Critiquing David H. Gorski, MD, PhD, FACS www.sciencebasedmedicine.org/editorial-staff/david-h-gorski-md-phd-managing-editor/

Critiquing David H. Gorski, MD, PhD, FACS http://www.sciencebasedmedicine.org/editorial-staff/david-h-gorski-md-phd-managing-editor/

“Our only goal is to promote high standards of science in medicine”
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http://www.sciencebasedmedicine.org/editorial-staff/
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So proclaims Science Based Medicine . org

6/10/2013 Gorski published:
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BBC Panorama investigates Stanislaw Burzynski
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http://www.sciencebasedmedicine.org/bbc-panorama-investigates-stanislaw-burzynski/
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“Burzynski hasn’t published anything other than case reports, tiny case series, and unconvincing studies, mostly (at least over the last decade or so) in crappy journals not even indexed on PubMed”
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Gorski’s above statement makes me wonder if PhD’s are handed out to any hack that requests one

Burzynski has published at least 4 publications which list all of the patients and information like:
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[2] 16. 2003
(Pgs. 95-96) data charts
(Pg. 95)
Case
Sex
Age
Date of initial diagnosis
Tumor histology
Tumour location
Tumour size
Previous therapies
Karnofsky performance status
KPS baseline
Date of recurrence
(Pg. 96)
Start date
Stop date
Days on treatment
Dosage
Response
Status / date of death
Progression date
Survival time (weeks) from start
Time (weeks) to progression
Last contact
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[9] 17. 2004
(Pgs. 316 + 318-321) data charts
(Pg. 316)
Gender
Age
Tumour histology
Tumour size (total of measured lesions)
Previous therapies
Karnofsky performance status
(Pg. 318)
Case
Age at admission
Sex
Ethnicity
Date of initial diagnosis
Pathology code
Visual Pathway Glioma (VPG)
Karnofsky baseline
Previous treatment
Multicentric tumour location
(Pg. 319)
” ”
(Pg. 320)
Case
Start date
Stop date
Days on treatment
Average dosage (IV treatment / PO treatment)
(Pg. 321)
Case
Response
Maximum response date
Time to maximum response (months)
Radiological PD as of 1/03/04
Progression Free Survival (PFS) (year)
Status
Karnofsky Performance Status (KPS) baseline
Karnofsky Performance Status (KPS) follow-up
Reason for withdrawal
Survival time from diagnosis (years)
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[10] 18. 6/2005
(Pgs. 169 + 171.–.172) data charts
(Pg. 169)
Gender
Tumor type
Tumor spread
Previous therapies
Age
Karnofsky performance status
(Pg. 171)
Case
Protocol
Gender
Age at Admission (years)
Ethnicity
Date of Initial Diagnosis
Tumor Type
Tumor Dissemination
Karnofsky Performance Status (KPS) Baseline
Previous treatment
(Pg. 172)
Case
Start Date
Stop Date
Days on Treatment
Average Dosage g/kg/d (A10 / AS2-1)

Case
Response
Radiological PD
Progression Free Survival (PFS) (month)
Status
Karnofsky Performance Status (KPS) Baseline
Karnofsky Performance Status (KPS) Follow-up
Reason for Withdrawal
Overall Survival from Diagnosis (OSD) (month)
Overall Survival from Start (OSS) (month)
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[12] 19. 3/2006
(Pgs. 42-45) data charts
(Pg. 42)
Gender
Age
Tumor history
Tumor size at baseline
Previous therapies
Karnofsky Performance Status
(Pg. 43)
Case
Protocol
Sex
Age (years)
Date of Initial Diagnosis
Tumor Type
Tumor Dissemination
Recurrence
Karnofsky Performance Status (KPS) Baseline
Previous Treatment
(Pg. 44)
Case
Start Date
Stop Date
Days On
Average Dosage g/kg/d (A10 / AS2-1)
(Pg. 45)
Case
Response
Radiological PD
Progression Free Survival (PFS) (months)
Status
Karnofsky Performance Status (KPS) Baseline
Karnofsky Performance Status (KPS) Follow-Up
Reason for Withdrawal
Overall Survival from Diagnosis (OSD) (month)
Overall Survival from Start of antineoplaston(OST) (month)
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Maybe Gorski should try “deconstructing” some of these, especially the ones where patients did NOT have chemotherapy or radiation therapy

I’ve even provided a handy reference list

But by George, I’m George Dubya dubious that Gorski can handle it, given his track record
� � � � � � � � � � � � � � � � �
[18] 12/2009 (Pg. 923)
1 – Special Exception (SE)
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[3] 1. 3/2004 (Pg. 52)
10 – subgroup
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[3] 1. 3/2004 (Pg. 55)
10 – Japan
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[11] 7. 7/2005 (Pg. 300)
10 – children
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[2] 16. 2003 (Pg. 98)
11 – Special Exception (SE)
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[7] 4. 10/2004 (Pg. 427)
11 – children
4 – children Study (ST)
7 – children Special Exception (SE)
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[1] 1. 10/2003 (Pg. 358)
12 – children
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[2] 16. 2003 (Pg. 91)
1st 12 – Study (ST)
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[4] 4. 9/2004 (Pg. 257)
12
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[9] 17. 2004 (Pg. 316)
1st 12 – children
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[15] 10. 6/2008 (Pg. 450)
1st 12 – children
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[10] 18. 6/2005 (Pgs. 169 + 176)
13 – children
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[8] 5. 10/2004 (Pg. 428)
17
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[20] 14. 6/2010 (Pg. ii95)
17
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[12] 19. 3/2006 (Pgs. 40-41 + 46)
18
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[3] 1. 3/2004 (Pg. 50)
19 – children
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[3] 1. 3/2004 (Pg. 55)
19 – Japan
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[14] 8. 10/2006 (Pg. 466)
19
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[16] 10/2008 (Pg. 821)
20
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[17] 12/2008 (Pg. 1067)
20
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[21] 15. 11/2010 (Pg. iv72)
20
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[5] 2. 10/2004 (Pg. 384)
22
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[6] 3. 10/2004 (Pg. 386)
31 – Special Exception (SE)
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[19] 13. 12/2009 (Pg. 951)
40
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[19] 13. 12/2009 (Pg. 951)
52 – Special Exception SE)
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[3] 1. 3/2004 (Pg. 55)
56 – Japan
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[6] 3. 10/2004 (Pg. 386)
60
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[3] 1. 3/2004 (Pg. 52)
62
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[3] 1. 3/2004 (Pg. 53)
80
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[13] 2006
30 (Pg. 173)
335 – children (Pg. 174)
1652 – adults (Pg. 174)
� � � � � � � � � � � � � � � � �
[18] 12/2009 (Pg. 923)
1 – evaluable Special Exception (SE)
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[2] 16. 2003 (Pg. 91)
1st 10 – evaluable Study (ST)
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[3] 1. 3/2004 (Pg. 52)
10 – evaluable subgroup
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[3] 1. 3/2004 (Pg. 55)
10 – evaluable Japan
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[11] 7. 7/2005 (Pg. 300)
10 – evaluable children
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[2] 16. 2003 (Pg. 98)
11 – evaluable Special Exception (SE)
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[7] 4. 10/2004 (Pg. 427)
11 – evaluable children
4 – evaluable children Study (ST)
7 – evaluable children Special Exception (SE)
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[1] 1. 10/2003 (Pg. 358)
12 – evaluable children
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[9] 17. 2004 (Pg. 316)
1st 12 – evaluable children
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[15] 10. 6/2008 (Pg. 450)
1st 12 – evaluable children
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[10] 18. 6/2005 (Pgs. 169 + 176)
13 – evaluable children
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[21] 15. 11/2010 (Pg. iv72)
13 – evaluable
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[8] 5. 10/2004 (Pg. 428)
17 – evaluable
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[20] 14. 6/2010 (Pg. ii95)
17 – evaluable
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[3] 1. 3/2004 (Pg. 51)
18 – evaluable children
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[12] 19. 3/2006 (Pgs. 40-41 + 46)
18 – evaluable
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[3] 1. 3/2004 (Pg. 55)
19 – evaluable Japan
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[14] 8. 10/2006 (Pg. 466)
19 – evaluable
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[16] 10/2008 (Pg. 821)
20 – evaluable
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[17] 12/2008 (Pg. 1067)
20 – evaluable
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[5] 2. 10/2004 (Pg. 384)
22 – evaluable
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[6] 3. 10/2004 (Pg. 386)
31 – evaluable Special Exception (SE)
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[19] 13. 12/2009 (Pg. 951)
52 – evaluable Special Exception SE)
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[3] 1. 3/2004 (Pg. 55)
56 – evaluable Japan
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[6] 3. 10/2004 (Pg. 386)
60 – evaluable
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[3] 1. 3/2004 (Pg. 52)
62 – evaluable
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[3] 1. 3/2004 (Pg. 53)
80 – evaluable
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[13] 2006
30 – evaluable (Pg. 173)
335 – children (Pg. 174)
1652 – adults (Pg. 174)
� � � � � � � � � � � � � � � � �
[1] 1. 10/2003 (Pg. 358)
escalating doses of ANP intravenous injections (IV) and subsequently capsules (po)
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[2] 16. 2003 (Pg. 91)
Patients received escalating doses of antineoplaston A10 and AS2-1 by intravenous bolus injections
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[2] 16. 2003 (Pg. 93)
Antineoplaston therapy was administered in gradually escalating doses by intermittent bolus injections 6 times a day using a portable Provider 6000 dual-channel pump (Abbott Laboratories, North Chicago, IL, USA)
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[5] 2. 10/2004 (Pg. 384)
ANP was given in escalating doses by intravenous bolus injections
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[9] 17. 2004 (Pg. 317)
Gradually escalating doses were administered by intermittent bolus injections 6 times a day using a portable Provider 6000 dual channel pump (Abbott Laboratories, North Chicago, IL, USA)
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[12] 19. 3/2006 (Pg. 40)
Antineoplastons A10 (A10I) and AS2-1 injections, were given in escalating doses by intravenous injections
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[20] 14. 6/2010 (Pg. ii95)
Patients received escalating doses of intravenous A10 and AS2-1 6 times daily
12 or more weeks – ANP
or
at least 4 weeks – ANP but developed progressive disease (PD)
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[21] 15. 11/2010 (Pg. iv72)
Patients received escalating doses of intravenous ANP 6 times daily
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 93)
Dose escalation was necessary to prevent peritumoral oedema
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[9] 17. 2004 (Pg. 317)
Gradual dose escalation was necessary to prevent peritumoral oedema
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[12] 19. 3/2006 (Pg. 44)
ANP was given by intravenous injections in escalating doses to prevent peritumoral oedema
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 93)
Treatment consisted of daily intravenous injections of antineoplaston A10 (300 mg / mL) and AS2-1 (80 mg / mL) through a Broviac or equivalent catheter
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[4] 4. 9/2004 (Pgs. 257-260)
he was admitted for administration of intravenous antineoplastons A10 and AS2-1 through a subclavian venous catheter by intermittent bolus injections 6 times per day using a portable pump
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[7] 4. 10/2004 (Pg. 427)
intravenous injection of ANP
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[8] 5. 10/2004 (Pg. 428)
intravenous infusions of ANP
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[9] 17. 2004 (Pg. 317)
300 mg / ML – Daily intravenous injections of A10
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[9] 17. 2004 (Pg. 317)
80 mg / ML – Daily intravenous injections of AS2-1
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[9] 17. 2004 (Pg. 317)
administered through a subclavian venous catheter
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[9] 17. 2004 (Pg. 315)
ANP intravenously initially and subsequently orally
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[10] 18. 6/2005 (Pg. 169)
intravenous infusions of 2 formulations of ANP, A10 and AS2-1
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[10] 18. 6/2005 (Pg. 170)
IV ANP
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[11] 7. 7/2005 (Pg. 300)
ANP was given intravenously daily through a subclavian venous catheter and double channel infusion pump
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[12] 19. 3/2006 (Pg. 42)
Treatment involved daily intravenous injections of A10I and AS2-1
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[12] 19. 3/2006 (Pg. 42)
The injections were administered every 4 hours through a subclavian venous catheter via a dual-channel infusion pump
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[14] 8. 10/2006 (Pg. 466)

