Does David H. “Orac” Gorski, M.D., Ph.D, really CARE about Breast Cancer patients?

Dr. Gorski (@gorskon @OracKnows @ScienceBasedMed
http://www.scienceblogs.com/Insolence
#ScienceBasedMedicine
http://www.sciencebasedmedicine.org)
is advertised as being a “Breast Cancer Specialist”

The question is, does he really CARE about Breast Cancer patients?

2000-2001, clinical studies were conducted on breast cancer patients in Egypt, using antineoplaston A10
======================================
Burzynski: Egypt antineoplaston publications:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/04/25/burzynski-egypt-antineoplaston-publication/
======================================
7/3/2000 they noted:
——————————————————————
Antineoplastons first described by Burzynski are naturally occurring peptides and amino acid derivatives, which control neoplastic growth
——————————————————————
Antineoplaston A-10 level measured in urine of:
31 breast cancer patients
17 normal women
——————————————————————
Significantly lower antineoplaston A-10 levels detected among patients with breast cancer
——————————————————————
Data suggest strong inverse association of urinary antineoplaston A-10 level with breast cancer
——————————————————————
Potential utility of antineoplaston A-10 as predictive test for women at risk of developing breast cancer
======================================
8/31/2000 they noted:
—————————————————————
Antineoplastons are naturally occurring cytodifferentiating agents
—————————————————————
Chemically, they are medium and small sized peptides, amino acid derivatives and organic acids, which exist in blood, tissues and urine
—————————————————————
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
======================================
12/2000 they noted:
—————————————————————
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
—————————————————————
DNA binding capacity of compounds evaluated against A10
—————————————————————
“3A” and “3C” had weaker biological profiles than lead compound A10
—————————————————————
“3B” and “3D” were several-fold more potent antiproliferative agents than A10 and tamoxifen and had significantly higher capacity to bind DNA than A10
======================================
10/1/2001 they noted:
—————————————————————
Reports on structural characterization of new antineoplaston (ANP) representatives
—————————————————————
Combination heat with pH modification had virtually no effect on obtained peaks, attesting to stability and purity of compounds
—————————————————————
One had superior affinity to DNA than prototype ANP-A10
======================================
8/2005 Antineoplastons such as A10 include naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH OF CELLS
——————————————————————
Findings indicate antineoplaston A10 ANTITUMOR EFFECT could be utilized as effective therapy for breast cancer patients
——————————————————————
Antineoplaston induces G1 arrest by PKCα and MAPK pathway in SKBR-3 breast cancer cells
Hideaki H TSUDA Antineoplaston A10
http://www.ncbi.nlm.nih.gov/pubmed/16012735
Antineoplaston induces G1 arrest by PKCo and MAPK pathway in SKBR-3 breast cancer cells
http://www.ncbi.nlm.nih.gov/m/pubmed/16012735
Antineoplaston induces G(1) arrest by PKCalpha and MAPK pathway in SKBR-3 breast cancer cells
http://www.spandidos-publications.com/or/14/2/489
Oncol Rep. 8/2005; 14(2):489-94
http://gyouseki.kurume-u.ac.jp/PDF/ichiran_2005.pdf
Oncol Rep 14(2):489-94 (2005)
http://research.kurume-u.ac.jp/K90RES.php?scode=49485632873864
Oncol Rep. 2005; 14:489–94
http://onlinelibrary.wiley.com/doi/10.1002/iub.574/abstract
Oncol. Rep. 14, 489–494
http://onlinelibrary.wiley.com/doi/10.1002/iub.574/full
Oncology Reports, 8/2005, Volume 14 Number 2
Pages: 489-494
http://onlinelibrary.wiley.com/store/10.1002/iub.574/asset/574_ftp.pdf?v=1&t=hbr9z60q&s=0b1c1e8655db9c54b45dbf72062e8b11cb7895ac
Oncology Reports, Spandidos Publications
Department of Surgery, Kurume University School of Medicine, Kurume, Fukuoka, Japan
======================================
� � � � � � � � � � � � � � � �
1/2008 Novel mechanism through which all-trans retinoic acid (ATRA) and antineoplaston, ANTICANCER DRUG, CAUSED CELL GROWTH INHIBITION IN BREAST CANCER CELLS through effects on intracellular pathways
——————————————————————
Antineoplaston caused down-regulation of PKCalpha protein expression, resulting in INHIBITION of ERK MAPK phosphorylation, with resultant INHIBITION of Rb phosphorylation leading to G(1) arrest

