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

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

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

“Burzynski … antineoplastons … “:

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

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

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

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

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

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

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[3] 1990 AS2-1 (AS)
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2 / 14.5% – Complete Remission
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3 / 21%- Partial Remission
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7 / 50%- Stabilization of disease with objective improvement
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2 / 14.5% – Progression
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1st patient enrolled in Complete Remission 17 months and off treatment 16 months
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[4] 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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Treatment of promyelocytic leukemia III.-60 cells resulted in rapid decline of myc oncogene expression followed by growth arrest and granulocyte differentiation
——————————————————————
results indicate PHENYLACETATE is effective in inducing tumor cell maturation and free of cytotoxic and carcinogenic effects, a combination that warrants attention to potential use in CANCER intervention
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Conclusions:
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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 in treatment of hyperammonemia (2-4); we propose use may be extended to CANCER preventation and therapy
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[5] 9/15/1992 results suggest PHENYLACETATE, used alone or in combination with other drugs, might offer safe and effective new approach to treatment of some hematopoietic neoplasms and severe hemoglobinopathies
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NaPA, which has an unpleasant odor, can be substituted by its pro-drug, sodium PHENYLBUTYRATE (NaPB), for oral administration
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Upon ingestion by humans, PHENYLBUTYRATE undergoes @-oxidation to PHENYLACETATE
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Both NaPA and NaPB already proved safe for the treatment of infants and adults
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It seems important therefore to further evaluate the clinical relevance of our experimental data
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[6] 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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[7] 2/1994 sodium PHENYLACETATE can induce cytostasis and reversal of MALIGNANT properties of cultured HUMAN GLIOBLASTOMA CELLS, when used at pharmacological concentrations that are well tolerated by children and adults
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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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data indicate PHENYLACETATE, acting through inhibition of protein prenylation and other mechanisms, may offer safe and effective novel approach to treatment of MALIGNANT GLIOMAS and perhaps other neoplasms as well
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[8] 4/1/1994 Phenylacetate has recently been shown to suppress TUMOR growth and promote differentiation in experimental models
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phase I trial of PHENYLACETATE conducted in 17 patients with advanced solid TUMORS
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99% of PHENYLACETATE elimination was accounted for by conversion to PHENYLACETYLGLUTAMINE, which was excreted in the urine
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1 of 6 patients with GLIOBLASTOMA MULTIFORME, whose steroid dosage has remained unchanged for duration of therapy, has sustained functional improvement for more than 9 months
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use of adaptive control with feedback for dosing of each patient enabled us to safely maintain stable PHENYLACETATE concentrations … which resulted in clinical improvement in some patients with advanced disease
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[9] 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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PHENYLACETATE, used at clinically achievable concentrations, prolongs survival of rats with MALIGNANT BRAIN TUMORS through induction of TUMOR differentiation
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role in treatment of BRAIN TUMORS and other CANCERS should be explored further
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[10] 9/1994 increasing incidence of melanoma and poor responsiveness of disseminated disease to conventional treatments call for development of new therapeutic approaches
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PHENYLACETATE, nontoxic differentiation inducer, can suppress growth of other NEUROECTODERMAL TUMORS, i.e., GLIOMAS, in laboratory models and HUMANS
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finding led us to explore efficacy of PHENYLACETATE and related aromatic fatty acids in MELANOMA
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PHENYLACETATE and PHENYLBUTYRATE found to a) induce selective cytostasis and maturation of cultured HUMAN MELANOMA CELLS, b) modulate expression of GENES implicated in TUMOR METATASIS (type IV collagenase and tissue inhibitor of metalloproteinases-2) and immunogenicity (HLA class I); and c) enhance efficacy of other agents of clinical interest
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in vitro ANTITUMOR activity observed with nontoxic, pharmacologic concentrations of PHENYLACETATE and PHENYLBUTYRATE, suggesting potential clinical use of drugs in treatment of MELANOMAS
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[11] 2/8/1995 (7/17/2006) PHENYLACETATE, a natural metabolite of phenylalanine which was originally described as a plant growth hormone, has recently gained attention as a possible differentiation inducer for a variety of HUMAN TUMOR CELL types
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Using the LA-N-5 cell line, we have determined that NaPA can stimulate the differentiation of neuroblastoma cells …
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NaPA and RA synergized in inducing differentiation, in that combination treatment resulted in cessation of cell growth along with morphologic and biochemical changes indicative of loss of malignant properties
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[12] 4/1995 (3/8/2013) PHENYLACETATE, an inducer of tumor cytostasis and differentiation, shows promise as relatively nontoxic antineoplastic agent
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PHENYLBUTYRATE, an odorless compound that also has activity in TUMOR models
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[13] 5/1995 Antineoplaston (Ap), new ANTITUMOR agent, clinically tested for effects on MALIGNANT BRAIN TUMORS
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1 – medulloblastoma
1 – pontine glioma
2 – anaplastic astrocytoma
2 – metastatic brain tumor
3 – glioblastoma (G,B)

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

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

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Effects of Ap on malignant brain tumors considered due to synergy, since administered with other drugs and acceleration of tumor cellular differentiation
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Ap useful as approach to remission maintenance therapy for brain tumors
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[14] 6/15/1995 growth-inhibiting and differentiating effects of sodium PHENYLACETATE against hematopoietic and solid TUMOR CELL lines has aroused clinical interest in its use as an ANTICANCER drug
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1 – refractory malignant glioma had partial response
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1 – hormone-independent prostate cancer achieved 50% decline in prostate specific antigen level, maintained 1 month
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High grade GLIOMAS and advanced prostate cancer are reasonable targets for Phase II clinical trials
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[15] 7/1995 aromatic fatty acids phenylacetate (PA) and phenylbutyrate (PB) induce tumour cell differentiation in experimental models and currently in clinical trials
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close association between enhanced TGF-alpha production and melanoma cell differentiation suggests this growth factor, often linked to mitogenesis, may play a novel role in tumour differentiation by PA and PB
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[16] 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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Using gene transfer models, we show PA caused cytostasis in ras-transformed mesenchymal cells, associated with increased expression of 2′,5′-oligoadenylate synthetase, an enzyme implicated in negative growth control
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PA also induced phenotypic reversion characterized by loss of anchorage-independent growth, reduced invasiveness and increased expression of collagen alpha type I, a marker of cell differentiation
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ANTI-TUMOR ACTIVITY of PA was observed in cases involving either Ha- or Ki-ras and was independent of mode of oncogene activation
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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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profound changes in TUMOR CELL and molecular biology were associated with reduced isoprenylation of ras-encoded p21
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Our results indicate PA CAN SUPPRESS GROWTH of ras-transformed cells, resistant otherwise to free-radical based therapies, through interference with p21ras isoprenylation, critical to signal transduction and maintenance of MALIGNANT phenotype
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[17] 10/1995 investigated effects of a nontoxic differentiation inducer, PHENYLACETATE (PA), on NEUROECTODERMAL TUMOR-derived CELL lines
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PHENYLACETATE decreased transforming growth factor (TGF)-beta 2 production by medulloblastoma Daoy cells
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in vitro antiproliferative and differentiation inducing effects of PA suggest that this agent warrants further evaluation as a potential therapeutic modality for the treatment of MEDULLOBLASTOMAS and MALIGNANT GLIOMA in HUMANS
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[18] 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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slowly metabolized fatty acid alters tumor cell lipid metabolism causing … inhibition of protein prenylation critical to MALIGNANT growth
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data suggest PHENYLACETATE and analogues may act through common mechanisms to INHIBIT GROWTH of vastly divergent, undifferentiated CELL types, and provide basis for development of new agents for treatment of HUMAN MALIGNANCIES
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[19] 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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Evaluation of usefulness of Antineoplastons in combination therapy based on imaging findings during course of treatment revealed DISAPPEARANCE or MEASUREABLE SHRINKAGE of TUMOR lasting more than one months:
15 tumors / 32.6%
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No increase in size of tumor for more than 3 months:
8 / 17.4%