ANP was given intravenously daily through a subclavian venous catheter and a double-channel infusion pump
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[15] 10. 6/2008 (Pg. 450)
Treatment consisted of intravenous infusions of antineoplastons (ANP) A10 and AS2-1
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[16] 10/2008 (Pg. 821)
ANP was administered intravenously daily through a subclavian central venous catheter by a double-channel infusion pump
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[17] 12/2008 (Pg. 1067)
ANP was administered intravenously daily through a subclavian venous catheter via a double-channel infusion pump
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[18] 12/2009 (Pg. 923)
The patient received intravenous injections of ANP every 4 hours through a subclavian central venous catheter via a double channel infusion pump followed by PO ANP only
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[18] 12/2009 (Pg. 923)
6/8/2000 – PO ANP
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[18] 12/2009 (Pg. 923)
IV ANP
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[19] 13. 12/2009 (Pg. 951)
ANP was administered daily through a subclavian venous catheter via a double channel infusion pump
� � � � � � � � � � � � � � � � �
[9] 17. 2004 (Pg. 317)
Intravenous injections were discontinued after determination of CR, PR, or stable disease (SD)
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[9] 17. 2004 (Pg. 317)
After discontinuation of injections, the patients continued A10 and AS2-1 in 0.5g capsules
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[18] 12/2009 (Pg. 923)
7/8/2004 – discontinued
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[18] 12/2009 (Pg. 923)
2/1999 – CR
� � � � � � � � � � � � � � � � �
[5] 2. 10/2004 (Pg. 384)
4.3 months – median duration of administration
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[21] 15. 11/2010 (Pg. iv72)
4.4 months – median duration of treatment
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[14] 8. 10/2006 (Pg. 466)
4 1/2 months – median duration of i.v. ANP
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[12] 19. 3/2006 (Pg. 40)
5 months – median duration of antineoplaston administration
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[8] 5. 10/2004 (Pg. 428)
5.2 months – administered median
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[19] 13. 12/2009 (Pg. 951)
5.4 months – median duration of treatment (ST)
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[19] 13. 12/2009 (Pg. 951)
5.6 months – median duration of treatment (SE)
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[7] 4. 10/2004 (Pg. 427)

5.7 months – average duration of ANP
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[16] 10/2008 (Pg. 821)
5.7 months – median duration of treatment
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[2] 16. 2003 (Pgs. 91 + 96)
6 months – median duration of treatment
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[17] 12/2008 (Pg. 1067)
6.5 months – median duration of treatment
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[1] 1. 10/2003 (Pg. 358)

9.5 months – median duration of IV ANP
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[11] 7. 7/2005 (Pg. 300)
9 1/2 months – median duration of administration
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[9] 17. 2004 (Pgs. 315 + 320)
16 months (1 year 4 months) average duration of intravenous ANP
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[15] 10. 6/2008 (Pg. 450)
16.5 months – median
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[9] 17. 2004 (Pg. 320)
19 months – average duration of oral ANP
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[10] 18. 6/2005 (Pgs. 168 + 170)
20 months (1 year 8 months) administered average duration
� � � � � � � � � � � � � � � � �
[1] 1. 10/2003 (Pg. 358)
28.6 months – median duration of po ANP
After obtaining at least minor response (SD), the treatment continued with po ANP
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[4] 4. 9/2004 (Pg. 257)
655 consecutive days – administration of antineoplastons A10 and AS2-1 with the exception of a few short interruptions
� � � � � � � � � � � � � � � � �
[16] 10/2008 (Pg. 821)
5.69 g/kg/day – median average dosage of A10
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[17] 12/2008 (Pg. 1067)
5.8 g/kg/day – median average dosages of A10
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[21] 15. 11/2010 (Pg. iv72)
6.0 g/kg/day – median average dosages of A10
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[5] 2. 10/2004 (Pg. 384)
6.37 g/kg/day – average dosage of Antineoplaston A10
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[1] 1. 10/2003 (Pg. 358)
7.95 g/kg/day – average dosage of A10
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[9] 17. 2004 (Pgs. 315 + 320)
7.95 g/kg/day – average dosage of A10
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[15] 10. 6/2008 (Pg. 450)
8.36 g/kg/day – average dosage of A10
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[19] 13. 12/2009 (Pg. 951)
9.0 g/kg/day – median of average dosages of A10 (ST)
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[14] 8. 10/2006 (Pg. 466)
9.2 g/kg/day – average dosage of A10
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[12] 19. 3/2006 (Pg. 40)
9.22 g/kg/day – average dosage of A10I
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[8] 5. 10/2004 (Pg. 428)
9.4 g/kg/d – median of average dosages of A10
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[19] 13. 12/2009 (Pg. 951)
9.4 g/kg/day – median of average dosages of A10 (SE)
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[10] 18. 6/2005 (Pgs. 168 + 170)
10.30 g/kg/day – average dosage of A10
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[7] 4. 10/2004 (Pg. 427)
10.6 g/kg/d – median of average dosages of A10
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[2] 16. 2003 (Pg. 91)
11.3 g/kg/day – average dosage of A10
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[11] 7. 7/2005 (Pg. 300)
12.16 g/kg/day – average dosage of A10
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[2] 16. 2003 (Pg. 96)
5.3-16.1 g/kg/day – dosage of A10
� � � � � � � � � � � � � � � � �
[1] 1. 10/2003 (Pg. 358)
0.28 g/kg/d – average dosage of A10 and AS2-1
After obtaining at least minor response (SD), the treatment continued with po ANP
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[9] 17. 2004 (Pg. 320)
0.28 g/kg/day – average dosage of A10 and AS2-1
� � � � � � � � � � � � � � � � �
[4] 4. 9/2004 (Pg. 257)
8.15 g/kg/d – maximum dosage of A10
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 96)
11.3 g/kg/day – average maximum dosage of A10
——————————————————————
[12] 19. 3/2006 (Pg. 42)
13.37 g/kg/day – maximum dosage of A10I (SD = 7.36 g/kg/day)
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 93)
20 g/kg/day – highest tolerated or effective dosage of A10 not exceeding
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 96)
331.4 kg – maximum total dose of A10
� � � � � � � � � � � � � � � � �
[5] 2. 10/2004 (Pg. 384)
0.24 g/kg/day – average dosage of Antineoplaston AS2-1
——————————————————————
[17] 12/2008 (Pg. 1067)
0.24 g/kg/day – median average dosages of AS2-1
——————————————————————
[16] 10/2008 (Pg. 821)
0.28 g/kg/day – median average dosage of AS2-1
——————————————————————
[19] 13. 12/2009 (Pg. 951)
0.3 g/kg/day – median of average dosages of AS2-1 (ST and SE)
——————————————————————
[21] 15. 11/2010 (Pg. iv72)
0.3 g/kg/day – median average dosages of AS2-1
——————————————————————
[12] 19. 3/2006 (Pg. 40)
0.31 g/kg/day – average dosage of AS2-1
——————————————————————
[14] 8. 10/2006 (Pg. 466)
0.32 g/kg/day – average dosage of AS2-1
——————————————————————
[9] 17. 2004 (Pgs. 315 + 320)
0.33 g/kg/day – average dosage of AS2-1
——————————————————————
[1] 1. 10/2003 (Pg. 358)
0.34 g/kg/d – average dosage of AS2-1
——————————————————————
[15] 10. 6/2008 (Pg. 450)
0.37 g/kg/day – average dosage of AS2-1
——————————————————————
[10] 18. 6/2005 (Pgs. 168 + 170)
0.38 g/kg/day – average dosage of AS2-1
——————————————————————
[2] 16. 2003 (Pg. 91)
0.4 g/kg/day – average dosage of AS2-1
——————————————————————
[7] 4. 10/2004 (Pg. 427)
0.4 g/kg/d – median of average dosages of AS2-1
——————————————————————
[8] 5. 10/2004 (Pg. 428)
0.4 g/kg/d – median of average dosages of AS2-1
——————————————————————
[11] 7. 7/2005 (Pg. 300)
0.41 g/kg/day – average dosage of AS2-1
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 96)
0.2-0.6 g/kg/day – dosage of AS2-1
� � � � � � � � � � � � � � � � �
[4] 4. 9/2004 (Pg. 257)
0.35 g/kg/d – maximum dosage of
AS2-1
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 96)
0.4 g/kg/day – average maximum dosage of AS2-1
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 93)
0.4 g/kg/day – highest tolerated or effective dosage of AS2-1 not exceeding
� � � � � � � � � � � � � � � � �
[12] 19. 3/2006 (Pg. 42)
0.49 g/kg/day – maximum dosage of AS2-1 (SD = 0.26 g/kg/day)
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 96)
23.9 kg – maximum total dose of AS2-1
� � � � � � � � � � � � � � � � �
[1] 1. 10/2003 (Pg. 358)
1 / 9% – nonevaluable due to only 4 weeks of treatment and lack of follow-up scans
This patient died while on treatment due to a brain infarct and was counted as a treatment failure
——————————————————————
[7] 4. 10/2004 (Pg. 427)
1 – nonevaluable
——————————————————————
[9] 17. 2004
1 – nonevaluable due to only receiving 4 weeks of ANP and no follow-up scans
This patient died while receiving ANP due to a nonhemorrhaging brain infarction and was considered a treatment failure (Pg. 320)
(only 4 weeks after initiation of ANP Pg. 321)
(There was no evidence that these were treatment related deaths Pg. 321)
——————————————————————
[2] 16. 2003 (Pg. 96)
Patient 2 unable to be evaluated because didn’t have follow-up MRI to determine response
——————————————————————
[2] 16. 2003 (Pg. 96)
Patient 11 unable to be evaluated because died of intratumoral hemorrhage and her duration of treatment was too short to short for evaluation of response
——————————————————————
[8] 5. 10/2004 (Pg. 428)
2 – nonevaluable due to lack of follow-up scans
——————————————————————
[7] 4. 10/2004 (Pg. 427)
3 Special Exception (SE) – nonevaluable
——————————————————————
[21] 15. 11/2010 (Pg. iv72)
7 – couldn’t be evaluated due to an inadequate duration of treatment and lack of follow-up magnetic resonance imaging (MRI) scans
——————————————————————
[19] 13. 12/2009 (Pg. 951)
12 – not evaluable due to too short a duration of treatment and lack of follow-up MRIs
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 97)
4 – died from the tumour
4 – died from aspiration pneumonia
2 – intratumoral bleeding
——————————————————————
[7] 4. 10/2004 (Pg. 427)
One CR patient developed recurrence after premature discontinuation of ANP and obtained a 2nd CR after ANP was restarted
This patient who initially had multiple metastases to the brain and spinal cord died due to aspiration pneumonia and was confirmed by autopsy as disease free
——————————————————————
[9] 17. 2004
1 patient who had stable disease discontinued ANP against medical advice and died 4.5 years later (Pgs. 315 + 320)
(There was no evidence that these were treatment related deaths Pg. 321)
——————————————————————
[10] 18. 6/2005
1 patient passed away after 6 years, 10 months from the start of the treatment (3 years after discontinuation of ANP)
The cause of death was recurrent pneumonia, possibly due (Pg. 170)
to chronic immunosuppression from chemotherapy administered prior to ANP (patient 1) (Pg. 172)
——————————————————————
[12] 19. 3/2006 (Pg. 45)
The deaths of 12 patients were most likely tumor related
——————————————————————
[12] 19. 3/2006 (Pg. 45)
There was a single death due to a pulmonary embolism
——————————————————————
[12] 19. 3/2006 (Pg. 45)
2 cases of death possibly resulting from aspiration pneumonia
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 97)
The 2 surviving patients weren’t previously treated with chemotherapy and radiation therapy and didn’t develop pneumonia or intratumoral bleeding
——————————————————————
[10] 18. 6/2005 (Pg. 169)
6 hadn’t received prior chemotherapy or radiation
——————————————————————
[10] 18. 6/2005 (Pg. 175)
6 long-term
——————————————————————
[12] 19. 3/2006 (Pgs. 40-41)
6 – didn’t have radiation therapy or chemotherapy
——————————————————————
[16] 10/2008 (Pg. 821)
No patients received radiation or chemotherapy before starting ANP, but 6 patients underwent surgery and 14 had biopsy only
——————————————————————
[18] 12/2009 (Pg. 923)
The tumor was inoperable
� � � � � � � � � � � � � � � � �
[2] 16. 2003
Patient 3 (Pg. 95)
Patient 8 (Pg. 95)
Case 10 (Pgs. 96-97)
——————————————————————
[3] 1. 3/2004
Case Study, Patient 1 (Pgs. 50-51)
Case Study, Patient 2 (Pgs. 51-52)
Case Study, Patient 3 (Pgs. 53-54)
Case Study, Patient 4 (Pg. 54)
Case Study, Patient 5 (Pg. 55)
——————————————————————
[9] 17. 2004
Case 8 (Pgs. 321-322)
Case 10 (Pgs. 321 + 323)
——————————————————————
[10] 18. 6/2005 (Pgs. 172-173)
Patient 4
——————————————————————
[10] 18. 6/2005 (Pgs. 173-174)
Patient 11
——————————————————————
[12] 19. 3/2006 (Pgs. 45-46)
Case Report Patient 12
� � � � � � � � � � � � � � � � �
[2] 16. 2003 (Pg. 94)
Trial design – Fleming
——————————————————————
[9] 17. 2004 (Pg. 317)
Trial design – Fleming
� � � � � � � � � � � � � � � � �
======================================
Gorski has claimed:
======================================
6/7/2013 “Unlike Mr. Merola, I am indeed very concerned with getting my facts correct”
——————————————————————
http://scienceblogs.com/insolence/2013/06/07/i-want-my-anp/
======================================
6/5/2013 “ … I do know cancer science”
——————————————————————
http://scienceblogs.com/insolence/2013/06/05/odds-and-ends-about-burzynski-clinic/
======================================
11/2/2012 “Personally, having pored over Burzynski’s publications … “
——————————————————————
http://scienceblogs.com/insolence/2012/11/02/stanislaw-burzynski-fails-to-save-another-patient/
======================================
5/8/2013 “I’ve searched Burzynski’s publications … “
——————————————————————
http://scienceblogs.com/insolence/2013/05/08/eric-merola-and-stanislaw-burzynskis-secret-weapon-against-the-skeptics-fabio-lanzoni-part-2/
======================================
☆AnthonyJeselnik☆
🚫GorskonOrac🚫
You tweeted 12:44pm-3/30/13📄