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
15(1):73-8
http://www.springerlink.com/content/p724x34746l56v73
Department of Surgery, Kurume University, Fukuoka, Japan
http://ci.nii.ac.jp/naid/10021288533
======================================
Burzynski has made it clear that:

… antineoplaston A10 rather than antineoplaston AS2-1 is main active drug
—————————————————————
Pg. 99
—————————————————————
http://www.burzynskiclinic.com/images/stories/Publications/960.pdf
—————————————————————
Burzynski has been using the “Parent” generation of antineoplastons in the phase II clinical trials, and could NOT just switch to new antineoplaston analogs which may produce better results

Also, Burzynski has made it clear that successive generations of antineoplastons have been developed which may also produce better results
—————————————————————
To those who seemed to think Burzynski’s phase II clinical trials were taking too long, he was following science based medicine’s:
—————————————————————
Pg. 94
—————————————————————
2-stage phase II clinical trial design proposed by Fleming [3]
—————————————————————
Pg. 100 References
—————————————————————
3. Fleming TR. One-sample multiple testing procedure for phase II clinical trials. Biometrics 1982; 38: 143-51
http://www.ncbi.nlm.nih.gov/pubmed/7082756/
Biometrics. 1982 Mar;38(1):143-51
http://www.ncbi.nlm.nih.gov/m/pubmed/7082756/
Biometrics Vol. 38, No. 1, Mar., 1982
http://www.jstor.org/discover/10.2307/2530297?uid=3739656&uid=2460338175&uid=2460337855&uid=2&uid=4&uid=83&uid=63&uid=3739256&sid=21102549294733
—————————————————————
To those who have made ridiculous statements to the effect that Burzynski is a murderer, and ignore that he has dealt with patients whom science based medicine’s chemotherapy therapy and / or radiation therapy did NOT work, what’s the difference when science based medicine fails?
——————————————————————
33 / 100% – DIED OF DISEASE PROGRESSION
——————————————————————
2004 – Supratentorial high-grade ASTROCYTOMA and DIFFUSE BRAINSTEM GLIOMA:
——————————————————————
two challenges for the pediatric oncologist
http://www.ncbi.nlm.nih.gov/pubmed/15047924/
Oncologist. 2004;9(2):197-206
http://www.ncbi.nlm.nih.gov/m/pubmed/15047924/
Oncologist 9, 197-206
http://m.theoncologist.alphamedpress.org/content/9/2/197.long
Division of Neuro-Oncology, Department of Hematology-Oncology, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA
======================================
David James (@StortSkeptic) tweeted at 7:08pm – 1 Aug 13:

The new Doctor Who will be Stanislaw #Burzynski. He manages to continually avoid getting cornered and he gets away with murder.
https://twitter.com/StortSkeptic/status/363088970239840256
—————————————————
To those who say that antineoplastons are toxic, what is the difference with science based medicine’s chemotherapy therapy or radiation therapy when we know that NOT all patients will experience all possible side-effects of a drug?

