Burzynski, Hideaki Tsuda (Japan), and the p53 gene

The p53 gene (Phosphoprotein, protein 53, TP53, Tumor protein 53) was supposedly “discovered in 1979, though I did find references to p53 from 1975:

Experiences with the unprepared homologous vein in the reconstruction of diseased and injured arteries

G Schulze-Bergmann and C Fernandez
Thorac Cardiovasc Surg 23(05):468-471 (1975),

We report that the core protein in the cytoplasm increases the amount of p21 via activating p53, and the core protein in the nucleus decreases the amount of p21 by the p53-independent pathway

and 1977:

Investigation of molecular motion in collagen using the spin-probe technique

T Nagamura and A E Woodward
Biopolymers 16(4):907-919 (1977),

We previously reported that OxLDL activates the tumor suppressor p53 in human fibroblasts [Biochem. Biophys. Res. Commun. 276 (2000) 718]

In the present work, we demonstrate that OxLDL increased intracellular levels of the kinase inhibitor p21waf1 (p21) and of the tumor suppressor Rb

5/1979
http://www.ncbi.nlm.nih.gov/m/pubmed/221923
Detection of a transformation-related antigen in chemically induced sarcomas and other transformed cells of the mouse
Proc Natl Acad Sci U S A. 1979 May;76(5):2420-4

p53 web-site:
http://p53.free.fr

It has been called:

“The most famous molecule in cancer research”

p53, a 53-kilodalton protein, was discovered in 1979

Researchers thought it might play a role in cancer

p53 is called:

“the guardian of the genome”

because of its role in conserving stability by preventing genome mutation

Is a tumor suppressor gene

p53, also known as TP53 or tumor protein (EC :2.7.1.37) is a gene that codes for a protein that regulates the cell cycle and hence functions as a tumor suppression

p53 is crucial in multicellular organisms, where it regulates the cell cycle and, thus, functions as a tumor suppressor that is involved in preventing cancer

p53 (also known as protein 53 or tumor protein 53), is a tumor suppressor protein that in humans is encoded by the TP53 gene

In humans, p53 is encoded by the TP53 gene located on the short arm of chromosome 17 (17p13.1)

More than a 1/2 of human cancers expressed a mutant p53 raised extensive clinical possibilities both for diagnosis and treatment

It is mutated in about half of all tumors

The p53 gene is often mutated in lung cancer

One of the most important molecules relating to cancer

Complete information for TP53 gene (protein-coding), tumor protein p53

The tumor suppressor gene p53 is mutated or deleted in over 50% of human tumors

The p53 gene is found in the nucleus of every cell in the human body

the p53 tumor suppressor gene and how it is transformed into a dominant oncogene in human cancer
present at the time of the discovery of p53 in 1979

It was only when the first alterations of the p53 gene in human cancers were discovered 10 years later, in 1989, that p53 started to become really popular, with the title of “molecule of the year”

Hideaki H. Tsuda (Japan) had learned about Burzynski and researched ANP’s independently and published:

1/20/1990 – Tsuda (Japan) – A10

Tsuda also researched the p53 gene and published papers re p53 while continuing ANP research:

p53 research

7/1991 (8/25/2005) – Tsuda H (Japan)
6/1/1992
7/1992 – Tsuda H
9/1992 – Tsuda H
11/1992 (8/25/2005) – Hitoshi Tsuda (Japan)
1993 – Tsuda H
4/1993
10/1993
10/1993
5/15/1994 – Tsuda H
6/1994
8/15/1994 – Tsuda H
12/1/1994 – Tsuda H
12/30/1994 – Tsuda H
3/1995
4/14/1995
6/1995 – Tsuda H
10/31/1995
11/1995 – Tsuda H
3/1996
4/1996
2/1997 – Tsuda H
3/1997 – Tsuda H
6/1997
8/1997
11 – 12/1997
12/1997 – Tsuda H
1998
1/1998
1/1998
3/1998
4/25/1998
7/1998 – Tsuda H
7/29/1998
9 – 10/1998 – Tsuda H
11/1998
3/1999
4/25/1999
5/24/1999 – Tsuda H
1/2000 – Tsuda H
1/2000
4/2000
4/2000 – Tsuda H
2001
5/2001 – Tsuda H
9/2001 – Tsuda H
2002
2002 – Tsuda H
1 – 2/2002
4/2002 – Tsuda H
6/2002
7/2002
2003
1/14/2003 – SRB
12/2003
2004
2/2004
3/2004 – SRB
5/2004 – SRB
9/2004
2005 – SRB
6/2005
8/25/2005 – Tsuda H
12/2005
2/8/2006 – Tsuda H
6/28/2007
7/2007 (6/27/2007)
10/2007
12/1/2007
2009
2009
7/2009 (5/7/2009)
11/2009 (8/6/2009) – Tsuda H
2/2010 – Tsuda H
4/2010 (1/29/2010)
5/2010 (3/5/2010) – Tsuda H
7/2011 (2/11/1011)
12/2011
4/2012 (5/12/2011)
8/2012 – Tsuda H
1/2013
2/6/2013 – Tsuda H