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

Odd how @BurzynskiMovie pretends I haven't deconstructed his "evidence" in depth before. http://t.co/uiGeNelAlb @bbcpanorama @vguyuk @fxnwo

— David Gorski (@gorskon) March 30, 2013

——————————————————————
Defend your tweet😅
#Burzynski—
(@FauxSkeptic) May 23, 2013
——————————————————————
David Gorski (@gorskon)
5/23/13, 9:32 AM
——————————————————————
@FauxSkeptic No need to defend my Tweet. The defense is in the link.
http://www.sciencebasedmedicine.org/index.php/stanislaw-burzynski-bad-medicine-a-bad-movie
——————————————————————
NO, Dr. Gorski, you have NOT “deconstructed his “evidence” in depth before”
Burzynski: Cancer Is Serious Business (Part I) consists of the documentary; as well as the documents on the movie web-site, which you have NOT “deconstructed … in depth before”

(What Gorski did is termed: “cherry-picking”)

Maybe #ScienceBasedMedicine needs to change this
——————————————————————
“Our only goal is to promote high standards of science in medicine”
======================================
� � � � � � � � � � � � � � � � �
References:
� � � � � � � � � � � � � � � � �
http://www.burzynskiclinic.com/scientific-publications.html
� � � � � � � � � � � � � � � � �
[1] 1. 10/2003 (Pg. 358)
——————————————————————
Interim Reports on Clinial Trials:
NEURO-ONCOLOGY
Phase II study of Antineoplastons A10 and AS2-1 (ANP) in children with recurrent and progressive multicentric glioma
A preliminary report

Click to access 970.pdf

Neuro-Oncology. 2003; 5: 358
Volume 5 Issue 4 October 2003
======================================
[2] 16. 2003 (Pgs. 91-101)
——————————————————————
Interim Reports on Clinial Trials
BT-11 – BRAIN STEM GLIOMA
Special exception (SE) to BT-11
DRUGS IN R&D
Phase II study of antineoplaston A10 and AS2-1 in patients with recurrent diffuse intrinsic brain stem glioma:
a preliminary report
recurrent diffuse intrinsic brain stem glioma
Drugs in R and D
(Drugs in Research and Development)
http://www.ncbi.nlm.nih.gov/pubmed/12718563
Drugs In R and D / Drugs in Research and Development:
http://www.ncbi.nlm.nih.gov/m/pubmed/12718563
Drugs R D. 2003;4(2):91-101

Click to access 960.pdf

Drugs in R&D 2003;4:91-101
======================================
[3] 1. 3/2004 (Pgs. 47-58)
——————————————————————
Review Articles on Clinical Trials:
INTEGRATIVE CANCER THERAPIES
The Present State of Antineoplaston Research

Click to access 994.pdf

Integrative Cancer Therapies 2004;3:47-58
Volume 3, No. 1, March 2004
DOI: 10.1177/1534735-403261964
======================================
[4] 4. 9/2004 (Pgs. 257-261)
——————————————————————
Case Reports:
INTEGRATIVE CANCER THERAPIES
Special exception (SE) to BT-11 BRAIN STEM GLIOMA
Long-term survival and complete response of a patient with recurrent diffuse intrinsic brain stem glioblastoma multiforme

Click to access 1145.pdf

Integrative Cancer Therapies 2004;3:257-261
Volume 3, Number 3 September 2004
======================================
[5] 2. 10/2004 (Pg. 384)
——————————————————————
Interim Reports on Clinial Trials:
NEURO-ONCOLOGY
BT-20 Patients With GLIOBLASTOMA MULTIFORME (GBM)
Phase II study of Antineoplastons A10 and AS2-1 (ANP) in recurrent glioblastoma multiforme

Click to access 1218.pdf

Neuro-Oncology. 2004; 6: 384
Volume 6 Issue 4 October 2004
Abstracts from the Society for Neuro-Oncology Ninth Annual Meeting, Toronto, Ontario, Canada, November 18-21, 2004
======================================
[6] 3. 10/2004 (Pg. 386)
——————————————————————
Interim Reports on Clinial Trials:
(DBSG) (Study (ST) and Special Exception (SE))
NEURO-ONCOLOGY
Long-term survivals in phase II studies of Antineoplastons A10 and AS2-1 (ANP) in patients with diffuse intrinsic brain stem glioma

Click to access 1219.pdf

Neuro-Oncology. 2004; 6: 386
Volume 6 Issue 4 October 2004
======================================
[7] 4. 10/2004 (Pg. 427)
——————————————————————
Interim Reports on Clinial Trials:
(AT/RT of CNS) (Study (ST) and Special Exception (SE))
NEURO-ONCOLOGY
BT-14 CHILDREN WITH RHABDOID TUMOR OF THE CENTRAL NERVOUS SYSTEM
Phase II studies of antineoplastons A10 and AS2-1 (ANP) in children with atypical teratoid/rhabdoid tumors (AT/RT) of the central nervous system
A preliminary report