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

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

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These metabolites are water soluble and have ANTITUMOR EFFECT, they are further degraded to PHENYLACETIC acid
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Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid in ratio of 1 to 4 shown to have ANTITUMOR EFFECT in tissue culture study, then formulated as Antineoplaston AS2-1
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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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We report effects of Antineoplaston A10 and AS2-1 on cell proliferation, cell morphology, cell cycle, and DNA in human hepatocellular carcinoma cell lines
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BOTH AGENTS INHIBITED CELL PROLIFERATION and increased number of cells in G0 and G1 phases and Antineoplaston AS2-1 induced APOPTOSIS
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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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[23] 8/23/1996 aromatic fatty acid PHENYLACETATE and analogs INDUCE TUMOR CYTOSTASIS and differentiation in experimental models
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studies using HUMAN PROSTATIC CARCINOMA, MELANOMA, and GLIOBLASTOMA cell lines showed a tight correlation between drug-induced cytostasis …
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results identify PHENYLACETATE and analogs as new class of aromatic fatty acids capable of activating hPPAR, and suggest nuclear receptor may mediate TUMOR cytostasis induced by these drugs
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[24] 9/1996 We examined hypothesis this postulate may not apply to evaluation of drugs such as PHENYLACETATE, a differentiating agent endowed with mechanisms of action different from those of classic cytotoxic chemotherapy
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Using HUMAN PROSTATIC CARCINOMA LNCaP cells as model, we show PHENYLACETATE induces PSA production despite inhibition of TUMOR CELL proliferation

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[25] 12/1996 PHENYLACETATE (PA) and related aromatic fatty acids constitute novel class of relatively nontoxic antineoplastic agents
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Using human breast carcinoma MCF-7 cells as model, we show PA-induced growth arrest associated with enhanced expression of cyclin-dependent kinase inhibitor p21Waf1/Cip1 …
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induction of p21WAF1/CIP1 mRNA by PA independent of cellular p53 status
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PA effectively induced p21WAF1/CIP1 mRNA and growth inhibition of wild-type mouse embryonal fibroblasts
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findings strongly support role for p21Waf1/Cip1 in PA-mediated inhibition of cell growth
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[26] 1996 Cytotoxic chemotherapies often give rise to multidrug resistance, which remains major problem in CANCER management
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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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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 parental counterparts
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PA and PB potentiated the cytotoxic activity of doxorubicin against MDR cells
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Taken together, our in vitro data indicate PA and PB, differentiation inducers of aromatic fatty acid class, may provide alternative approach to treatment of MDR TUMORS
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[27] 8/1997 aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB) are novel ANTITUMOR AGENTS currently under clinical evaluation
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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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In present studies, we characterized interactions between aromatic fatty acids and radiation, using as a model cell lines derived from CANCERS of PROSTATE, BREAST, BRAIN and COLON
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in vitro findings identify aromatic fatty acids PA and PB as new class of non-toxic modulators of radiation response, antagonistic effect of these compounds on radiation response needs further examination
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data strongly suggest that for PA or PB to have role in clinical radiotherapy, appropriate scheduling of combination therapies must take into account time-dependent effects in order to achieve clinical radiosensitization
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[28] 11-12/1997 Antineoplaston AS2-1 EXHIBITS CYTOSTATIC GROWTH INHIBITION of human hepatocellular carcinoma cells in vitro and showed minimum adverse effects in phase I clinical trial
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2 clinical cases of liver cancer (hepatocellular carcinoma and multiple liver metastases from colon cancer) in whom we believe antineoplaston A2-1 useful as maintenance therapy after transcatheter arterial embolization (TAE) and microwave coagulation necrosis (MCN)
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2 patients have continued to be in good condition for more than 2 years without limitation of normal activities
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Antineoplaston AS2-1 may be effective and useful as maintenance agent after TAE and MCN in patients with liver cancer
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[29] 1997 PHENYLACETATE and analogs represent new class of pleiotropic growth regulators that alter TUMOR CELL biology by affecting GENE EXPRESSION at both transcriptional and post transcriptional levels
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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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[30] 5 – 6/1998 Antineoplastons A10 and AS2-1 EXHIBIT GROWTH INHIBITION OF CANCER CELLS by diverse modes of action
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Observed ANTITUMOR RESPONSES within 2-3 weeks of combination treatment of chemoradiation therapy and antineoplastons A10 and AS2-1 in phase I clinical study conducted in Kurume University Hospital
——————————————————————
Reviewed 3 clinical cases of advanced cancer (multiple metastatic lung cancer, thalamic glioma and primary lung cancer) in which we believed antineoplaston A10 and AS2-1 may be contributing to RAPID ANTITUMOR RESPONSE
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Possible use of this combination for induction therapy in advanced cancer
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[31] 11-12/1998 Antineoplaston A10 injection (antineoplaston A10 I) exhibited CYSTOSTATIC GROWTH INHIBITION OF HUMAN HEPATOCELLULAR CARCINOMA (HCC) CELLS in vitro and showed minimum adverse effects in phase I clinical trial
——————————————————————
2 cases of advanced HCC treated with antineoplaston A10 I
——————————————————————
Both cases showed interesting responses to antineoplaston A10 I
——————————————————————
One showed massive coagulation necrosis of tumors after intra-arterial infusion of antineoplaston A10 I and other showed RESOLUTION of portal vein TUMOR thrombosis with systemic infusion of antineoplaston A10 I
——————————————————————
Usefulness of anti-neoplaston A10 I in terminal staged HCC is discussed
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[32] 3/1999 determine response rate, time to treatment failure, and toxicity of phenylacetate in patients with recurrent malignant glioma …
————————————————————
Adult patients
————————————————————
43 – enrolled 12/1994-12/ 1996
40 – assessable
————————————————————
Reversible symptoms
————————————————————
fatigue
somnolence
were primary toxicities
————————————————————
only mild hematologic toxicity
————————————————————
30 / 75% – failed treatment within 2 months
————————————————————
7 / 17.5% – stable disease
————————————————————
3 – 7.5% – response defined as more than 50% reduction in tumor
————————————————————
Median time to treatment failure
————————————————————
2 months
————————————————————
35 – died
————————————————————
median survival
————————————————————
8 months
————————————————————
PHENYLACETATE HAS LITTLE ACTIVITY at this dose schedule in PATIENTS with RECURRENT MALIGNANT GLIOMA
————————————————————
Further studies with drug would necessitate evaluation of different dose schedule
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[33] 7/3/2000 Antineoplastons first described by Burzynski are naturally occurring peptides and amino acid derivatives, which CONTROL NEOPLASTIC GROWTH
——————————————————————
data suggest strong inverse association of urinary antineoplaston A-10 level with breast cancer
————————————————————
finding was stimulus for further investigations of antineoplaston A-10 levels in some benign as well as other malignant diseases to determine utility of approach as predictive test for women at risk of developing breast cancer
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[34] 8/31/2000 Antineoplastons are naturally occurring CYTODIFFERENTIATING AGENTS
—————————————————————
Findings confirm presence of immune defects among patients with breast cancer and results should stimulate development of new strategies to induce and augment immunity for treatment of breast cancer
—————————————————————
Antineoplaston A-10 may provide rational basis for designing trials to employ its immune modulatory potentials as adjuvant therapy in breast cancer patients
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[35] 12/2000 4 new piperidinedione A10 analogs synthesized and tested for antimitotic activity on human breast cancer cell line against prototype A10 and antibreast cancer drug tamoxifen
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“3B” and “3D” were several-fold more potent ANTIPROLIFERATIVE AGENTS than A10 and tamoxifen and had significantly higher capacity to bind DNA than A10
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[36] 8/2001 No partial remission or complete remission was seen, but 7 patients had stable disease for more than 6 months while on drug
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PB may have role as cytostatic agent and should be additionally explored in combination with cytotoxics and other novel drugs
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[37] 2002 p53 tumor suppressor gene plays important role in protecting cells from developing undesirable proliferation
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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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non-toxic p53 gene activator would induce cancer cell apoptosis and help damaged cancer cells to recover
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combination use of chemotherapeutics or radiation with non-toxic p53 gene activator will be crucial in cancer therapy, damaging DNA with chemotherapeutics or radiation on one hand and promoting apoptosis induction with p53 gene activator on the other
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Strategy would be most efficient for remission induction and maintenance CANCER therapy
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Antineoplastons are naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH
——————————————————————
Antineoplaston A10 and AS2-1 are chemically identified and synthesized antineoplastons PROVEN TO INHIBIT CANCER CELL GROWTH by arresting cell cycle in G1 phase and INHIBITING TUMOR GROWTH by reducing mitosis
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Agents thought to be good candidates for clinically easily applicable non-toxic p53 gene activators
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CASES OF ADVANCED CANCER RESPONDED WELL to combination treatment using chemotherapeutics and irradiation with antineoplaston A10 and AS2-1 in clinical trials being conducted in Kurume University Hospital
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[38] 3 – 4/2003 Phase II clinical trail to clarify whether antineoplaston AS2-1, mixture of sodium salts of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid at ratio of 1:4, prolongs recurrence-free interval of HCC patients who undergo frequent treatments for recurrence
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10 patients enrolled in trial
2 in stage I
6 in stage II
1 in stage III
1 in stage IV-B
at initial diagnosis