The successive generations of antineoplastons may be even better and have less potential side-effects
=====================================
10/1/2010 As degradation product of Antineoplaston A10 in vivo, PHENYLACETYL GLUTAMINE showed ANTITUMOR ACTIVITIES
——————————————————————
Designed and radiosynthesized PHENYLACETYL GLUTAMINE derivative, achieved under mild reaction condition
——————————————————————
radiochemical purity of (S)-2-((S)-2-(4-(3-fluoropropyl)benzamido)-3-phenylpropanamido)pentanedioic acid ([18F]FBPPA) was 98%, and best radiochemical yield was up to 46%
——————————————————————
results revealed it might become potential PET imaging agent for DETECTING TUMORS
——————————————————————
Antineoplaston A10 phenylacetyl glutamine (PG) – (S)-2-((S)-2-(4-(3-[18F]fluoropropyl)benzamido)-3-phenylpropanamido)pentanedioic acid labeled with 18F
http://www.springerlink.com/content/tj0177485773007t
(S)-2-((S)-2-(4-(3-[18 F] fluoropropyl) benzamido)-3-phenylpropanamido) pentanedioic acid labeled with 18 F
http://link.springer.com/article/10.1007%2Fs10967-010-0633-2?LI=true
Journal of Radioanalytical and Nuclear Chemistry, 2010, 286, 1, 135
http://www.springerlink.com/content/tj0177485773007t
October 2010, Volume 286, Issue 1, pp 135-140
http://link.springer.com/article/10.1007%2Fs10967-010-0633-2
DOI
10.1007/s10967-010-0633-2
http://link.springer.com/article/10.1007/s10967-010-0633-2/fulltext.html
Burzynski References: 5. – 6.
http://onlinelibrary.wiley.com/doi/10.1021/js960120y/abstract

http://www.springerlink.com/content/tj0177485773007t
======================================
Antineoplastons as a blood or urine “cancer test”:
—————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/02/22/antineoplastons-as-a-blood-or-urine-cancer-test/
======================================

Burzynski: Why has the FDA NOT granted Accelerated Approval for Antineoplastons A10 (Atengenal) and AS2-1 (Astugenal) ?

======================================
1996 – Accelerated approval started by United States Food and Drug Administration Commissioner, Dr. David A. Kessler
(.4:18 – .6:10):
http://www.youtube.com/watch?v=1buiXWr_QTQ
======================================
Tamoxifen:
======================================
7/1997 – A phase I study of high-dose tamoxifen for the treatment of refractory malignant GLIOMAS OF CHILDHOOD
http://www.ncbi.nlm.nih.gov/pubmed/9815790/
Clin Cancer Res. 1997 Jul;3(7):1109-15
http://www.ncbi.nlm.nih.gov/m/pubmed/9815790/
Clin Cancer Res July 1997 3; 1109
http://m.clincancerres.aacrjournals.org/content/3/7/1109.full.pd
Departments of Neurosurgery, Children’s Hospital of Pittsburgh, Pittsburgh, Pennsylvania, USA

http://clincancerres.aacrjournals.org/content/3/7/1109
Children with malignant GLIOMAS THAT PROGRESSED AFTER CONVENTIONAL THERAPY
——————————————————————
0 / 0% – EXHIBITED CLEAR-CUT TUMOR regression
——————————————————————
17 months (1 year 5 months) – longest survivor lived for after beginning tamoxifen
======================================
2000 – Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse BRAINSTEM GLIOMAS:

results of a Brazilian cooperative study
http://www.ncbi.nlm.nih.gov/pubmed/10715294/
Brainstem Glioma Cooperative Group
http://www.ncbi.nlm.nih.gov/m/pubmed/10715294/
J Clin Oncol 18, 1246-1253
http://m.jco.ascopubs.org/content/18/6/1246.long
——————————————————————
22 – assessable patients
——————————————————————
10.3 months – Median Survival
——————————————————————
4 / 18% – remain alive without tumoral progression
——————————————————————
8 / 37.0% {+/- 2 / 9.5%} (mean +/- SD) – 1-year Survival rate
——————————————————————
treatment combination PRODUCED NO SIGNIFICANT CHANGE in overall POOR prognosis of patients

