[34] 12/2000 NO CLEAR PROOF OF EFFICACY
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NO BETTER THAN SURVIVAL BEFORE THE INTRODUCTION OF temozolomide
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[35] 2002 p53 tumor suppressor gene plays important role in protecting cells from developing undesirable proliferation
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Mutant p53 gene or malfunctioning p53 protein found in more than 50% of cancer cells impedes DNA repair or apoptosis induction
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MAY BE WHY SOME CANCERS GAIN RESISTANCE TO CHEMOTHERAPY AND RADIATION AND BECOME MORE RESISTANT AFTER FREQUENT CANCER TREATMENTS
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[36] 2004 outcome for patients with either type of tumor is POOR when STANDARD multimodality THERAPY IS USED
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children are ideal candidates for INNOVATIVE TREATMENT approaches
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33 / 100% – DIED OF DISEASE PROGRESSION
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administration of temozolomide after RT DIDN’T ALTER POOR PROGNOSIS associated with newly diagnosed diffuse BRAINSTEM GLIOMA in children
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[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
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[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
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[39] 10/12/2011 Afinitor (ubependymal giant cell ASTROCYTOMA (SEGA) brain tumor)
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none of their tumors went away completely
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[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
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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
http://www.ncbi.nlm.nih.gov/m/pubmed/1372534/
Cancer Res 1992;52:1988-1992
http://m.cancerres.aacrjournals.org/content/52/7/1988.abstract
Cancer Res April 1, 1992 52; 1988v I
http://cancerres.aacrjournals.org/content/52/7/1988
Cancer Res. 1992 Apr 1;52(7):1988-92
Click to access 1988.full.pdf
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
http://www.ncbi.nlm.nih.gov/pubmed/1378939/
N Engl J Med. 1992 Aug 20;327(8):569-70
http://www.ncbi.nlm.nih.gov/m/pubmed/1378939/
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
http://www.ncbi.nlm.nih.gov/pubmed/1381630/
Blood. 1992 Sep 15;80(6):1576-81
http://www.ncbi.nlm.nih.gov/m/pubmed/1381630/
Blood September 15, 1992 vol. 80 no. 6 1576-1581
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.full.pd
Blood 80:1576, 1992
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.abstract
Blood 80(6):1576–1581
Click to access 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
http://www.ncbi.nlm.nih.gov/pubmed/8486788/
J Clin Invest. 1993 May;91(5):2288-95
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J Clin Invest. 1993 May; 91(5): 2288–2295
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC288233/
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
� � � � � � � � � � � � � � � � �
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
http://m.bloodjournal.hematologylibrary.org/content/82/7/2203.full.pd
Blood October 1, 1993 vol. 82 no. 7 2203-2209
http://m.bloodjournal.hematologylibrary.org/content/82/7/2203.abstract
1993 82: 2203-2209
Click to access 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
� � � � � � � � � � � � � � � � �
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
Click to access 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
References: 8-12
BURZYNSKI
Reference: 13
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Drugs Exp Clin Res. 1990;16(7):361-9
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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
Click to access 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
� � � � � � � � � � � � � � � � �
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
� � � � � � � � � � � � � � � � �
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
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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
� � � � � � � � � � � � � � � �
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
� � � � � � � � � � � � � � � � �
Stockhammer G, Manley GT, Johnson R, et al: (SAMID D) Inhibition of proliferation and induction of differentiation in medulloblastoma and astrocytoma-derived cell lines with PHENYLACETATE. J Neurosurg 83:672-681, 1995
http://www.ncbi.nlm.nih.gov/pubmed/7674018/
J Neurosurg. 1995 Oct;83(4):672-81
http://www.ncbi.nlm.nih.gov/m/pubmed/7674018/
Cotzias Laboratory of Neuro-Oncology, Memorial Sloan-Kettering Cancer Center, New York, New York, USA
http://thejns.org/doi/abs/10.3171/jns.1995.83.4.0672?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed&
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[14] 1995
� � � � � � � � � � � � � � � � �
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
Click to access 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
Click to access 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
� � � � � � � � � � � � � � � � �
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
Click to access 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
Click to access 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
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[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
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[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
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[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
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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
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[30] 5/1996
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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
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[31] 7/1997
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A phase I study of high-dose tamoxifen for the treatment of refractory malignant gliomas of childhood
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Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse BRAINSTEM GLIOMAS:
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Temozolomide and ANAPLASTIC ASTROCYTOMA:
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A novel strategy for remission induction and maintenance in cancer therapy
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[36] 2004
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Supratentorial high-grade ASTROCYTOMA and DIFFUSE BRAINSTEM GLIOMA:
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References:
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Cited By:
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DOI: 10.1002/cncr.20741
Department of Hematology-Oncology, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA
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Cancer 103, 133-139
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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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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
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http://www.fda.gov/AboutFDA/CentersOffices/OfficeofMedicalProductsandTobacco/CDER/ucm231967.htm
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