——————————————————————
10 / 100% – experienced 35 recurrence-free intervals
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Recurrence-free intervals during antineoplaston AS2-1 administration SIGNIFICANTLY LONGER than without
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Patients who experienced recurrence-free intervals with and without antineoplaston AS2-1 SHOWED LONGER INTERVALS during antineoplaston AS2-1 administration
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2 patients in stage I showed LONGER RECURRENCE-FREE INTERVALS than those in more advanced stages
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Antineoplastons AS2-1 couldn’t prevent recurrence of HCC but PROLONGED RECURRENCE-FREE INTERVAL between regional treatments and IMPROVED SURVIVAL RATE OF PATIENTS
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[39] 2003 Case of survival for nearly 8 years after treatment of unresectable multiple liver metastases from colon cancer, using microwave ablation and NONTOXIC ANTITUMOR AGENT, antineoplastons
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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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Computed tomography scans done 1 and 4 years after initial diagnosis showed recurrent tumors
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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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======================================
Burzynski has made it clear that PHENYLACETATE, by itself, does NOT achieve the results of antineoplastons (PHENYLACETATE, PHENYLGLUTAMINATE, PHENYLACETYLISOGLUTIMINATE, PHENYLBUTYRATE)
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[40] 2003
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Pg. 92
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Antineoplaston A10 and AS2-1 are synthetic derivatives of phenylacetate (PN) acid, glutamine and isoglutamine
——————————————————————
A10 is sterile solution of sodium phenylacetylisoglutiminate (isoPG) in 4 : 1 ratio
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Antineoplaston AS2-1 is sterile solution of sodium phenylacetate (PN) and phenylacetylglutaminate (PG) in 4 : 1 ratio
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Pg. 93
======================================
combination of antineoplaston A10 and AS2-1 used instead of single drugs
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Based on previous observations, combination treatment has provided better results than single drugs
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Pg. 97
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active ingredient of antineoplaston AS2-1 is PHENYLACETATE,
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Pg. 98
——————————————————————
known to modulate expression of ras oncogenes and tumor suppressor gene p53
——————————————————————
ras oncogene protein p21ras
——————————————————————
farneslyation of p21ras, which is inhibited by antineoplaston AS2-1
——————————————————————
Antineoplaston AS2-1 also activates p53 gene
——————————————————————
protein p53 activates p21 gene, which directs synthesis of p21WAF1/Cip1 protein
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Induction of p21WAF1/Cip1 suppresses human glioma cell proliferation
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proposed mechanism of action of 2 ingredients of antineoplaston A10, sodium phenylacetylglutamine (PG) and sodium phenylacetylisoglutimine (IsoPG), is inhibition of glutamine incorporation into proteins of neoplastic cells
——————————————————————
Antineoplaston A10 has demonstrated 5 effects related to therapeutic indication in patients with brain tumors: cytostatic, antimitogenic, antiproliferative and inhibitory effects, and differentiation of tumors
——————————————————————
[22-25]
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Initial clinical studies with antineoplaston therapy included testing of separate ingredients phenylacetate (PN) (antineoplaston AS5) and phenylacetylglutaminate (PG) (antineoplaston AS2-5)
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[26-28]
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studies failed to show marked anticancer activity of phenylacetate (PN) in malignant glioma, confirmed by phase II study by North
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Pg. 99
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American Brain Tumor Consortium
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[29]
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Based on results, further studies of phenylacetate (PN) as single agent in patients with malignant glioma were not recommended
——————————————————————
subsequent study by Buckner et al.
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[30]
——————————————————————
confirmed conclusion because patients receiving antineoplaston AS2-1 didn’t respond to treatment
——————————————————————
main difference between Buckner’s study is dosage of antineoplaston A10, which was approximately 50 times lower in Buckner’s study
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[31]
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2 patients who participated in our study (cases 3 and 8) developed recurrence on lower dosages of antineoplaston A10, but responded again with Complete Response (CR) when dosage of antineoplaston A10 was increased
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In these 2 patients, antineoplaston AS2-1 didn’t seem to have effect on 2nd response, which suggests antineoplaston A10 rather than antineoplaston AS2-1 is main active drug
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[41] 8/2005 Antineoplastons such as A10 include naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH OF CELLS
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Findings indicate antineoplaston A10 ANTITUMOR EFFECT could be utilized as effective therapy for breast cancer patients
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[42] 2006 Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which CONTROL NEOPLASTIC GROWTH
——————————————————————
Antineoplaston A10 (3-pehnylacetylamino-2,6-piperidinedion) is first chemically identified antineoplastons and when administered orally is hydrolysed in pancreatic juice to PHENYLACETYLGLUTAMINE and PHENYLACETYLISOGLUTAMINE in ration of 4 to 1
——————————————————————
These metabolites are water soluble and have ANTITUMOR EFFECT, are further degraded to PHENYLACETIC acid
——————————————————————
Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETYLISOGLUTAMINE in ratio of 4 to 1 formulated as Antineoplaston A10 injectable formulation
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Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid in ratio of 1 to 4 also shown to have ANTITUMOR EFFECT in tissue culture study, then formulated as Antineoplaston AS2-1
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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 this TUMOR recurs frequently despite initial successful treatment
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BOTH AGENTS INHIBITED CELL PROLIFERATION and increased number of cells in G0 and G1 phases and Antineoplaston AS2-1 induced apoptosis, we also describe clinical experience of hepatocellula carcinoma (HCC) patient whose tumor, after incomplete trancathere arterial embolization (TAE) for 7cm 7cm HCC, has been stable for more than 15 months during which time he has been taking Antineoplaston AS2-1 continuously WITHOUT ANY SERIOUS ADVERSE EFFECTS
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[43] 1/2008 Novel mechanism through which all-trans retinoic acid (ATRA) and antineoplaston, ANTICANCER DRUG, CAUSED CELL GROWTH INHIBITION IN BREAST CANCER CELLS through effects on intracellular pathways
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Antineoplaston caused down-regulation of PKCalpha protein expression, resulting in INHIBITION of ERK MAPK phosphorylation, with resultant INHIBITION of Rb phosphorylation leading to G(1) arrest
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[44] 10/1/2010 As degradation product of Antineoplaston A10 in vivo, PHENYLACETYL GLUTAMINE showed ANTITUMOR ACTIVITIES
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Designed and radiosynthesized PHENYLACETYL GLUTAMINE derivative, achieved under mild reaction condition
——————————————————————
radiochemical purity of (S)-2-((S)-2-(4-(3-fluoropropyl)benzamido)-3-phenylpropanamido)pentanedioic acid ([18F]FBPPA) was 98%, and best radiochemical yield was up to 46%
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results revealed it might become potential PET imaging agent for DETECTING TUMORS
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References:
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[1] 7/1971
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Neish, W. J. P. Phenylacetic acid as a potential therapeutic agent for the treatment of HUMAN CANCER. Experientia (Basel), 27: 860-861, 1971
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[2] 1976
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Biological active peptides in human urine: III. Inhibitors of the growth of human leukemia, osteosarcoma, and HeLa cells
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S R Burzynski, …
Physiol Chem Phys 8(1):13-22 (1976), PMID .1066715
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[3] 1990
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BURZYNSKI, S. R., Kubove E., Burzynski, B. Treatment of hormonally refractory CANCER of the prostate with ANTINEOPLASTON AS2-1. Drugs Exp. Clin. Res., 16: 361-369, 1990
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[4] 4/1/1992
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SAMID, D., Shack, S., and Sherman, l.. T.
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Cancer Res., 52: 1988-1992, 1992
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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
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SAMID D, Shack S, Ti-Sherman L PHENYLACETATE-A novel nontoxic inducer of TUMOR CELL differentiation. Cancer Res 52:1988, 1992
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[5] 9/15/1992
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SAMID, D., Yeh, A., and Prasanna, P. Induction of erythroid differentiation and fetal
hemoglobin production in HUMAN leukemic cells treated with PHENYLACETATE. Blood, 80: 1576-81, 1992
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SAMID D, Yen A, Prasanna P . Induction of erythroid differentiation and fetal hemoglobin production in HUMAN leukemic cells treated with PHENYLACETATE . Blood. 1992;80:1576
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Blood, 80: 1576-1581, 1992
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Blood. 1992 Sep 15;80(6):1576-81
http://m.bloodjournal.hematologylibrary.org/content/80/6/1576.full.pdf
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD
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[6] 5/1993
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SAMID D, Shack S , Myers CE . Selective growth arrest and phenotypic reversion of prostate CANCER CELLS in vitro by nontoxic pharmacological concentrations of PHENYLACETATE . J. Clin. Invest . 1993;91:2288
http://www.ncbi.nlm.nih.gov/pubmed/8486788/
J Clin Invest. 1993 May;91(5):2288-95
http://www.ncbi.nlm.nih.gov/m/pubmed/8486788/
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC288233/