Click to access 1146.pdf

Neuro-Oncology. 2004; 6: 427
Volume 6 Issue 4 October 2004
Abstracts from the Eleventh International Symposium on Pediatric Neuro-Oncology, Boston, Massachusetts, June 13-16, 2004
======================================
[8] 5. 10/2004 (Pg. 428)
——————————————————————
Interim Reports on Clinial Trials:
NEURO-ONCOLOGY
BT-12 CHILDREN WITH PRIMITIVE NEUROECTODERMAL TUMORS (PNET)
Treatment of primitive neuroectodermal tumors (PNET) with antineoplastons A10 and AS2-1 (ANP)
Preliminary results of phase II studies

Click to access 1147.pdf

Neuro-Oncology. 2004; 6: 428
Volume 6 Issue 4 October 2004
Abstracts from the Eleventh International Symposium on Pediatric Neuro-Oncology
======================================
[9] 17. 2004 (Pgs. 315-326)
——————————————————————
Interim Reports on Clinial Trials:
DRUGS IN R&D
Drugs in R and D
(Drugs in Research and Development)
Pg. 317
BT-13 – children with low-grade astrocytoma
BT-23 – children with visual pathway gliomas
Phase II study of antineoplaston A10 and AS2-1 in children with recurrent and progressive multicentric glioma
A Preliminary Report
http://www.ncbi.nlm.nih.gov/pubmed/15563234
Drugs R&D 2004;5(6):315-326
http://www.ncbi.nlm.nih.gov/m/pubmed/15563234
Drugs R D. 2004;5(6):315-26

Click to access 1194.pdf

======================================
[10] 18. 6/2005 (Pgs. 168-177)
——————————————————————
Interim Reports on Clinial Trials:
INTEGRATIVE CANCER THERAPIES
BT-12 children with PRIMITIVE NEUROECTODERMAL TUMORS (PNET)
CAN-01 (CAN-1) PATIENTS WITH REFRACTORY MALIGNANCIES
Long-term survival of high-risk pediatric patients with primitive neuroectodermal tumors treated with Antineoplastons A10 and AS2-1
http://www.ncbi.nlm.nih.gov/pubmed/15911929
Integrative Cancer Therapies 2005;4(2):168-177
http://www.ncbi.nlm.nih.gov/m/pubmed/15911929
Integr Cancer Ther. 2005 Jun;4(2):168-77

Click to access 1220.pdf

DOI: 10.1177/1534735405276835
http://m.ict.sagepub.com/content/4/2/168.long?view=long&pmid=15911929
Volume 4 Number 2 June 2005
======================================
[11] 7. 7/2005 (Pg. 300)
——————————————————————
Interim Reports on Clinial Trials:
BT-11 BRAIN STEM GLIOMA
Targeted therapy with ANP in children less than 4 years old with inoperable brain stem gliomas. Neuro-Oncology. 2005; 7:300

Click to access 1224.pdf

Volume 7 Issue 3 July 2005
Abstracts from the World Federation of Neuro-Oncology Meeting
======================================
[12] 19. 3/2006 (Pgs. 40-47)
——————————————————————
Interim Reports on Clinial Trials:
BT-03

BT-11 BRAIN STEM GLIOMA (BSG)
BT-18
6. MIXED GLIOMA
ADULT PATIENTS WITH MIXED GLIOMA
“mixed glioma”, a type of primary malignant brain tumor (PMBT)
BT-22
8. CHILDREN WITH PRIMARY MALIGNANT BRAIN TUMORS
CAN-01 (CAN-1)
PATIENTS WITH REFRACTORY MALIGNANCIES
Burzynski, S.R., Janicki, T.J., Weaver, R.A., Burzynski, B. Targeted therapy with Antineoplastons A10 and AS2-1 of high grade, recurrent, and progressive brainstem glioma. Integrative Cancer Therapies 2006;5(1):40-47
http://www.ncbi.nlm.nih.gov/pubmed/16484713
Integr Cancer Ther. 2006 Mar;5(1):40-7
http://www.ncbi.nlm.nih.gov/m/pubmed/16484713
DOI: 10.1177/1534735405285380

Click to access 5825.pdf

�
http://m.ict.sagepub.com/content/5/1/40.long?view=long&pmid=16484713
======================================
[13] 2006 (Pgs. 167-168)
——————————————————————

Click to access 1252.pdf

======================================
[14] 8. 10/2006 (Pg. 466)
——————————————————————
Interim Reports on Clinial Trials:
BT-11 BRAIN STEM GLIOMA
Treatment of multicentric brainstem gliomas with antineoplastons (ANP) A10 and AS2-1. Neuro-Oncology. 2006; 8:466

Click to access 2105.pdf

Volume 8 Issue 4 October 2006
Abstracts for the Eleventh Annual Meeting of the Society for Neuro-Oncology (SNO)
======================================
[15] 10. 6/2008 (Pg. 450)
——————————————————————
NEURO-ONCOLOGY
Interim Reports on Clinical Trials:
(OPG)
BT-23 – CHILDREN WITH VISUAL PATHWAY GLIOMA
Phase II study of antineoplastons A10 and AS2-1 (ANP) in children with optic pathway glioma:
A preliminary report

Click to access 7287.pdf

Neuro-Oncology 2008; 10:450
Volume 10 Issue 3 June 2008
======================================
[16] 10/2008 (Pg. 821)
——————————————————————
NEURO-ONCOLOGY
Phase II study of antineoplastons A10 and AS2-1 (ANP) in patients with newly diagnosed anaplastic astrocytoma:
A preliminary report

Click to access 7853.pdf

Neuro-Oncology 2008; 10:821
Volume 10 Issue 5 October 2008
======================================
[17] 12/2008 (Pg. 1067)
——————————————————————
NEURO-ONCOLOGY
Phase II study of antineoplastons A10 and AS2-1 infusions (ANP) in patients with recurrent anaplastic astrocytoma

Click to access 7898.pdf

Neuro-Oncology 2008; 10:1067
Volume 10 Issue 6 December 2008
======================================
[18] 12/2009 (Pg. 923)
——————————————————————
Case Reports:
NEURO-ONCOLOGY
Over a 10-year survival and complete response of a patient with diffuse intrinsic brainstem glioma (DBSG) treated with antineoplastons (ANP)

Click to access 8638.pdf

Neuro-Oncology 2009; 11:923
Volume 11 Issue 6 December 2009
======================================
[19] 13. 12/2009 (Pg. 951)
——————————————————————
Interim Reports on Clinial Trials:
BT-11 BRAIN STEM GLIOMA
(Study (ST) and Special Exception (SE))
Phase II study of antineoplastons A10 and AS2-1 in patients with brainstem glioma
Protocol BC-BT-11

Click to access 8639.pdf

Neuro-Oncology 2009, 11:951.
Volume 11 Issue 6 December 2009
Abstracts from the Third Quadrennial Meeting of the World Federation of Neuro-Oncology (WFNO) and the Sixth Meeting of the Asian Society for Neuro-Oncology (ASNO), May 11-14, 2009, Yokohama, Japan
======================================
[20] 14. 6/2010 (Pg. ii95)
——————————————————————
Interim Reports on Clinical Trials:
BT-13 – CHILDREN WITH LOW GRADE ASTROCYTOMA
A Phase II Study of Antineoplaston A-10 and AS-1 Injections in children with low-grade astrocytomas

Click to access 8397.pdf

Neuro-Oncology 2010; 12, ii95.
Volume 12 Issue 6 June 2010
Antineoplaston A10 (Atengenal)
Antineoplaston AS2-1 (Astugenal)
======================================
[21] 15. 11/2010 (Pg. iv72)
——————————————————————
Interim Reports on Clinical Trials:
BT-18 – ADULT PATIENTS WITH MIXED GLIOMA
Preliminary Results of a Phase II Study of Antineoplastons A10 and AS2-1 (ANP) in Adult Patients with Recurrent Mixed Gliomas

Click to access 8637.pdf

Neuro-Oncology 2010; 12:iv72.
Volume 12 Supplement 4 November 2010
======================================

Advertisement

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

6/4/2013 Gorski made a remarkable admission:
======================================
http://scienceblogs.com/insolence/2013/06/04/stanislaw-burzynski-versus-the-bbc/
======================================
“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” ?
======================================
Gorski has claimed:
======================================
6/7/2013 “Unlike Mr. Merola, I am indeed very concerned with getting my facts correct”
——————————————————————
http://scienceblogs.com/insolence/2013/06/07/i-want-my-anp/
======================================
6/5/2013 “ … I do know cancer science”
——————————————————————
http://scienceblogs.com/insolence/2013/06/05/odds-and-ends-about-burzynski-clinic/
======================================
11/2/2012 “Personally, having pored over Burzynski’s publications … “
——————————————————————
http://scienceblogs.com/insolence/2012/11/02/stanislaw-burzynski-fails-to-save-another-patient/
======================================
5/8/2013 “I’ve searched Burzynski’s publications … “
——————————————————————
http://scienceblogs.com/insolence/2013/05/08/eric-merola-and-stanislaw-burzynskis-secret-weapon-against-the-skeptics-fabio-lanzoni-part-2/
======================================
☆AnthonyJeselnik☆
🚫GorskonOrac🚫
You tweeted 12:44pm-3/30/13📄

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

Odd how @BurzynskiMovie pretends I haven't deconstructed his "evidence" in depth before. http://t.co/uiGeNelAlb @bbcpanorama @vguyuk @fxnwo

— David Gorski (@gorskon) March 30, 2013

——————————————————————
Defend your tweet😅
#Burzynski—
(@FauxSkeptic) May 23, 2013
——————————————————————
David Gorski (@gorskon)
5/23/13, 9:32 AM
——————————————————————
@FauxSkeptic No need to defend my Tweet. The defense is in the link.
http://www.sciencebasedmedicine.org/index.php/stanislaw-burzynski-bad-medicine-a-bad-movie
——————————————————————
NO, Dr. Gorski, you have NOT “deconstructed his “evidence” in depth before”
Burzynski: Cancer Is Serious Business (Part I) consists of the documentary; as well as the documents on the movie web-site, which you have NOT “deconstructed … in depth before”