Most tumors responded initially to treatment but recurred as study progressed

Based on POOR RESULTS, recommend ALTERNATIVE TREATMENTS be tested in patients with this type of tumor
======================================
Temodar (Temozolomide):
======================================
Temozolomide received accelerated approval by the U.S. Food and Drug Administration 1/1999 for treatment of ANAPLASTIC ASTROCYTOMA (brain cancer) patients
——————————————————————
54 patients
——————————————————————
12 / 22% – response rate
——————————————————————
5 / 9% – Complete Response rate
——————————————————————
50 weeks (16-114 weeks) – Median duration of all responses
——————————————————————
64 weeks (52-114 weeks) – Median duration of Complete Response
——————————————————————
4.4 months – Median Progression-Free Survival
——————————————————————
15.9 months (1 year 3.9 months) – Median Overall Survival
——————————————————————
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
——————————————————————
http://clincancerres.aacrjournals.org/content/11/19/6767.full
======================================
Was the United States Food and Drug Administration’s 1/1999 accelerated approval based on the PUBLISHED FINAL RESULTS OF A PHASE II (2) CLINICAL TRIAL?
======================================
12/2000 – Temozolomide and ANAPLASTIC ASTROCYTOMA:

new indication

NO CLEAR PROOF OF EFFICACY
http://www.ncbi.nlm.nih.gov/pubmed/11475493/
Prescrire Int. 2000 Dec;9(50):170-1.
http://www.ncbi.nlm.nih.gov/m/pubmed/11475493/
(1) Temozolomide recently licensed in France for treating patients with ANAPLASTIC ASTROCYTOMA who are in relapse or progression after standard therapy
——————————————————————
(2) clinical dossier contains only one non comparative trial
——————————————————————
(3) 111 patients with ANAPLASTIC ASTROCYTOMA or oligoanaplastic astrocytoma had not all had the standard treatment with surgery, radiotherapy and chemotherapy
——————————————————————
54 patients – subgroup who met criteria
——————————————————————
16 months (1 year 4 months) – Median Global Survival
——————————————————————
31 months (2 years 7 months) – Median Global Survival from start of initial treatment
——————————————————————
NO BETTER THAN SURVIVAL BEFORE THE INTRODUCTION OF temozolomide
======================================
The answer is: NO

1/1999 – FDA Accelerated Approval
9/1999 – Phase 2 publication
======================================
9/1999 – Multicenter phase II trial of temozolomide in patients with ANAPLASTIC ASTROCYTOMA or anaplastic oligoastrocytoma at first relapse

Temodal Brain Tumor Group
http://www.ncbi.nlm.nih.gov/pubmed/10561351/
J Clin Oncol. 1999 Sep;17(9):2762-71.
http://www.ncbi.nlm.nih.gov/m/pubmed/10561351/
University of Texas M.D. Anderson Cancer Center, Houston, TX, USA
======================================
http://www.drugs.com/pro/temodar.html
======================================
http://www.pharmainfo.net/fda-articles/fda-safety-page-fatal-medication-errors-associated-temodar
======================================
TEMODAR ADVERSE EVENTS REPORTED TO THE FDA OVER TIME:
http://www.drugcite.com/?q=TEMODAR
======================================
ADVERSE EVENTS:
Primary Suspect Reports: 4,436
Total Reports: 6,350
http://www.adverseevents.com/drugdetail.php?AEDrugID=1794&BrandName=TEMODAR
======================================
http://www.temodar.com/temodar/index.do
======================================
2004 – Supratentorial high-grade ASTROCYTOMA and DIFFUSE BRAINSTEM GLIOMA:

two challenges for the pediatric oncologist
http://www.ncbi.nlm.nih.gov/pubmed/15047924/
Oncologist. 2004;9(2):197-206.
http://www.ncbi.nlm.nih.gov/m/pubmed/15047924/
Oncologist 9, 197-206
http://m.theoncologist.alphamedpress.org/content/9/2/197.long
Division of Neuro-Oncology, Department of Hematology-Oncology, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA

neoplasms predominantly involve supratentorial hemispheres or pons, in which case tumors are usually called DIFFUSE BRAINSTEM GLIOMAS

supratentorial neoplasms
——————————————————————
diagnosis of DIFFUSE BRAINSTEM GLIOMA based upon typical imaging, dispensing with need for surgery in majority of cases