http://m.jci.org/articles/view/116457
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[7] 2/15/1994
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SAMID, D., Ram, Z., Hudgins, W. R., Shack, S., Liu, L., Waibridge, S., Oldfield, E. H., and Myers, C. E. Selective activity of PHENYLACETATE against MALIGNANT GLIOMAS: resemblance to fetal brain damage in phenylketonuria. Cancer Res., 54: 891-895, 1993
http://www.ncbi.nlm.nih.gov/pubmed/8313377/
Cancer Res. 1994 Feb 15;54(4):891-5
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Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
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[8] 4/1/1994
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A phase I and pharmacokinetic study of intravenous PHENYLACETATE in PATIENTS with CANCER
http://www.ncbi.nlm.nih.gov/pubmed/8137283/
Cancer Res 54(7):1690-4 (1994), PMID.8137283
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Cancer Res April 1, 1994 54:1690
http://cancerres.aacrjournals.org/content/54/7/1690
Cancer Res. 1994 Apr 1;54(7):1690-4.
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Cancer Res . 1994;54:
http://cancerres.aacrjournals.org/content/54/7/1690
Clinical Pharmacology Branch, National Cancer Institute, NIH, Bethesda, Maryland
http://m.cancerres.aacrjournals.org/content/54/7/1690.full.pdf
A A Thibault, …, D D SAMID et al.
http://cancerres.aacrjournals.org/content/54/7/1690.full.pdf?sid=78d246d7-a4ee-4980-bdaf-b299dc98cbe8
Thibault A, Cooper MR, Figg WD, Venzon DJ, Sartor O, Tompkins AE, et al. (SAMID D)
↵1 This study was supported in part by a grant from Elan Pharmaceutical Research Co.
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[9] 6/1/1994
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Growth inhibition, TUMOR maturation, and extended survival in experimental BRAIN TUMORS in rats treated with PHENYLACETATE.
http://www.ncbi.nlm.nih.gov/pubmed/8187079/
Ram Z, SAMID D, Walbridge S, et al:
http://www.ncbi.nlm.nih.gov/m/pubmed/8187079/
Cancer Res 54:2934-2927, 1994
http://m.cancerres.aacrjournals.org/content/54/11/2934.abstract?ijkey=03bc67e581ef77536842806b949046916458d548&keytype2=tf_ipsecsha
Cancer Res. 1994 Jun 1;54(11):2923-7.
http://m.cancerres.aacrjournals.org/content/54/11/2923.abstract
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland
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Cancer Res. 1994 Jun 1;54(11):2923-7
http://cancerres.aacrjournals.org/content/54/11/2923
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[10] 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
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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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[11] 2/8/1995
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PHENYLACETATE synergizes with retinoic acid in inducing the differentiation of human neuroblastoma cells.
http://www.ncbi.nlm.nih.gov/pubmed/7829265/
Int J Cancer. 1995 Feb 8;60(4):507-14
http://www.ncbi.nlm.nih.gov/m/pubmed/7829265/
Department of Pathology and Laboratory Medicine (Neuropathology), UCLA School of Medicine
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910600414/abstract
Int J Cancer 60:507-514, 1995
Int J Cancer. 1995 Feb 8;60(4):507-14.
International Journal of Cancer
Volume 60, Issue 4, pages 507–514, 8 February 1995
Article first published online: 17 JUL 2006
DOI: 10.1002/ijc.2910600414
Sidell N, Wada R, Han G, et al: (SAMID D)
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[12] 4/1995
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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://jcp.sagepub.com/content/35/4/368
Piscitelli SC, Thibault A, Figg WD, et al: (SAMID D)
DOI: 10.1002/j.1552-4604.1995.tb04075.x
Pharmacy Department, National Institutes of Health, Bethesda, Maryland, USA
http://m.jcp.sagepub.com/content/35/4/368.abstract?ijkey=74bff0d86ce76b404728762fe2a1bfde1641fa41&keytype2=tf_ipsecsha
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[13] 5/1995
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The effect of Antineoplaston, a new ANTITUMOR AGENT on MALIGNANT BRAIN TUMORS
http://www.ncbi.nlm.nih.gov/pubmed/7474850
Kurume Med J. 1995;42(3):133-40
http://www.ncbi.nlm.nih.gov/m/pubmed/7474850
Department of Neurosurgery, Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/3/42_3_133/_article
Tsuda H (Japan)
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/3/42_3_133/_article/references
Burzynski References: 1 – 2 and 4
SAMID Reference: 7 (who learned from Burzynski re PHENYLACETATE)
Lee (Japan) A-10 Reference: 3
Nishidi (Japan) A-10 Reference: 6
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/3/42_3_133/_pdf
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[14] 6/15/1995
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Phase I study of PHENYLACETATE administered twice daily to PATIENTS with CANCER. Cancer 75:2932-8, 1995
http://www.ncbi.nlm.nih.gov/pubmed/7773944/
Cancer 75(12):2932-8 (1995), PMID.7773944
http://www.ncbi.nlm.nih.gov/m/pubmed/7773944
A A Thibault, D D SAMID, … C E CE Myers
Cancer. 1995 Jun 15;75(12):2932-8
Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
Thibault A, SAMID D, Cooper MR, et al:
Thibault, A., SAMID, D., Cooper, M. A., Figg, W. 0., Tompkins, A. C., Patronas, N., Headlea, 0. J., Kohler, 0. A., Venzon, 0. J., and Myers, C. E. Cancer (Phila.), 75: 2932-2938, 1995.
http://onlinelibrary.wiley.com/doi/10.1002/1097-0142(19950615)75:12%3C2932::AID-CNCR2820751221%3E3.0.CO;2-P/abstract
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[15] 7/1995
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Transcriptional upregulation of TGF-α by PHENYLACETATE and PHENYLBUTYRATE is associated with differentiation of HUMAN MELANOMA CELLS
http://www.ncbi.nlm.nih.gov/pubmed/7578983/
Liu L., Hudgins W. R., Miller A. C., Chen L. C., SAMID D.
http://www.sciencedirect.com/science/article/pii/S1043466685700610
Cytokine, 7: 449-456, 1995.
Cytokine Volume 7, Issue 5, July 1995, Pages 449–456
Cytokine. 1995 Jul;7(5):449-56.
a Clinical Pharmacology Branch, National Cancer Institute, Armed Forces of Radiation Research Institute, Bethesda, Maryland, USA
b Radiation Biochemistry Department, Armed Forces of Radiation Research Institute, Bethesda, Maryland, USA
http://dx.doi.org/10.1006/cyto.1995.0061
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[16] 9/27/1995
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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.
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International Journal of Cancer
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[18] 10/12/1995
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Cytostatic activity of PHENYLACETATE and derivatives against TUMOR CELLS:
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[19] 1995
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Toxicological study on antineoplastons A-10 and AS2-1 in cancer patients
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Lipid metabolism as a target for BRAIN CANCER therapy:
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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland, USA
Prasanna P, Thibault A, Liu L, et al: (SAMID D)
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[21] 5/1996
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PHENYLACETATE is an inhibitor of prostatic growth and development in culture.
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Lipshutz JH, SAMID D, Cunha GR:
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Volume 155, Issue 5, Pages 1762-1770, May 1996
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[22] 1996
� � � � � � � � � � � � � � � �
Inhibitory effect of antineoplaston A10 and AS2-1 on human hepatocellular carcinoma
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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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[23] 8/23/1996
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Pineau T, Hudgins WR, Liu L, et al: (SAMID D) Activation of a human peroxisome proliferator-activated receptor by the ANTITUMOR agent PHENYLACETATE and its analogs. Biochem Pharmacol 52:659-667, 1996
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Biochem Pharmacol. 1996 Aug 23;52(4):659-67
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Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD, USA
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[24] 9/1996
� � � � � � � � � � � � � � � �
The differentiating agent PHENYLACETATE increases prostate-specific antigen production by prostate cells
http://www.ncbi.nlm.nih.gov/pubmed/8827086/
Prostate 29:177-182, 1996
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Prostate. 1996 Sep;29(3):177-82
Walls R, Thibault A, Liu L, et al: (SAMID D)
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland, USA
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[25] 12/1996
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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
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Laboratory of Cellular and Molecular Biology, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, Maryland, USA
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[26] 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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Miller AC, Whittaker T, Thibault A, et al: (SAMID D)
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Armed Forces Radiobiology, Research Institute, Bethesda, MD, USA
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[28] 11-12/1997
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Antineoplaston AS2-1 for maintenance therapy in liver cancer
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Oncology Reports
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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
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[29] 1997
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PHENYLACETATE and PHENYLBUTYRATE as novel, nontoxic differentiation inducers
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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD USA
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[30] 5 – 6/1998
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Oncology Reports
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[31] 11-12/1998
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Antineoplaston treatment for advanced hepatocellular carcinoma
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Oncology Reports, Spandidos Publications
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[32] 3/1999
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Phase II study of PHENYLACETATE in patients with recurrent MALIGNANT GLIOMA:
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(A10) – Potential utility of antineoplaston A-10 levels in breast cancer
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Cancer Letters, Elsevier Science
Department of Pharmacognosy, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