(What Gorski did is termed: “cherry-picking”)
======================================
7/22/2013 I published the below article on my blog:
======================================
Critiquing: In which Orac does Stanislaw Burzynski propagandist Eric Merola a favor…:
——————————————————————
https://stanislawrajmundburzynski.wordpress.com/2013/07/22/critiquing-in-which-orac-does-stanislaw-burzynski-propagandist-eric-merola-a-favor/
======================================
“… because Gorski and others do NOT seem to understand how antineoplastons (ANP) A10 (Atengenal) and AS2-1 (Astugenal) work, I provide the relevant Burzynski publications and page #’s for them to review:
——————————————————————
It’s not like The Skeptics are going to help Gorski since they usually post inane comments that frequently go off topic on his Respectful Insolence blog
——————————————————————
Gorski, here’s:
——————————————————————
“the scientific rationale … to expect that (antineoplastons) might have antitumor activity”
� � � � � � � � � � � � � � � �
[1] 7/1971 Phenylacetic acid as potential therapeutic agent for treatment of HUMAN CANCER
� � � � � � � � � � � � � � � �
[2] 1976 Medium-sized peptides isolated from normal humans urine were tested for effect on DNA, RNA, and protein synthesis, and mitosis, in tissue culture of human myeloblastic leukemia, osteosarcoma, and HeLa cells
——————————————————————
active peptides produce up to 97% inhibition of DNA synthesis and mitosis in neoplastic cells in tissue culture
� � � � � � � � � � � � � � � �
[3] 1990 AS2-1 (AS)
� � � � � � � � � � � � � � � �
2 / 14.5% – Complete Remission
——————————————————————
3 / 21%- Partial Remission
——————————————————————
7 / 50%- Stabilization of disease with objective improvement
——————————————————————
2 / 14.5% – Progression
——————————————————————
1st patient enrolled in Complete Remission 17 months and off treatment 16 months
� � � � � � � � � � � � � � � � �
[4] 4/1/1992 PHENYLACETATE-novel nontoxic inducer of TUMOR CELL differentiation
——————————————————————
Sodium PHENYLACETATE found to affect growth and differentiation of TUMOR CELLS in vitro at concentrations achieved in humans with no significant adverse effects
——————————————————————
Treatment of promyelocytic leukemia III.-60 cells resulted in rapid decline of myc oncogene expression followed by growth arrest and granulocyte differentiation
——————————————————————
results indicate PHENYLACETATE is effective in inducing tumor cell maturation and free of cytotoxic and carcinogenic effects, a combination that warrants attention to potential use in CANCER intervention
——————————————————————
Conclusions:
——————————————————————
Sodium PHENYLACETATE is investigational new drug approved for human use by U.S. Food and Drug Administration
——————————————————————
drug already established as safe and effective in treatment of hyperammonemia (2-4); we propose use may be extended to CANCER preventation and therapy
� � � � � � � � � � � � � � � �
[5] 9/15/1992 results suggest PHENYLACETATE, used alone or in combination with other drugs, might offer safe and effective new approach to treatment of some hematopoietic neoplasms and severe hemoglobinopathies
——————————————————————
NaPA, which has an unpleasant odor, can be substituted by its pro-drug, sodium PHENYLBUTYRATE (NaPB), for oral administration
——————————————————————
Upon ingestion by humans, PHENYLBUTYRATE undergoes @-oxidation to PHENYLACETATE
——————————————————————
Both NaPA and NaPB already proved safe for the treatment of infants and adults
——————————————————————
It seems important therefore to further evaluate the clinical relevance of our experimental data
� � � � � � � � � � � � � � � �
[6] 5/1993 nontoxic differentiation inducer, sodium PHENYLACETATE (NaPA)
——————————————————————
in vitro antineoplastic activity was observed with drug concentrations that have been achieved in humans with no significant toxicities, suggesting PA, used alone or in combination with other antitumor agents, warrants evaluation in treatment of advanced prostatic CANCER
� � � � � � � � � � � � � � � �
[7] 2/1994 sodium PHENYLACETATE can induce cytostasis and reversal of MALIGNANT properties of cultured HUMAN GLIOBLASTOMA CELLS, when used at pharmacological concentrations that are well tolerated by children and adults
——————————————————————
Systemic treatment of rats bearing intracranial GLIOMAS resulted in SIGNIFICANT TUMOR SUPPRESSION with no apparent toxicity to host
——————————————————————
data indicate PHENYLACETATE, acting through inhibition of protein prenylation and other mechanisms, may offer safe and effective novel approach to treatment of MALIGNANT GLIOMAS and perhaps other neoplasms as well
� � � � � � � � � � � � � � � �
[8] 4/1/1994 Phenylacetate has recently been shown to suppress TUMOR growth and promote differentiation in experimental models
——————————————————————
phase I trial of PHENYLACETATE conducted in 17 patients with advanced solid TUMORS
——————————————————————
99% of PHENYLACETATE elimination was accounted for by conversion to PHENYLACETYLGLUTAMINE, which was excreted in the urine
——————————————————————
1 of 6 patients with GLIOBLASTOMA MULTIFORME, whose steroid dosage has remained unchanged for duration of therapy, has sustained functional improvement for more than 9 months
——————————————————————
use of adaptive control with feedback for dosing of each patient enabled us to safely maintain stable PHENYLACETATE concentrations … which resulted in clinical improvement in some patients with advanced disease
� � � � � � � � � � � � � � � �
[9] 6/1/1994 PHENYLACETATE is naturally occurring plasma component that suppresses growth of TUMOR CELLS and induces differentiation in vitro
——————————————————————
Treatment with PHENYLACETATE extended survival … without associated adverse effects
——————————————————————
PHENYLACETATE, used at clinically achievable concentrations, prolongs survival of rats with MALIGNANT BRAIN TUMORS through induction of TUMOR differentiation
——————————————————————
role in treatment of BRAIN TUMORS and other CANCERS should be explored further
� � � � � � � � � � � � � � � �
[10] 9/1994 increasing incidence of melanoma and poor responsiveness of disseminated disease to conventional treatments call for development of new therapeutic approaches
——————————————————————
PHENYLACETATE, nontoxic differentiation inducer, can suppress growth of other NEUROECTODERMAL TUMORS, i.e., GLIOMAS, in laboratory models and HUMANS
——————————————————————
finding led us to explore efficacy of PHENYLACETATE and related aromatic fatty acids in MELANOMA
——————————————————————
PHENYLACETATE and PHENYLBUTYRATE found to a) induce selective cytostasis and maturation of cultured HUMAN MELANOMA CELLS, b) modulate expression of GENES implicated in TUMOR METATASIS (type IV collagenase and tissue inhibitor of metalloproteinases-2) and immunogenicity (HLA class I); and c) enhance efficacy of other agents of clinical interest
——————————————————————
in vitro ANTITUMOR activity observed with nontoxic, pharmacologic concentrations of PHENYLACETATE and PHENYLBUTYRATE, suggesting potential clinical use of drugs in treatment of MELANOMAS
� � � � � � � � � � � � � � � �
[11] 2/8/1995 (7/17/2006) PHENYLACETATE, a natural metabolite of phenylalanine which was originally described as a plant growth hormone, has recently gained attention as a possible differentiation inducer for a variety of HUMAN TUMOR CELL types
——————————————————————
Using the LA-N-5 cell line, we have determined that NaPA can stimulate the differentiation of neuroblastoma cells …
——————————————————————
NaPA and RA synergized in inducing differentiation, in that combination treatment resulted in cessation of cell growth along with morphologic and biochemical changes indicative of loss of malignant properties
� � � � � � � � � � � � � � � �
[12] 4/1995 (3/8/2013) PHENYLACETATE, an inducer of tumor cytostasis and differentiation, shows promise as relatively nontoxic antineoplastic agent
——————————————————————
PHENYLBUTYRATE, an odorless compound that also has activity in TUMOR models
� � � � � � � � � � � � � � � �
[13] 5/1995 Antineoplaston (Ap), new ANTITUMOR agent, clinically tested for effects on MALIGNANT BRAIN TUMORS
——————————————————————
1 – medulloblastoma
1 – pontine glioma
2 – anaplastic astrocytoma
2 – metastatic brain tumor
3 – glioblastoma (G,B)
——————————————————————
All underwent radiochemotherapy and surgical resection of tumors except:
1 – pontine glioma
2 – anaplastic astrocytoma
2 – metastatic brain tumor
——————————————————————
Complete Response:
1 – anaplastic astrocytoma
Partial Response:
1 – metastatic brain tumor
1 – pontine glioma
No change:
1 – anaplastic astrocytoma
1 – multiple brain metastasis
Progression of disease:
3 – glioblastomas
1 – medulloblastoma
showed continuous increase in tumor size
——————————————————————
Effects of Ap on malignant brain tumors considered due to synergy, since administered with other drugs and acceleration of tumor cellular differentiation
——————————————————————
Ap useful as approach to remission maintenance therapy for brain tumors
� � � � � � � � � � � � � � � �
[14] 6/15/1995 growth-inhibiting and differentiating effects of sodium PHENYLACETATE against hematopoietic and solid TUMOR CELL lines has aroused clinical interest in its use as an ANTICANCER drug
——————————————————————
1 – refractory malignant glioma had partial response
——————————————————————
1 – hormone-independent prostate cancer achieved 50% decline in prostate specific antigen level, maintained 1 month
——————————————————————
High grade GLIOMAS and advanced prostate cancer are reasonable targets for Phase II clinical trials
� � � � � � � � � � � � � � � �
[15] 7/1995 aromatic fatty acids phenylacetate (PA) and phenylbutyrate (PB) induce tumour cell differentiation in experimental models and currently in clinical trials
——————————————————————
close association between enhanced TGF-alpha production and melanoma cell differentiation suggests this growth factor, often linked to mitogenesis, may play a novel role in tumour differentiation by PA and PB
� � � � � � � � � � � � � � � �
[16] 9/27/1995 (7/17/2006) Alterations in expression of ras oncogenes are characteristic of wide variety of human neoplasms
——————————————————————
Accumulating evidence has linked elevated ras expression with disease progression and FAILURE of TUMORS to RESPOND to CONVENTIONAL THERAPIES, including radiotherapy and certain chemotherapies
——————————————————————
observations led us to investigate response of ras-transformed cells to differentiation-inducer PHENYLACETATE (PA)
——————————————————————
Using gene transfer models, we show PA caused cytostasis in ras-transformed mesenchymal cells, associated with increased expression of 2′,5′-oligoadenylate synthetase, an enzyme implicated in negative growth control
——————————————————————
PA also induced phenotypic reversion characterized by loss of anchorage-independent growth, reduced invasiveness and increased expression of collagen alpha type I, a marker of cell differentiation
——————————————————————
ANTI-TUMOR ACTIVITY of PA was observed in cases involving either Ha- or Ki-ras and was independent of mode of oncogene activation
——————————————————————
Interestingly, in contrast to their relative resistance to radiation and doxorubicin, ras-transformed cells were significantly more sensitive to PA than their parental cells
——————————————————————
profound changes in TUMOR CELL and molecular biology were associated with reduced isoprenylation of ras-encoded p21
——————————————————————
Our results indicate PA CAN SUPPRESS GROWTH of ras-transformed cells, resistant otherwise to free-radical based therapies, through interference with p21ras isoprenylation, critical to signal transduction and maintenance of MALIGNANT phenotype
� � � � � � � � � � � � � � � �
[17] 10/1995 investigated effects of a nontoxic differentiation inducer, PHENYLACETATE (PA), on NEUROECTODERMAL TUMOR-derived CELL lines
————————————————————
PHENYLACETATE decreased transforming growth factor (TGF)-beta 2 production by medulloblastoma Daoy cells
————————————————————
in vitro antiproliferative and differentiation inducing effects of PA suggest that this agent warrants further evaluation as a potential therapeutic modality for the treatment of MEDULLOBLASTOMAS and MALIGNANT GLIOMA in HUMANS
� � � � � � � � � � � � � � � �
[18] 10/12/1995 aromatic fatty acid PHENYLACETATE, a common metabolite of phenylalanine, shows promise as a relatively non-toxic drug for CANCER treatment