Radiation therapy is mainstay of treatment for children with DIFFUSE BRAINSTEM GLIOMAS
——————————————————————
2 years – Less than 10% of children with diffuse brainstem gliomas survive
——————————————————————
outcome for patients with either type of tumor is POOR when standard multimodality therapy is used

children are ideal candidates for INNOVATIVE TREATMENT approaches
——————————————————————
3-21 years Patients were eligible for current multiinstitutional study
——————————————————————
33 patients (6.4 years – Median age at diagnosis) enrolled
——————————————————————
33 / 100% – DIED OF DISEASE PROGRESSION
——————————————————————
12 months (1 year) – Median Survival
——————————————————————
16 / 48% – estimated 1-year Survival rate (standard error, 1 / 8%)
——————————————————————
administration of temozolomide after RT DIDN’T ALTER POOR PROGNOSIS associated with newly diagnosed diffuse BRAINSTEM GLIOMA in children
======================================
1/1/2005 (11/24/2004) – Role of temozolomide after radiotherapy for newly diagnosed diffuse BRAINSTEM GLIOMA in children:

results of a multiinstitutional study (SJHG-98)
http://www.ncbi.nlm.nih.gov/pubmed/15565574
Cancer. 2005 Jan 1;103(1):133-9.
http://www.ncbi.nlm.nih.gov/m/pubmed/15565574
Cancer 103, 133-139
http://onlinelibrary.wiley.com/doi/10.1002/cncr.20741/abstract;jsessionid=6717837591CCC8FCBD8E46163808E221.d03t01
Cancer
Volume 103, Issue 1, pages 133–139, 1 January 2005
http://onlinelibrary.wiley.com/doi/10.1002/cncr.20741/full
Article first published online: 24 NOV 2004
References:
http://onlinelibrary.wiley.com/doi/10.1002/cncr.20741/references
Cited By:
http://onlinelibrary.wiley.com/doi/10.1002/cncr.20741/citedby
DOI: 10.1002/cncr.20741

Department of Hematology-Oncology, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA
——————————————————————
33 patients: (33 / 100% – 6.4 years: Median age)
——————————————————————
33 / 100% – ALL DIED OF DISEASE PROGRESSION
——————————————————————
12 months (1 year) – Median Survival
——————————————————————
16 / 48% – 1 year estimated Survival rate
——————————————————————
Table 1. Results of radiation therapy in combination with chemotherapy for newly diagnosed, diffuse, intrinsic BRAIN STEM GLIOMA

Author
Study Type
Patients Total No.
Treatment Radiation Therapy
Additional Chemotherapy
Efficacy
OS MST CR PR SD PD

Multiinstitutional 33 56 Temozolomide, irinotecan 0 0 12 NA NA NA

response rates based on evaluable patients
32 54 Topotecan

CR – complete response
GCSF – granulocyte colony stimulating factor
HD – high dose tamoxifen
HDB – high dose chemotherapy and autologous bone marrow transplantation HF – hyperfractionated
M – months
MST – median survival time
NA – not available
OS – overall survival
PD – progressive disease
PR – partial response
SD – stable disease
UNK – unknown
* 1 patient had radiological improvement