� � � � � � � � � � � � � � � �
[34] 8/31/2000
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Cancer Letters – Elsevier
Cancer Letters, Elsevier Science
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Department of Pharmacognosy, Faculty of Pharmacy, Mansoura University, Egypt

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[35] 12/2000
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(antineoplaston A10) – Novel piperidinedione analogs as inhibitors of breast cancer cell growth
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Arch Pharm (Weinheim), John Wiley & Sons, Inc.
Department of Medicinal Chemistry, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt

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[36] 8/2001
� � � � � � � � � � � � � � � �
A phase Idose escalation and bioavailability study of oral sodium PHENYLBUTYRATE in patients with refractory solid tumor malignancies
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Clin Cancer Res 7(8):2292-300 (2001), PMID.11489804
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[37] 2002
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A novel strategy for remission induction and maintenance in cancer therapy
H Tsuda A10 and AS2-1
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Oncol Rep 9(1):65-8 (2002)
Oncology Reports, Spandidos Publications
Department of Anesthesiology, Kurume University, School of Medicine, Fukuoka-ken, Japan
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[38] 3 – 4/2003
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The preventive effect of antineoplaston AS2-1 on HCC recurrence
Hideaki H TSUDA Phase II Clinical Trial
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Oncol Rep. 2003 Mar-Apr;10(2):391-7
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Oncol Rep. 2003;10:391-397
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Spandidos Publications
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Oncology Reports 10: 391-397, 2003
Oncol Rep 10 (2):391-7 (2003)
Oncol Rep 2003;10:391–7
Department of Anesthesiology, Kurume Daiichi Social Insurance Hospital, Kushihara Kurumeshi, Fukuoka, Japan
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[39] 2003
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Long-term survival following treatment with antineoplastons for colon cancer with unresectable multiple liver metastases: report of a case
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Long-Term Survival Following Treatment with Antineoplastons for Colon Cancer with Unresectable Multiple Liver Metastases:
Report of a Case
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Surg Today. 2003;33(6):448-53
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Surgery Today, Springer
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DOI: 10.1007/s10595-002-2503-2
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Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan
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� � � � � � � � � � � � � � � �
Antineoplaston induces G1 arrest by PKCα and MAPK pathway in SKBR-3 breast cancer cells
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Oncology Reports, 8/2005, Volume 14 Number 2
Pages: 489-494
http://onlinelibrary.wiley.com/store/10.1002/iub.574/asset/574_ftp.pdf?v=1&t=hbr9z60q&s=0b1c1e8655db9c54b45dbf72062e8b11cb7895ac
Oncology Reports, Spandidos Publications
Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan
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[42] 2006
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Inhibitory Effect of Antineoplaston A10 and AS2-1 on Human Hepatocellular Carcinoma
Tsuda H, et al
http://www.ncbi.nlm.nih.gov/pubmed/8755117
Kurume Med J. 1996;43(2):137-47
http://www.ncbi.nlm.nih.gov/m/pubmed/8755117
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article
Kurume Medical Journal
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_pdf
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[43] 1/2008
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Preclinical studies of molecular-targeting diagnostic and therapeutic strategies against breast cancer
http://www.ncbi.nlm.nih.gov/pubmed/18224398
antineoplaston
http://www.ncbi.nlm.nih.gov/m/pubmed/18224398
Breast Cancer 15(1):73-8 (2008)
DOI: 10.1007/s12282-007-0015-y
http://link.springer.com/article/10.1007%2Fs12282-007-0015-y
Breast Cancer. 2008;15(1):73-8. doi: 10.1007/s12282-007-0015-y
http://www.springerlink.com/content/p724x34746l56v73
15(1):73-8
http://ci.nii.ac.jp/naid/10021288533
Breast Cancer: January 2008, Volume 15, Issue 1, pp 73-78
Department of Surgery, Kurume University, Fukuoka, Japan
Burzynski Reference: 12
Tsuda (Japan) Antineoplaston Reference: 13
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[44] 10/2010
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Antineoplaston A10 phenylacetyl glutamine (PG)
http://www.springerlink.com/content/tj0177485773007t
(S)-2-((S)-2-(4-(3-[18F]fluoropropyl)benzamido)-3-phenylpropanamido)pentanedioic acid labeled with 18F
http://link.springer.com/article/10.1007%2Fs10967-010-0633-2?LI=true
(S)-2-((S)-2-(4-(3-[18 F] fluoropropyl) benzamido)-3-phenylpropanamido) pentanedioic acid labeled with 18 F
http://www.springerlink.com/content/tj0177485773007t
Journal of Radioanalytical and Nuclear Chemistry, 2010, 286, 1, 135
http://link.springer.com/article/10.1007%2Fs10967-010-0633-2
October 2010, Volume 286, Issue 1, pp 135-140
http://link.springer.com/article/10.1007/s10967-010-0633-2/fulltext.html
DOI
10.1007/s10967-010-0633-2

http://onlinelibrary.wiley.com/doi/10.1021/js960120y/abstract
Burzynski References: 5. – 6.
http://www.springerlink.com/content/tj0177485773007t
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QUESTIONS the Critics and Cynics, “The Skeptics™” do NOT want to ANSWER

1. One “Orac” (Dr. David H. Gorski @oracknows @sciencebasedmed @gorskon #sciencebasedmedicine
http://www.scienceblogs.com/Insolence
http://www.sciencebasedmedicine.org)
claimed:


“Burzynski naturally has lots of excuses for why the trial failed and tried to blame the investigators, but his complaints are not convincing.”