————————————————————
slowly metabolized fatty acid alters tumor cell lipid metabolism causing … inhibition of protein prenylation critical to MALIGNANT growth
————————————————————
data suggest PHENYLACETATE and analogues may act through common mechanisms to INHIBIT GROWTH of vastly divergent, undifferentiated CELL types, and provide basis for development of new agents for treatment of HUMAN MALIGNANCIES
� � � � � � � � � � � � � � � �
[19] 1995 Antineoplastons, firstly described by Burzynski, are naturally occurring peptides and amino acid derivatives which CONTROL NEOPLASTIC GROWTH
——————————————————————
toxicological study of Antineoplastons A-10 and AS2-1 in combination with other anticancer agents or radiation in 42 patients
46 tumors with terminal stage cancer
——————————————————————
Antineoplaston A-10 oral formulation
14 – patients
A-10 injectable formulation
25 – patients
——————————————————————
Antineoplaston AS2-1 oral formulation
33 – patients
AS2-1 injectable formulation
10 – patients
——————————————————————
Major adverse effects that may have been related to agents used in combination with other conventional chemotherapeutic agents or radiation:
liver dysfunction
myelosuppression
general weakness
these effects weren’t seen when either Antineoplaston was administered alone
——————————————————————
Minor adverse effects observed in single use of either Antineoplaston A-10 or AS2-1:
reduced albumin
increased alkaline phosphatase
increased amylase
reduced cholesterol
peripheral edema
eosinophilia
fingers rigidity
excess gas
headache
hypertension
maculopapullar rash
palpitation
adverse effects didn’t limit to continuation of either agent
——————————————————————
Evaluation of usefulness of Antineoplastons in combination therapy based on imaging findings during course of treatment revealed DISAPPEARANCE or MEASUREABLE SHRINKAGE of TUMOR lasting more than one months:
15 tumors / 32.6%
——————————————————————
No increase in size of tumor for more than 3 months:
8 / 17.4%
——————————————————————
Mean survival time of patients SIGNIFICANTLY LONGER than patients with tumors showing progressive increasing
——————————————————————
Antineoplaston A-10 and AS2-1 LESS TOXIC than conventional chemotherapeutics and useful in maintenance therapy for CANCER patients
� � � � � � � � � � � � � � � �
[20] 2/1996 (11/23/2002)
sodium salt of PHENYLACETATE acid (NaPA) … acted synergistically with lovastatin to SUPPRESS MALIGNANT GROWTH
————————————————————
used at pharmacologically attainable concentrations … compounds induced profound cytostasis and LOSS of MALIGNANT PROPERTIES
————————————————————
results indicate targeting lipid metabolism with … aromatic fatty acid NaPA, may offer novel approach to treatment of MALIGNANT GLIOMAS
� � � � � � � � � � � � � � � �
[21] 5/1996 recently investigated as ANTICANCER AGENT because decreased growth and increased differentiation of variety of human NEOPLASMS, including PROSTATE CANCER in which a phase I trial has recently been completed
————————————————————
PA’s GROWTH-INHIBITORY effects on a variety of cell lines
————————————————————
PA MARKEDLY DECREASED rat PROSTATIC GROWTH and ductal morphogenesis at concentrations that have previously been well tolerated in patients
————————————————————
Synthesis of DNA also significantly decreased per organ with PA
————————————————————
In common with earlier studies, we found PA INHIBITS PROSTATIC GROWTH
————————————————————
studies indicate there may be role for PA in treating BPH or elucidating mechanisms
� � � � � � � � � � � � � � � �
[22] 1996
Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which CONTROL NEOPLASTIC GROWTH
——————————————————————
These metabolites are water soluble and have ANTITUMOR EFFECT, they are further degraded to PHENYLACETIC acid
——————————————————————
Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid in ratio of 1 to 4 shown to have ANTITUMOR EFFECT in tissue culture study, then formulated as Antineoplaston AS2-1
——————————————————————
reported CYTOSTATIC INHIBITORY EFFECT of A10 on HUMAN HEPATOCELLULAR CARCINOMA CELLS and differentiation inducing effect of AS2-1 on various TUMOR CELLS suggest potential benefit for treatment of HUMAN HEPATOCELLULAR CARCINOMA since TUMOR recurs frequently despite initial successful treatment
——————————————————————
We report effects of Antineoplaston A10 and AS2-1 on cell proliferation, cell morphology, cell cycle, and DNA in human hepatocellular carcinoma cell lines
——————————————————————
BOTH AGENTS INHIBITED CELL PROLIFERATION and increased number of cells in G0 and G1 phases and Antineoplaston AS2-1 induced APOPTOSIS
——————————————————————
clinical experience of HEPATOCELLULAR CARCINOMA (HCC) patient whose TUMOR, after incomplete trancathere arterial embolization (TAE) for a 7cm 7cm HCC, has been stable for more than 15 months during which time he has been taking Antineoplaston AS2-1 continuously WITHOUT ANY SERIOUS ADVERSE EFFECTS
� � � � � � � � � � � � � � � �
[23] 8/23/1996 aromatic fatty acid PHENYLACETATE and analogs INDUCE TUMOR CYTOSTASIS and differentiation in experimental models
————————————————————
studies using HUMAN PROSTATIC CARCINOMA, MELANOMA, and GLIOBLASTOMA cell lines showed a tight correlation between drug-induced cytostasis …
————————————————————
results identify PHENYLACETATE and analogs as new class of aromatic fatty acids capable of activating hPPAR, and suggest nuclear receptor may mediate TUMOR cytostasis induced by these drugs
� � � � � � � � � � � � � � � �
[24] 9/1996 We examined hypothesis this postulate may not apply to evaluation of drugs such as PHENYLACETATE, a differentiating agent endowed with mechanisms of action different from those of classic cytotoxic chemotherapy
————————————————————
Using HUMAN PROSTATIC CARCINOMA LNCaP cells as model, we show PHENYLACETATE induces PSA production despite inhibition of TUMOR CELL proliferation
� � � � � � � � � � � � � � � �
[25] 12/1996 PHENYLACETATE (PA) and related aromatic fatty acids constitute novel class of relatively nontoxic antineoplastic agents
————————————————————
Using human breast carcinoma MCF-7 cells as model, we show PA-induced growth arrest associated with enhanced expression of cyclin-dependent kinase inhibitor p21Waf1/Cip1 …
————————————————————
induction of p21WAF1/CIP1 mRNA by PA independent of cellular p53 status
————————————————————
PA effectively induced p21WAF1/CIP1 mRNA and growth inhibition of wild-type mouse embryonal fibroblasts
————————————————————
findings strongly support role for p21Waf1/Cip1 in PA-mediated inhibition of cell growth
� � � � � � � � � � � � � � � �
[26] 1996 Cytotoxic chemotherapies often give rise to multidrug resistance, which remains major problem in CANCER management
————————————————————
In pursuit of alternative treatments for chemoresistant TUMOR CELLS, we tested response of multidrug-resistant (MDR) TUMOR CELL lines to aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB), 2 differentiation inducers currently in clinical trials
————————————————————
Both compounds induced cytostasis and maturation of multidrug-resistant BREAST, OVARIAN, and COLON CARCINOMA CELLS with no significant effect on cell viability
————————————————————
MDR cells generally more sensitive to GROWTH ARREST by PA and PB than parental counterparts
————————————————————
PA and PB potentiated the cytotoxic activity of doxorubicin against MDR cells
————————————————————
Taken together, our in vitro data indicate PA and PB, differentiation inducers of aromatic fatty acid class, may provide alternative approach to treatment of MDR TUMORS
� � � � � � � � � � � � � � � �
[27] 8/1997 aromatic fatty acids PHENYLACETATE (PA) and PHENYLBUTYRATE (PB) are novel ANTITUMOR AGENTS currently under clinical evaluation
————————————————————
ability to induce TUMOR differentiation in laboratory models and low clinical toxicity profile makes them promising candidates for COMBINATION with CONVENTIONAL THERAPIES
————————————————————
In present studies, we characterized interactions between aromatic fatty acids and radiation, using as a model cell lines derived from CANCERS of PROSTATE, BREAST, BRAIN and COLON
————————————————————
in vitro findings identify aromatic fatty acids PA and PB as new class of non-toxic modulators of radiation response, antagonistic effect of these compounds on radiation response needs further examination
————————————————————
data strongly suggest that for PA or PB to have role in clinical radiotherapy, appropriate scheduling of combination therapies must take into account time-dependent effects in order to achieve clinical radiosensitization
� � � � � � � � � � � � � � � �
[28] 11-12/1997 Antineoplaston AS2-1 EXHIBITS CYTOSTATIC GROWTH INHIBITION of human hepatocellular carcinoma cells in vitro and showed minimum adverse effects in phase I clinical trial
——————————————————————
2 clinical cases of liver cancer (hepatocellular carcinoma and multiple liver metastases from colon cancer) in whom we believe antineoplaston A2-1 useful as maintenance therapy after transcatheter arterial embolization (TAE) and microwave coagulation necrosis (MCN)
——————————————————————
2 patients have continued to be in good condition for more than 2 years without limitation of normal activities
——————————————————————
Antineoplaston AS2-1 may be effective and useful as maintenance agent after TAE and MCN in patients with liver cancer
� � � � � � � � � � � � � � � �
[29] 1997 PHENYLACETATE and analogs represent new class of pleiotropic growth regulators that alter TUMOR CELL biology by affecting GENE EXPRESSION at both transcriptional and post transcriptional levels
————————————————————
Based on findings, NaPA and NaPB entered clinical trials at NATIONAL CANCER INSTITUTE
————————————————————
Ongoing phase I studies with NaPA, involving adults with PROSTATE and BRAIN CANCER, confirmed therapeutic levels can be achieved with no significant toxicities, and provide preliminary evidence for benefit to patients with advanced disease (Thibault et al., submitted)
� � � � � � � � � � � � � � � �
[30] 5 – 6/1998 Antineoplastons A10 and AS2-1 EXHIBIT GROWTH INHIBITION OF CANCER CELLS by diverse modes of action
——————————————————————
Observed ANTITUMOR RESPONSES within 2-3 weeks of combination treatment of chemoradiation therapy and antineoplastons A10 and AS2-1 in phase I clinical study conducted in Kurume University Hospital
——————————————————————
Reviewed 3 clinical cases of advanced cancer (multiple metastatic lung cancer, thalamic glioma and primary lung cancer) in which we believed antineoplaston A10 and AS2-1 may be contributing to RAPID ANTITUMOR RESPONSE
——————————————————————
Possible use of this combination for induction therapy in advanced cancer
� � � � � � � � � � � � � � � �
[31] 11-12/1998 Antineoplaston A10 injection (antineoplaston A10 I) exhibited CYSTOSTATIC GROWTH INHIBITION OF HUMAN HEPATOCELLULAR CARCINOMA (HCC) CELLS in vitro and showed minimum adverse effects in phase I clinical trial
——————————————————————
2 cases of advanced HCC treated with antineoplaston A10 I
——————————————————————
Both cases showed interesting responses to antineoplaston A10 I
——————————————————————
One showed massive coagulation necrosis of tumors after intra-arterial infusion of antineoplaston A10 I and other showed RESOLUTION of portal vein TUMOR thrombosis with systemic infusion of antineoplaston A10 I
——————————————————————
Usefulness of anti-neoplaston A10 I in terminal staged HCC is discussed
� � � � � � � � � � � � � � � �
[32] 3/1999 determine response rate, time to treatment failure, and toxicity of phenylacetate in patients with recurrent malignant glioma …
————————————————————
Adult patients
————————————————————
43 – enrolled 12/1994-12/ 1996
40 – assessable
————————————————————
Reversible symptoms
————————————————————
fatigue
somnolence
were primary toxicities
————————————————————
only mild hematologic toxicity
————————————————————
30 / 75% – failed treatment within 2 months
————————————————————
7 / 17.5% – stable disease
————————————————————
3 – 7.5% – response defined as more than 50% reduction in tumor
————————————————————
Median time to treatment failure
————————————————————
2 months
————————————————————
35 – died
————————————————————
median survival
————————————————————
8 months
————————————————————
PHENYLACETATE HAS LITTLE ACTIVITY at this dose schedule in PATIENTS with RECURRENT MALIGNANT GLIOMA
————————————————————
Further studies with drug would necessitate evaluation of different dose schedule