Cancer 103, 133-139
——————————————————————
3-21 years – eligible for current multiinstitutional study
——————————————————————
33 – (Median age at diagnosis
6.4 years) enrolled
——————————————————————
ALL PATIENTS DIED OF DISEASE PROGRESSION
——————————————————————
12 months (1 year) – Median Survival
——————————————————————
48% – estimated 1-year Survival rate (standard error 8%)
——————————————————————
administration of temozolomide after RT DIDN’T ALTER POOR PROGNOSIS associated with newly diagnosed diffuse BRAINSTEM GLIOMA in children
======================================
2/2008 (2/2/2007)
Treatment of children with diffuse intrinsic BRAIN STEM GLIOMA
with radiotherapy, vincristine and oral VP-16:

a Children’s Oncology Group phase II study
http://www.ncbi.nlm.nih.gov/pubmed/17278121
Pediatr Blood Cancer. 2008 Feb;50(2):227-30
http://www.ncbi.nlm.nih.gov/m/pubmed/17278121
University of Rochester Medical Center, Rochester, New York, USA.

http://onlinelibrary.wiley.com/doi/10.1002/pbc.21154/abstract;jsessionid=DE7A67EFBAC1A184F6805F11CFC4F30B.d02t02
Article first published online: 2 FEB 2007
DOI: 10.1002/pbc.21154

prognosis for children with BRAIN STEM GLIOMA remains grim

The Pediatric Oncology Group (POG, now part of Children’s Oncology Group) conducted study using agents in combination with standard external beam radiation for children with newly diagnosed BRAIN STEM GLIOMA
——————————————————————
Children eligible
3-21 years of age, had MRI-evidence of diffuse intrinsic pontine glioma, and had neurologic deficits of <6 months duration
——————————————————————
30 eligible and evaluable for Survival / toxicity
——————————————————————
8 years (3-14 years) – Median age
——————————————————————
7 / 23% – Partial Response following radiation
18 / 60% – Stable Disease
2 / 7% – Progressive Disease
3 / 10% – Response Not measured
——————————————————————
30 / 100% CHILDREN DIED
——————————————————————
Overall Survival 1 year
27 +/- 7%
2 years, 3 +/- 2%
——————————————————————
9 months (3-36 months) – Median Survival
——————————————————————
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
======================================
Avastin (Bevacizumab):
======================================
5/6/2009 – U.S. Food and Drug Administration (FDA) granted accelerated approval of Avastin (bevacizumab) for people with GLIOBLASTOMA (brain cancer) with progressive disease following prior therapy

effectiveness of Avastin in AGGRESSIVE form of BRAIN CANCER based on improvement in objective response rate

Currently, NO DATA available from randomized controlled trials demonstrating improvement in disease-related symptoms or increased survival with Avastin in GLIOBLASTOMA
——————————————————————
11.3 months – Progression-Free Survival
——————————————————————
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
——————————————————————
22 / 26% – tumor responses observed of 85 patients treated with Avastin alone
——————————————————————
4.2 months – Median duration of response in patients
——————————————————————
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

56 patients treated with Avastin alone
——————————————————————
11 / 20% of patients – Responses were observed
——————————————————————
3.9 months – Median duration of response
——————————————————————
http://www.cancer.gov/cancertopics/druginfo/fda-bevacizumab
FDA – “People with this type of brain cancer have had no new treatments in more than a decade”
http://www.drugs.com/newdrugs/fda-grants-accelerated-approval-avastin-brain-cancer-glioblastoma-has-progressed-following-prior-1342.html
——————————————————————
Avastin is gene-targeted therapy, which can only target certain specific genes
======================================
Afinitor (Everolimus):
======================================
Afinitor (ubependymal giant cell ASTROCYTOMA (SEGA) brain tumor)
——————————————————————
10/29/2010 – FDA granted accelerated approval for Afinitor after single Phase 2 study of only 28 patients
——————————————————————
32% experienced 50% reduction of tumor
——————————————————————
none of their tumors went away completely
======================================
Was the United States Food and Drug Administration’s 10/29/2010 accelerated approval based on the PUBLISHED FINAL RESULTS OF A PHASE II (2) CLINICAL TRIAL?
======================================
10/12/2011 (8/1/2011) – Everolimus tablets for patients with subependymal giant cell ASTROCYTOMA
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3389821/
Expert Opin Pharmacother. Author manuscript; available in PMC 2012 July 5.
Published in final edited form as:
Expert Opin Pharmacother. 2011 October; 12(14): 2265–2269.
Published online 2011 August 1. doi: 10.1517/14656566.2011.601742
PMCID: PMC3389821
NIHMSID: NIHMS385824
——————————————————————
http://www.fda.gov/AboutFDA/CentersOffices/OfficeofMedicalProductsandTobacco/CDER/ucm231967.htm
======================================
The answer is: NO