When I requested that he respond to Burzynski’s comments re the study, he would NOT touch it with the proverbial ZZ Top

“Ten-Foot Pole”

What Critic, Cynic, or one of “The Skeptics™” is going to show more Bravery and Courage than “Orac”?
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2. If antineoplastons do NOT work, why, after Dvorit D. SAMID learned of them from Burzynski, did all the research, clinical studies, and phase I, phase II, and phase III clinical trials really start to get underway on
PHENYLACETYLGLUTAMINATE (PAG or PG)
PHENYLACETATE (PN)

and
PHENYLBUTYRATE (PB)?
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3. This individual claims to be a “cancer researcher”

If this individual’s “research” is so poor as a “cancer researcher,” what does that say about “research” re the “War on Cancer”?

My review of C0nc0rdance:
https://stanislawrajmundburzynski.wordpress.com/2013/03/23/my-review-of-c0nc0rdance/
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4. This individual claims to be a “Doctor,” “oncologist,” “breast cancer specialist,” and “cancer researcher”

If this individual’s “research” is so poor as a “cancer researcher,” what does that say about “research” re the “War on Cancer”?

Paging Doctor David H. Gorski, Paging Doctor David H. Gorski: There’s Mud in your Ears … Doktor Gorski?:
https://stanislawrajmundburzynski.wordpress.com/2013/05/28/paging-doctor-david-h-gorski-paging-doctor-david-h-gorski-theres-mud-in-your-ears-doktor-gorski/
He did NOT even refer to the below publication by Burzynski regarding “Treatment of Recurrent Triple-Negative Breast Cancer:”

8/2011 – Successful Treatment of Recurrent Triple-Negative Breast Cancer with Combination of Targeted Therapies
http://www.scirp.org/journal/PaperDownload.aspx?DOI=10.4236/jct.2011.23050
Journal of Cancer Therapy, 2011, 2, 372-376
doi:10.4236/jct.2011.23050 Published Online August 2011
(http://www.SciRP.org/journal/jct)
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5. Critics, Cynics, “The Skeptics™” state that Burzynski is NOT an oncologist, but can offer no explanation as to why this is supposedly “relevant,” they cannot explain if oncologists are somehow “better” than biochemists, nor do they want to answer the question:

“Does Burzynski work with any oncologists, and are any of them listed on his phase II clinical trial publications”?

http://www.burzynskiclinic.com/scientific-publications.html
Interim Reports on Clinial Trials:

16. 2003

DRUGS IN R&D
Drugs in R and D
(Drugs in Research and Development)

BT-11

BRAIN STEM GLIOMA

Phase II study of antineoplaston A10 and AS2-1 in patients with recurrent diffuse intrinsic BRAIN STEM GLIOMA:

a preliminary report.
http://www.ncbi.nlm.nih.gov/pubmed/12718563
Burzynski, S.R.
Lewy, R.I.
Weaver, R.A.
Axler, M.L.
Janicki, T.J.
Jurida, G.F.
Paszkowiak, J.K.
Szymkowski, B.G.
Khan, M.I.
Bestak, M.

http://www.ncbi.nlm.nih.gov/m/pubmed/12718563
Drugs R D. 2003;4(2):91-101
Drugs in R&D 2003;4:91-101
http://www.burzynskiclinic.com/images/stories/Publications/960.pdf
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6. The British Broadcasting Corporation (BBC) Panorama program indicated that 776 Burzynski patients with brain tumours were treated in trials before 2008
http://t.co/nFpwlQg275
15.5% (120) survived more than 5 years

Critics, Cynics, “The Skeptics™”, what’s your survival rate?
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7. March 29, 1996

Then United States Food and Drug Administration Commissioner, David A. Kessler told the American people:

1. We will eliminate unnecessary paperwork … that used to delay or discourage … cancer research … by non-commercial clinical investigators

2. The … FDA’s initiatives … will allow …the agency … to rely on smaller trialsfewer patients … if there is evidence … of partial response in clinical trials

I don’t want to get into any particular … agent … except let me point out … that … the information needs to be part … of clinical trials

3. We will accept … less information … up front –

4. we’re going to require further study AFTERapproval … because the science … has matured

5. The important – point … is that information needs to be gathered … through scientific means … through clinical – trials … and I think – that’s … that’s very important uhh very … important point

You can’t … just … use an agent here – or there … you have to use it … as part of a clinical trial … so we can get information … on whether the drug works

6. The uhh agency has … many … trials … has has approved trials … for patients … with antineoplastons

7. We are committed to providing expanded accessavailabilityfor American patients for any drugthere’s reason to believemay work
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/03/22/antineoplastons-has-the-fda-kept-its-promise-to-the-american-people
——————————————————————
A. What is the FDA’s definition of “unnecessary paperwork”?

B. What is the FDA’s definition of “smaller trials”?

C. What is the FDA’s definition of “fewer patients”?

D. What is the FDA’s definition of “evidence … of partial response“?

E. What is the FDA’s definition of “less information … up front”?

F. What is the FDA’s definition of “we’re going to require further study AFTER … approval”?

G. What is the FDA’s definition of “We are committed to providing expanded access … availability … for American patients for any drug … there’s reason to believe … may work”?

https://stanislawrajmundburzynski.wordpress.com/2013/06/08/what-is-misdirection-critiquing-antineoplastons-has-the-fda-kept-its-promise-to-the-american-people/
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8. The British Broadcasting Corporation (BBC) Panorama program indicated that 776 Burzynski patients with brain tumours were treated in trials before 2008
http://t.co/nFpwlQg275
Is that what the FDA means by:

rely on … fewer patients?
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9. 4/27/2013 (37:20) Fabio stated that
Burzynski had provided the FDA with 2.5 million pages of clinical trial documents

Is that what the FDA means by:

“unnecessary paperwork”?

and

“less information … up front”?
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10. Is this what the FDA means by:
https://stanislawrajmundburzynski.wordpress.com/2013/06/08/what-is-misdirection-critiquing-antineoplastons-has-the-fda-kept-its-promise-to-the-american-people/
if there is evidence … of partial response in clinical trials?
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11. Why was the United States Food and Drug Administration requiring that radiation be used in the Phase 3 Clinical Trial when Burzynski has shown better results with antineoplastons when radiation is NOT used?
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12. Who wants to defend the excuse that The Lancet gave for NOT Publishing the documentation which Burzynski sent to them, which is referred to in Burzynski: Cancer is Serious Business, Part II?
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13. Review Articles on Clinical Trials: 2. 2006 – Treatments for Astrocytic Tumors in Children: Current and Emerging Strategies. Pediatric Drugs 2006;8:167-178.
http://www.burzynskiclinic.com/images/stories/Publications/1252.pdf
2006 Adis – Pediatr Drugs 2006; 8 (3)

pg 174

2.3. Targeted Therapy

1652 adults
335 children
[147]


indicates 1,799 Burzynski patients

Is that what the FDA means by:

rely on … fewer patients?
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13. The FDA approved phase III (3) clinical trials for Antineoplastons A10 (Atengenal) and AS2-1 (Astugenal); which means that they have shown evidence of effectiveness, yet they have NOT granted Accelerated Approval for them, even though they have done so for other treatments which had NOT yet published the final results of phase II (2) clinical trials, and which did NOT have as good Complete Response, Partial Response, Stable Disease, Minor Response, Progressive Disease, Objective Response, Progression-Free Survival, etc., rates:

Burzynski: Why has the FDA NOT granted Accelerated Approval for Antineoplastons A10 (Atengenal) and AS2-1 (Astugenal) ?:
https://stanislawrajmundburzynski.wordpress.com/2013/07/28/burzynski-why-has-the-fda-not-granted-accelerated-approval-for-antineoplastons-a10-astengenal-and-as2-1-astugenal/

(Additional QUESTIONS being added)

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References:

1.