� � � � � � � � � � � � � � � �
[33] 7/3/2000 Antineoplastons first described by Burzynski are naturally occurring peptides and amino acid derivatives, which CONTROL NEOPLASTIC GROWTH
——————————————————————
data suggest strong inverse association of urinary antineoplaston A-10 level with breast cancer
————————————————————
finding was stimulus for further investigations of antineoplaston A-10 levels in some benign as well as other malignant diseases to determine utility of approach as predictive test for women at risk of developing breast cancer
� � � � � � � � � � � � � � � �
[34] 8/31/2000 Antineoplastons are naturally occurring CYTODIFFERENTIATING AGENTS
—————————————————————
Findings confirm presence of immune defects among patients with breast cancer and results should stimulate development of new strategies to induce and augment immunity for treatment of breast cancer
—————————————————————
Antineoplaston A-10 may provide rational basis for designing trials to employ its immune modulatory potentials as adjuvant therapy in breast cancer patients
� � � � � � � � � � � � � � � �
[35] 12/2000 4 new piperidinedione A10 analogs synthesized and tested for antimitotic activity on human breast cancer cell line against prototype A10 and antibreast cancer drug tamoxifen
—————————————————————
“3B” and “3D” were several-fold more potent ANTIPROLIFERATIVE AGENTS than A10 and tamoxifen and had significantly higher capacity to bind DNA than A10
� � � � � � � � � � � � � � � �
[36] 8/2001 No partial remission or complete remission was seen, but 7 patients had stable disease for more than 6 months while on drug
————————————————————
PB may have role as cytostatic agent and should be additionally explored in combination with cytotoxics and other novel drugs
� � � � � � � � � � � � � � � �
[37] 2002 p53 tumor suppressor gene plays important role in protecting cells from developing undesirable proliferation
——————————————————————
Mutant p53 gene or malfunctioning p53 protein found in more than 50% of cancer cells impedes DNA repair or apoptosis induction
——————————————————————
May be why some cancers gain resistance to chemotherapy and radiation and become more resistant after frequent cancer treatments
——————————————————————
non-toxic p53 gene activator would induce cancer cell apoptosis and help damaged cancer cells to recover
——————————————————————
combination use of chemotherapeutics or radiation with non-toxic p53 gene activator will be crucial in cancer therapy, damaging DNA with chemotherapeutics or radiation on one hand and promoting apoptosis induction with p53 gene activator on the other
——————————————————————
Strategy would be most efficient for remission induction and maintenance CANCER therapy
——————————————————————
Antineoplastons are naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH
——————————————————————
Antineoplaston A10 and AS2-1 are chemically identified and synthesized antineoplastons PROVEN TO INHIBIT CANCER CELL GROWTH by arresting cell cycle in G1 phase and INHIBITING TUMOR GROWTH by reducing mitosis
——————————————————————
Agents thought to be good candidates for clinically easily applicable non-toxic p53 gene activators
——————————————————————
CASES OF ADVANCED CANCER RESPONDED WELL to combination treatment using chemotherapeutics and irradiation with antineoplaston A10 and AS2-1 in clinical trials being conducted in Kurume University Hospital
� � � � � � � � � � � � � � � �
[38] 3 – 4/2003 Phase II clinical trail to clarify whether antineoplaston AS2-1, mixture of sodium salts of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid at ratio of 1:4, prolongs recurrence-free interval of HCC patients who undergo frequent treatments for recurrence
——————————————————————
10 patients enrolled in trial
2 in stage I
6 in stage II
1 in stage III
1 in stage IV-B
at initial diagnosis
——————————————————————
10 / 100% – experienced 35 recurrence-free intervals
——————————————————————
Recurrence-free intervals during antineoplaston AS2-1 administration SIGNIFICANTLY LONGER than without
——————————————————————
Patients who experienced recurrence-free intervals with and without antineoplaston AS2-1 SHOWED LONGER INTERVALS during antineoplaston AS2-1 administration
——————————————————————
2 patients in stage I showed LONGER RECURRENCE-FREE INTERVALS than those in more advanced stages
——————————————————————
Antineoplastons AS2-1 couldn’t prevent recurrence of HCC but PROLONGED RECURRENCE-FREE INTERVAL between regional treatments and IMPROVED SURVIVAL RATE OF PATIENTS
� � � � � � � � � � � � � � � �
[39] 2003 Case of survival for nearly 8 years after treatment of unresectable multiple liver metastases from colon cancer, using microwave ablation and NONTOXIC ANTITUMOR AGENT, antineoplastons
——————————————————————
72-year-old man diagnosed with adenocarcinoma of ascending colon and 14 bilateral liver metastases underwent right hemicolectomy combined with microwave ablation of 6 metastatic liver tumors
——————————————————————
Antineoplaston A10 given intravenously, followed by oral antineoplaston AS2-1
——————————————————————
Computed tomography scans done 1 and 4 years after initial diagnosis showed recurrent tumors
——————————————————————
Patient underwent 2nd and 3rd microwave ablation of recurrent tumors, and has survived for nearly 8 years WITHOUT SUFFERING ANY SERIOUS ADVERSE EFFECTS
——————————————————————
Currently FREE FROM CANCER
——————————————————————
Demonstrates potential effectiveness of NONTOXIC ANTITUMOR AGENT, antineoplastons, for controlling liver metastases from colon cancer
� � � � � � � � � � � � � � � �
======================================
Burzynski has made it clear that PHENYLACETATE, by itself, does NOT achieve the results of antineoplastons (PHENYLACETATE, PHENYLGLUTAMINATE, PHENYLACETYLISOGLUTIMINATE, PHENYLBUTYRATE)
======================================
� � � � � � � � � � � � � � � �
======================================
[40] 2003
——————————————————————
Pg. 92
——————————————————————
Antineoplaston A10 and AS2-1 are synthetic derivatives of phenylacetate (PN) acid, glutamine and isoglutamine
——————————————————————
A10 is sterile solution of sodium phenylacetylisoglutiminate (isoPG) in 4 : 1 ratio
——————————————————————
Antineoplaston AS2-1 is sterile solution of sodium phenylacetate (PN) and phenylacetylglutaminate (PG) in 4 : 1 ratio
——————————————————————
Pg. 93
======================================
combination of antineoplaston A10 and AS2-1 used instead of single drugs
——————————————————————
Based on previous observations, combination treatment has provided better results than single drugs
——————————————————————
Pg. 97
——————————————————————
active ingredient of antineoplaston AS2-1 is PHENYLACETATE,
——————————————————————
Pg. 98
——————————————————————
known to modulate expression of ras oncogenes and tumor suppressor gene p53
——————————————————————
ras oncogene protein p21ras
——————————————————————
farneslyation of p21ras, which is inhibited by antineoplaston AS2-1
——————————————————————
Antineoplaston AS2-1 also activates p53 gene
——————————————————————
protein p53 activates p21 gene, which directs synthesis of p21WAF1/Cip1 protein
——————————————————————
Induction of p21WAF1/Cip1 suppresses human glioma cell proliferation
——————————————————————
proposed mechanism of action of 2 ingredients of antineoplaston A10, sodium phenylacetylglutamine (PG) and sodium phenylacetylisoglutimine (IsoPG), is inhibition of glutamine incorporation into proteins of neoplastic cells
——————————————————————
Antineoplaston A10 has demonstrated 5 effects related to therapeutic indication in patients with brain tumors: cytostatic, antimitogenic, antiproliferative and inhibitory effects, and differentiation of tumors
——————————————————————
[22-25]
——————————————————————
Initial clinical studies with antineoplaston therapy included testing of separate ingredients phenylacetate (PN) (antineoplaston AS5) and phenylacetylglutaminate (PG) (antineoplaston AS2-5)
——————————————————————
[26-28]
——————————————————————
studies failed to show marked anticancer activity of phenylacetate (PN) in malignant glioma, confirmed by phase II study by North
——————————————————————
Pg. 99
——————————————————————
American Brain Tumor Consortium
——————————————————————
[29]
——————————————————————
Based on results, further studies of phenylacetate (PN) as single agent in patients with malignant glioma were not recommended
——————————————————————
subsequent study by Buckner et al.
——————————————————————
[30]
——————————————————————
confirmed conclusion because patients receiving antineoplaston AS2-1 didn’t respond to treatment
——————————————————————
main difference between Buckner’s study is dosage of antineoplaston A10, which was approximately 50 times lower in Buckner’s study
——————————————————————
[31]
——————————————————————
2 patients who participated in our study (cases 3 and 8) developed recurrence on lower dosages of antineoplaston A10, but responded again with Complete Response (CR) when dosage of antineoplaston A10 was increased
——————————————————————
In these 2 patients, antineoplaston AS2-1 didn’t seem to have effect on 2nd response, which suggests antineoplaston A10 rather than antineoplaston AS2-1 is main active drug
� � � � � � � � � � � � � � � �
[41] 8/2005 Antineoplastons such as A10 include naturally occurring peptides and amino acid derivatives that CONTROL NEOPLASTIC GROWTH OF CELLS
——————————————————————
Findings indicate antineoplaston A10 ANTITUMOR EFFECT could be utilized as effective therapy for breast cancer patients
� � � � � � � � � � � � � � � �
[42] 2006 Antineoplastons, first described by Burzynski, are naturally occurring peptides and amino acid derivatives which CONTROL NEOPLASTIC GROWTH
——————————————————————
Antineoplaston A10 (3-pehnylacetylamino-2,6-piperidinedion) is first chemically identified antineoplastons and when administered orally is hydrolysed in pancreatic juice to PHENYLACETYLGLUTAMINE and PHENYLACETYLISOGLUTAMINE in ration of 4 to 1
——————————————————————
These metabolites are water soluble and have ANTITUMOR EFFECT, are further degraded to PHENYLACETIC acid
——————————————————————
Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETYLISOGLUTAMINE in ratio of 4 to 1 formulated as Antineoplaston A10 injectable formulation
——————————————————————
Mixture of PHENYLACETYLGLUTAMINE and PHENYLACETIC acid in ratio of 1 to 4 also shown to have ANTITUMOR EFFECT in tissue culture study, then formulated as Antineoplaston AS2-1
——————————————————————
Reported CYTOSTATIC INHIBITORY EFFECT of A10 on HUMAN HEPATOCELLULAR CARCINOMA CELLS and differentiation inducing effect of AS2-1 on various TUMOR CELLS suggest potential benefit for treatment of HUMAN HEPATOCELLULAR CARCINOMA since this TUMOR recurs frequently despite initial successful treatment
——————————————————————
BOTH AGENTS INHIBITED CELL PROLIFERATION and increased number of cells in G0 and G1 phases and Antineoplaston AS2-1 induced apoptosis, we also describe clinical experience of hepatocellula carcinoma (HCC) patient whose tumor, after incomplete trancathere arterial embolization (TAE) for 7cm 7cm HCC, has been stable for more than 15 months during which time he has been taking Antineoplaston AS2-1 continuously WITHOUT ANY SERIOUS ADVERSE EFFECTS
� � � � � � � � � � � � � � � �
[43] 1/2008 Novel mechanism through which all-trans retinoic acid (ATRA) and antineoplaston, ANTICANCER DRUG, CAUSED CELL GROWTH INHIBITION IN BREAST CANCER CELLS through effects on intracellular pathways
——————————————————————
Antineoplaston caused down-regulation of PKCalpha protein expression, resulting in INHIBITION of ERK MAPK phosphorylation, with resultant INHIBITION of Rb phosphorylation leading to G(1) arrest
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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
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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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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD
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Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland
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[7] 2/15/1994
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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
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Clinical Pharmacology Branch, National Cancer Institute, NIH, Bethesda, Maryland