10/29/2010 – FDA Accelerated Approval
10/12/2011 – publication
� � � � � � � � � � � � � � � � �
COMPARE COMBINED:
� � � � � � � � � � � � � � � � �
======================================
ANAPLASTIC ASTROCYTOMA
==========================
22% – Objective Response: Objective response = complete response and partial response – Antineoplastons
�
22% – response rate: Temodar
——————————————————————
11% – Complete Response: Antineoplastons
�
9% – Complete Response rate: Temodar
——————————————————————
17+ years – Maximum Survival : patient with ANAPLASTIC ASTROCYTOMA – Antineoplastons
�
50 weeks (16-114 weeks) – Median duration of all responses: Temodar
——————————————————————
17+ years – Maximum Survival : patient with ANAPLASTIC ASTROCYTOMA – Antineoplastons
�
64 weeks (52-114 weeks) – Median duration of Complete Response: Temodar
——————————————————————
6 months – 7 / 39% Progression-Free Survival: Antineoplastons
�
4.4 months – Median Progression-Free Survival: Temodar
——————————————————————
5 years – 4 / 22% Overall Survival: Antineoplastons
�
2 years – 7 / 39% Overall Survival: Antineoplastons
�
2 years – Most patients with brainstem glioma fail standard radiation therapy and chemotherapy and do not survive longer
�
15.9 months (1 year 3.9 months) – Median Overall Survival: Temodar
� � � � � � � � � � � � � � � � �
COMPARE COMBINED:
� � � � � � � � � � � � � � � � �
======================================
GLIOBLASTOMA
======================================
39% – Progression-Free Survival (PFS) at 6 months: Antineoplastons
�
5.28 months – Median Progression-Free Survival (PFS): Antineoplastons
�
11.3 months – Progression-Free Survival: Avastin
——————————————————————
32% – % of Patients Showing Objective Response = complete response and partial response: Antineoplastons
�
26% – tumor responses observed Avastin
——————————————————————
42% – special exception (SE): Overall survival (OS) – 2 years: Antineoplastons
�
36% – BT-11: Overall survival (OS) – 2 years: Antineoplastons
�
19% – special exception (SE): Overall survival (OS) – 5 years: Antineoplastons
�
25% – BT-11: Overall survival (OS) – 5 years: Antineoplastons
�
4.2 months – Median duration of response in patients: Avastin
——————————————————————
9 / 32% – # and % of Patients Showing Objective response = complete response and partial response – Antineoplastons
�
11 / 20% of patients – Responses were observed: Avastin
——————————————————————
5+ years – Maximum Survival : patient with GLIOBLASTOMA – Antineoplastons
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3.9 months – Median duration of response: Avastin
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COMPARE COMBINED:
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ASTROCYTOMA
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47% / 7 – % and # of Patients Showing Objective response = complete response (6) and partial response (1) – Antineoplastons
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32% experienced 50% reduction of tumor – Afinitor
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Burzynski: Complete Response, Partial Response, Stable Disease, Progressive Disease, Objective Response, and Response:
https://stanislawrajmundburzynski.wordpress.com/2013/07/04/burzynski-complete-response-partial-response-stable-disease-progressive-disease-objective-response-and-response/
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Burzynski: Progression-Free Survival:
https://stanislawrajmundburzynski.wordpress.com/2013/07/04/burzynski-progression-free-survival/
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WHAT IS MISDIRECTION ? Critiquing “Antineoplastons: Has the FDA kept its promise to the American people ?”:
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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