Post #73 – Didymus Judas Thomas

At the Tu-Quack Center Oracles of Deny to Respond tree

1/30/2013

Post #52 – Orac

“You do realize that that means that the Mayo trial failed to find evidence of efficacy, just as I said, don’t you?”

“The default of a finding like that is that there is no evidence of efficacy, not that failure to have adequate numbers to show an effect means that there’s an effect there”

“If SRB wants to convince skeptics that his treatments work better than conventional therapy, let him publish the evidence in a peer-reviewed journal in a manner that it can be independently verified”

“Thus far, he has failed to do so.”

Orac, I thoroughly enjoyed; with a dismissive limp wrist, you posted:

“Burzynski naturally has lots of excuses for why the trial failed and tried to blame the investigators, but his complaints are not convincing.”
http://scienceblogs.com/insolence/2013/01/21/quoth-joe-mercola-i-love-me-some-burzynski-antineoplastons
Now, why don’t you tackle those ?’s?

1. “[T]he study tested a dosing regimen known to be ineffective.”

2. “[D]osages used in the study “were meant for the treatment of a single small lesion…”

3. “5 of the 6 evaluable patients had either multiple nodules or tumors larger than” said single small lesion.

4. “As the provider,” SRB “strongly suggested to the NCI that these patients receive a much higher dose, consistent with their greater tumor load.”

5. “[T]he study was closed when” SRB “insisted that the NCI either increase the dosage or inform the patients that the drug manufacturer believed that the treatment was unlikely to be effective at the dosages being used (letter to Dr M. Sznol, NCI, on 4/20/1995).”

6. “A review of the clinical data in the article … proves the validity of” SRB’s “position” per SRB

7. “Their study patients had extremely low plasma antineoplaston levels.”

8. SRB’s “phase 2 study dosage regimen produced plasma phenylacetylglutamine levels that are 35 times greater, phenylacetylisoglutamine levels 53 times greater, and phenylacetate levels 2 times greater than those reported…’”

9. “The clinical outcomes reported … based on their inadequate dosage schedule, differ dramatically from” SRB’s “phase 2 studies in which a higher dosage regimen was used.”

10. “They reported no tumor regression. In contrast, in 1 of” SRB’s “ongoing studies on protocol BT-9, 4 of 8 evaluable patients with astrocytoma had objective responses.’”

11. “The difference in outcomes is primarily due to the difference in dosage schedules,” per SRB

12. “Another factor that may have caused a lack of response in the study by … is that the duration of treatment was too brief.”

13. “Almost all the patients in their study received treatment for less than 30 days.”

14. “1 patient received only 9 days of treatment.”

15. “The current studies indicate that objective tumor responses are usually observed after 3 months of therapy.”

16. “An additional 8 months of treatment is usually needed to obtain a maximal therapeutic effect.”

17. “[A]mbiguities in the response evaluation and analysis in the article…”

a) “In 2 patients, tumor necrosis was attributed to “radionecrosis.””

b) “However, such an interpretation is clouded by the fact that antineoplaston-induced necrosis can be indistinguishable from radionecrosis.”

c) “Moreover, the analysis … could have highlighted the 2 patients with recurrent glioblastoma who survived for more than I year.”

d) “This is of interest because these patients typically have a life expectancy of 3 to 6 months.”

18. “It is regrettable that, at the time of the study … the sponsor, NCI, decided against the higher dosing regimen that I proposed and closed the study.”
https://stanislawrajmundburzynski.wordpress.com/2013/03/24/stanislaw-rajmund-burzynski-m-d-ph-d-and-freedom-of-speech/
IMPORTANT: The live “debate” that wasn’t-A Film Producer, A Cancer Doctor, And Their Critics:
https://stanislawrajmundburzynski.wordpress.com/2013/04/29/important-the-live-debate-that-wasnt-a-film-producer-a-cancer-doctor-and-their-critics/
Post #85 – Orac – April 28, 2013

“Well, DJT tried to comment last night and got caught in the moderation trap.”

“I’m not letting DJT through.”

“He’s been banned for very good reason, and I will not rescind the ban.”
http://scienceblogs.com/insolence/2013/04/26/all-truth-comes-from-public-debate-a-corollary-to-crank-magnetism/
My below blog contained a copy of the comment I submitted to his blog:
https://stanislawrajmundburzynski.wordpress.com/2013/04/27/important-the-live-debate-a-film-producer-a-cancer-doctor-and-their-critics/
All Mr. Hinton would have to do is ask “Orac” to respond to my post 73 on his blog, and it would be all over, since “Orac” has adopted his “Hold the Mayo” attitude, and shows no indication that he would ever be brave enough to touch it with the proverbial ZZ Top

“Ten Foot Pole”

because he’s probably aware of what would happen if he did

One of “Orac’s” “Oracolytes” posted on Forbes (#Forbes):
onforb.es/11pwse9

http://t.co/vh3cgAR6hW
“I already offered you a forum on a science blog to debate with a real respected surgical oncologist, with a guarantee that he never moderates the “debate”.”
http://www.forbes.com/sites/peterlipson/2013/04/19/a-film-producer-a-cancer-doctor-and-their-critics
IMPORTANT: The live “debate”-A Film Producer, A Cancer Doctor, And Their Critics:
https://stanislawrajmundburzynski.wordpress.com/2013/04/27/important-the-live-debate-a-film-producer-a-cancer-doctor-and-their-critics/
This is Dr. David H. Gorski’s blog

Dr. Gorski censored (blocked) my comments

We are supposed to believe that he’s now NOT going to block someone’s comments???
http://scienceblogs.com/insolence/2013/04/26/all-truth-comes-from-public-debate-a-corollary-to-crank-magnetism/
#66 – Didymus Judas Thomas

IMPORTANT: The live “debate”-A Film Producer, A Cancer Doctor, And Their Critics | Didymus Judas Thomas’ Hipocritical Oath Blog

April 27, 2013

Your comment is awaiting moderation.

Seriously ? Gorski ? Let’s remember that it is YOU who would NOT answer my questions, and instead inacted your “Hold the Mayo” posture re post 73

Let’s review your

“deconstructed his “evidence” in depth before” claim

1/21/2013 Orac posted THIS blog:

“Quoth Joe Mercola:

I love me some Burzynski antineoplastons

Posted by Orac on January 21, 2013″

” … In particular, a multicenter phase II trial carried out by investigators at the Mayo Clinic was a big failure, with a median survival of 5.2 months in patients with anaplastic oligoastrocytoma, anaplastic astrocytoma, or glioblastoma multiforme that had recurred after radiation therapy”

“Burzynski naturally has lots of excuses for why the trial failed and tried to blame the investigators, but his complaints are not convincing”
http://scienceblogs.com/insolence/2013/01/21/quoth-joe-mercola-i-love-me-some-burzynski-antineoplastons
I challenged “Orac” about this and this reply was posted which included my point at the beginning of the reply:

1/29/2013

“An excellent explanation of how dubious Stanislaw Burzynski’s activities are”

Posted by Orac on January 28, 2013
http://scienceblogs.com/insolence/2013/01/28/an-excellent-explanation-of-how-dubious-stanislaw-burzynskis-activities-are
Post #52 – Orac

January 29, 2013

“CONCLUSION: Although we could not confirm any tumor regression in patients in this study, THE SMALL SAMPLE SIZE PRECLUDES DEFINITIVE CONCLUSIONS ABOUT TREATMENT EFFICACY.”

“You do realize that that means that the Mayo trial failed to find evidence of efficacy, just as I said, don’t you?”

“The default of a finding like that is that there is no evidence of efficacy, not that failure to have adequate numbers to show an effect means that there’s an effect there”

“If SRB wants to convince skeptics that his treatments work better than conventional therapy, let him publish the evidence in a peer-reviewed journal in a manner that it can be independently verified”

“Thus far, he has failed to do so”

I responded to Orac, quoting his reply at the beginning of my reply:

Post #73 – Didymus Judas Thomas

At the Tu-Quack Center Oracles of Deny to Respond tree

January 30, 2013

Post #52 – Orac

“You do realize that that means that the Mayo trial failed to find evidence of efficacy, just as I said, don’t you?”