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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.
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Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland

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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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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.
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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
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The Journal of Clinical Pharmacology
Volume 35, Issue 4, pages 368–373, April 1995
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Article first published online: 8 MAR 2013
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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
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The effect of Antineoplaston, a new ANTITUMOR AGENT on MALIGNANT BRAIN TUMORS
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Department of Neurosurgery, Kurume University School of Medicine, Japan
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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
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Cancer 75(12):2932-8 (1995), PMID.7773944
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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.
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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
Volume 63, Issue 1, Article first published online: 17 JUL 2006
DOI: 10.1002/ijc.2910630122
Shack S, Chen L-C, Miller AC, et al: (SAMID D)
http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910630122/abstract
Shack, S., Chen, L-C., Miller, A. C., Danesi, A., and SAMID, D. Int. J. Cancer, 63: 124-129, 1995
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[17] 10/1995
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Stockhammer G, Manley GT, Johnson R, et al: (SAMID D) Inhibition of proliferation and induction of differentiation in medulloblastoma and astrocytoma-derived cell lines with PHENYLACETATE. J Neurosurg 83:672-681, 1995
http://www.ncbi.nlm.nih.gov/pubmed/7674018/
J Neurosurg. 1995 Oct;83(4):672-81
http://www.ncbi.nlm.nih.gov/m/pubmed/7674018/
Cotzias Laboratory of Neuro-Oncology, Memorial Sloan-Kettering Cancer Center, New York, New York, USA
http://thejns.org/doi/abs/10.3171/jns.1995.83.4.0672?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed&
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[18] 10/12/1995
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Cytostatic activity of PHENYLACETATE and derivatives against TUMOR CELLS:
Correlation with lipophilicity and inhibition of protein prenylation.
http://www.ncbi.nlm.nih.gov/pubmed/7488244/
Biochem Pharmacol. 1995 Oct 12;50(8):1273-9
http://www.ncbi.nlm.nih.gov/m/pubmed/7488244/
Biochem Pharmacol 50:1273-1279, 1995
http://www.sciencedirect.com/science/article/pii/0006295295020133
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD, USA
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[19] 1995
� � � � � � � � � � � � � � � �
Toxicological study on antineoplastons A-10 and AS2-1 in cancer patients
Kurume Med J. 1995;42(4):241-9
http://www.ncbi.nlm.nih.gov/pubmed/8667595
Tsuda H
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://www.ncbi.nlm.nih.gov/m/pubmed/8667595
Burzynski References: 1 – 3 and 5
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_article
Nishida et al. (Japan) A-10 Reference: 4 and 7
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_article/references
Muldoon et al. A-10 Reference: 6
http://www.jstage.jst.go.jp/article/kurumemedj1954/42/4/42_4_241/_pdf
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[20] 2/1996
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Lipid metabolism as a target for BRAIN CANCER therapy:
Synergistic activity of lovastatin and sodium PHENYLACETATE against human glioma cells
http://www.ncbi.nlm.nih.gov/pubmed/8592143/
J Neurochem 66:710-716, 1996
http://www.ncbi.nlm.nih.gov/m/pubmed/8592143/
J Neurochem. 1996 Feb;66(2):710-6.
http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.1996.66020710.x/abstract
DOI: 10.1046/j.1471-4159.1996.66020710.x
http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.1996.66020710.x/abstract;jsessionid=913EBF64F1FA2FD0D08BD94FDDE391D5.d03t01
Article first published online: 23 NOV 2002
http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.1996.66020710.x/abstract;jsessionid=E929EA030144CC973FECF4DAA1D9D50C.d01t04
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.
http://www.ncbi.nlm.nih.gov/pubmed/8627880/
J Urol 155:1762-1770, 1996
http://www.ncbi.nlm.nih.gov/m/pubmed/8627880/
J Urol. 1996 May;155(5):1762-70
Lipshutz JH, SAMID D, Cunha GR:
The Journal of Urology
Volume 155, Issue 5, Pages 1762-1770, May 1996
Department of Medicine, University of California, San Francisco, USA
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[22] 1996
� � � � � � � � � � � � � � � �
Inhibitory effect of antineoplaston A10 and AS2-1 on human hepatocellular carcinoma
Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/pubmed/8755117
Kurume Med J. 1996;43(2):137-47
http://www.ncbi.nlm.nih.gov/m/pubmed/8755117
Department of Anesthesiology, Kurume University School of Medicine, Japan
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article
Burzynski References: 1 – 3, 5 and 7
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_article/references
SAMID Reference: 13 (who learned from Burzynski re PHENYLACETATE)
http://www.jstage.jst.go.jp/article/kurumemedj1954/43/2/43_2_137/_pdf
Nishida et al. (Japan) A10 Reference: 4 and 10
Muldoon et al. A10 Reference: 8
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[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
http://www.ncbi.nlm.nih.gov/pubmed/8759039/
Biochem Pharmacol. 1996 Aug 23;52(4):659-67
http://www.ncbi.nlm.nih.gov/m/pubmed/8759039/
Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD, USA
http://www.sciencedirect.com/science/article/pii/0006295296003401
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[24] 9/1996
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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
http://www.ncbi.nlm.nih.gov/m/pubmed/8827086/
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
� � � � � � � � � � � � � � � �
Gorospe M, Shack S, Guyton KZ, et al: (SAMID D)
Up-regulation and functional role of p21Waf1/Cip1 during growth arrest of HUMAN BREAST CARCINOMA MCF-7 cells by PHENYLACETATE. Cell Growth Differ 7:1609-1615, 1996
http://www.ncbi.nlm.nih.gov/pubmed/8959328/
Cell Growth Differ. 1996 Dec;7(12):1609-15
http://www.ncbi.nlm.nih.gov/m/pubmed/8959328/
Laboratory of Cellular and Molecular Biology, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, Maryland, USA

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[26] 5/1996
� � � � � � � � � � � � � � � �
Shack, S., Miller, A., Liu, L., Prasanna, P., Thibault, A., and SAMID, D.. Vulnerability of multidrug-resistant TUMOR CELLS to the aromatic fatty acids PHENYLACETATE and PHENYLBUTYRATE. Clin. Cancer Res., 2: 865-872, 1996
http://www.ncbi.nlm.nih.gov/pubmed/9816242/
Clin Cancer Res. 1996 May;2(5):865-72
http://www.ncbi.nlm.nih.gov/m/pubmed/9816242/
Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892, USA
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