“The default of a finding like that is that there is no evidence of efficacy, not that failure to have adequate numbers to show an effect means that there’s an effect there”

“If SRB wants to convince skeptics that his treatments work better than conventional therapy, let him publish the evidence in a peer-reviewed journal in a manner that it can be independently verified”

“Thus far, he has failed to do so”

Orac, I thoroughly enjoyed; with a dismissive limp wrist, you posted:

“Burzynski naturally has lots of excuses for why the trial failed and tried to blame the investigators, but his complaints are not convincing.”
http://scienceblogs.com/insolence/2013/01/21/quoth-joe-mercola-i-love-me-some-burzynski-antineoplastons
Now, why don’t you tackle those ?’s?

[SOURCE: Feb. 1999 Mayo Clinic Publication pg 2, 3 PDF]
http://burzynskimovie.com/images/stories/transcript/Documents/Feb99MayoClinicPubANP.pdf
2/1999 – A10 and AS2-1 – Phase II – Mayo Clinic Proceedings http://www.ncbi.nlm.nih.gov/m/pubmed/10069350
Phase II Study of Antineoplastons A10 (NSC 648539) and AS2-1 (NSC 620261) in Patients With Recurrent Glioma Objective:
http://www.mayoclinicproceedings.org/article/S0025-6196(11)63835-4/fulltext
To assess the pharmacokinetics, toxicity, and efficacy of antineoplastons A10 (NSC 648539) and AS2-1 (NSC 620261)
http://linkinghub.elsevier.com/retrieve/pii/S0025-6196(11)63835-4
Design:
http://www.sciencedirect.com/science/article/pii/S0025619611638354
We initiated a phase II trial in order to determine whether evidence of antitumor activity of A10 and AS2-1 could be documented
http://download.journals.elsevierhealth.com/pdfs/journals/0025-6196/PIIS0025619611638354.pdf
Comment in Jun; 74 (6): 641-2
http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.2003.01098.x/full
Mayo Clin Proc 74(2):9 (1999)
http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.2003.01098.x/references
1999 Elsevier Ltd.
http://onlinelibrary.wiley.com/store/10.1046/j.1365-2796.2003.01098.x/asset/j.1365-2796.2003.01098.x.pdf?v=1&t=hbs6xce2&s=3423e3cd1955667e8e8cdf33323faf0bd85b6a29
DOI: 10.4065/74.2.137
http://onlinelibrary.wiley.com/store/10.1046/j.1365-2796.2003.01098.x/asset/j.1365-2796.2003.01098.x.pdf?v=1&t=hbrndkdf&s=e0af2d3bfb13841852d92a839d3a4932a5f4bb48
Mayo Clin Proc 1999; 74: 137–45

Burzynski responded by pointing out:

6/1999 – A10 and AS2-1 – SRB http://www.ncbi.nlm.nih.gov/m/pubmed/10377942
Efficacy of antineoplastons A10 and AS2-1
S R Burzynski
Mayo Clin Proc 74 (6): 641-2 (1999),
Mayo Clin Proc. 1999 Jun; 74 (6): 641-2 Comment on Mayo Clin Proc. 1999 Feb; 74 (2): 137-45 PMID .10377942 Elsevier Science
http://www.mayoclinicproceedings.org/article/S0025-6196(11)64143-8/fulltext
Mayo Clinic Proc. 1999; 74: 641–642 (letter) 74 (6): 641-2
http://linkinghub.elsevier.com/retrieve/pii/S0025-6196(11)64143-8
Mayo Clin Proc 74 (6): 1 (1999), 1999 Elsevier Ltd.
http://download.journals.elsevierhealth.com/pdfs/journals/0025-6196/PIIS0025619611641438.pdf
DOI: 10.4065/74.6.641

This was responded to:

6/1999 – Mayo Clin Proc 74(6):2 (1999), DOI: 10.4065/74.6.641-a
http://www.mayoclinicproceedings.org/article/S0025-6196(11)64144-X/fulltext
Mayo Clinic Proceedings
Volume 74, Issue 6 , Pages 641-642, June 1999
http://download.journals.elsevierhealth.com/pdfs/journals/0025-6196/PIIS002561961164144X.pdf
References:

1. SAMID D , Shack S, Sherman LT. Phenylacetate: a novel nontoxic inducer of tumor cell differentiation. Cancer Res . 1992; 52:1988–1992
http://www.ncbi.nlm.nih.gov/m/pubmed/1372534/

http://m.cancerres.aacrjournals.org/content/52/7/1988.abstract

http://m.cancerres.aacrjournals.org/content/52/7/1988.full.pdf

http://cancerres.aacrjournals.org/content/52/7/1988
2. Danesi R, Nardini D, Basolo F, Del Tacca M, SAMID D . Myers CEo Phenylacetate inhibits protein isoprenylation and growth of the androgen-independent LNCaP prostate cancer cells transfected with the T24 Ha-ras oncogene. Mol Pharmacal. 1996; 49:972–979
http://www.ncbi.nlm.nih.gov/m/pubmed/8649357/

http://m.molpharm.aspetjournals.org/content/49/6/972.long
3. Chang SM, Kuhn LG, Robins HI, et al. Phase II study of phenylacetate in patients with recurrent malignant glioma: a North American Brain Tumor Consortium report. J Clin Oneal. 1999; 17:984–990
http://www.ncbi.nlm.nih.gov/m/pubmed/10071293/

http://m.jco.ascopubs.org/content/17/3/984.long
4. Thibault A, Cooper MR, Figg WD, et al. (SAMID D). A phase I and pharmacokinetic study of intravenous phenylacetate in patients with cancer. Cancer Res. 1994; 54:1690–1694
http://www.ncbi.nlm.nih.gov/m/pubmed/8137283/

http://m.cancerres.aacrjournals.org/content/54/7/1690.abstract

http://m.cancerres.aacrjournals.org/content/54/7/1690.full.pdf

http://cancerres.aacrjournals.org/content/54/7/1690
PII: S0025-6196(11)64144-X

doi: 10.1016/S0025-6196(11)64144-X

1999 Mayo Foundation for Medical Education and Research.
Elsevier Inc.

The above four (4) references in the response to Burzynski might be relevant if all that antineoplastons consisted of was phenylacetate

Phenylacetylglutaminate (PAG or PG) and Phenylacetate (PN) are metabolites of Phenylbutyrate (PB) and are constituents of antineoplaston AS2-1

Antineoplastons AS2-1 and AS2-5 are DERIVED FROM A10

AS2-1=4:1 mixture of PHENYLACETIC ACID (PA) and Phenylacetylglutamine (PAG or PG)

National Cancer Institute (NCI) at the National Institutes of Health (NIH)
Antineoplastons
General Information:
http://www.cancer.gov/cancertopics/pdq/cam/antineoplastons/healthprofessional/page2
This is “what would happen” if “Orac” did have the “Bravery,” “Courage,” “Gumption,” “Intestinal Fortitude,” “Testicular Fortitude,” to address this issue:
http://burzynskimovie.com/images/stories/transcript/Documents/BurzynskiTriesToExposeNCI.pdf
Burzynski: Managing social conflict in complementary and alternative medicine research: the case of antineoplastons:
https://stanislawrajmundburzynski.wordpress.com/2013/04/26/burzynski-managing-social-conflict-in-complementary-and-alternative-medicine-research-the-case-of-antineoplastons/
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2.
Antineoplastons: Phenylacetylglutaminate (PG or PAG), Phenylacetate (PN), and Phenylbutyrate (PB):
https://stanislawrajmundburzynski.wordpress.com/2013/06/17/phenylacetylglutaminate-pg-or-pag-phenylacetate-pn-and-phenylbutyrate-pb/
Phenylacetylglutamine (PG or PAG):
https://stanislawrajmundburzynski.wordpress.com/2013/06/18/phenylacetylglutamine-pg-or-pag/
Phenylacetate (PN):
https://stanislawrajmundburzynski.wordpress.com/2013/06/18/phenylacetate-pn/
Phenylbutyrate (PB):
https://stanislawrajmundburzynski.wordpress.com/2013/06/18/phenylbutyrate-pb/
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