(Publications with “Tsuda” out to the right indicate publications with “p53” in the title, those without “Tsuda” are publications with “p53” in the text, “SRB” indicates Burzynski publications re ANP’s and p53)

The p53 gene like the Rb gene, is a tumor suppressor gene, i.e., its activity stops the formation of tumors
http://www.ncbi.nlm.nih.gov/books/NBK22268

It is now clearly understood that, in cancer, the ras gene can cause a cancer signal to be made (genes that cause cancer are called oncogenes)

It is also known that another gene (p53) normally suppresses tumours (and turns off the cancer process), but somehow fails in cancer patients

Burzynski showed that antineoplastons both turn off the ras gene and restimulate the p53 suppressor

He thinks of antineoplastons as switches turning some things off and others back on

Antineoplastons provide the messages which tell the genes to act

Without enough of these crucial peptides the risk of cancer is higher

Antineoplastons work on at least 100 genes

They ´turn off´ oncogenes which spread cancers; while ´turning on´ tumour surpressor genes which stop cancers growing and spreading

In about 30-40% of all cancers, an oncogene, or cancer gene, known as “ras” is activated

When activated, ras allows a protein to stick to the cell and send an abnormal signal

If we can deactivate ras, we can slow down cancer

Abnormal methylation or mutation of the ras gene causes abnormal activation

Antineoplastons normalize
DNA methylation and deactivate ras oncogene protein, making a gene behave normally

Tumor suppressor genes normally cause proteins to be made that provoke apoptosis — a process that naturally destroys cancer cells

This goes on all the time in healthy tissue

In cancer cells, tumor suppressor genes are shut down; they don’t work

The idea is to reactivate them

The p53 gene is an important tumor suppressor gene

And it is of great interest to us because it’s not working in about 70% of white Americans with brain tumors

In Japanese patients, it doesn’t work in 50 – 60%

One of the antineoplastons reactivates p53

What causes the gene to shut down?

First, abnormal methylation and mutation of the gene itself, and antineoplastons reverse this

Also, three important enzymes relate to how cancer cells multiply

All three involve methylation

We’ve discovered that in normal cells, the enzymes stick together briefly, and then come apart

In cancer cells, they stick together and make the cells keep replicating

It’s as though a switch is stuck in the “on” position

At least three of our antineoplastons make the enzymes disassociate

When the enzymes are normalized, the cancer cells undergo apoptosis, or cell death

This also has to do with normalizing the behavior of cancer cells

“Histone deacetylase inhibitors” are a new class of drugs being tested for cancer

Some of the antineoplastons are natural histone deacetylase inhibitors

Acetylation is a process related to methylation

Both affect how genes behave

One affects the other, so it’s important to address both processes

When cancer cells are treated with drugs that modulate both, you get a better response

We’ve noticed that people who get antineoplastons for cancer treatment receive other benefits as well — for example, they are resistant to common viral infections

Their blood cholesterol is normalized and they are less susceptible to breast cancer and enlargement of the prostate

Their skin is healthier, they are less depressed, and they have more energy

2/6/2013 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/23384409
A simple immunohistochemical panel comprising 2 conventional markers, Ki67 and p53, is a powerful tool for predicting patient outcome in luminal-type breast cancer
BMC Clin Pathol. 2013 Feb 6;13:5. doi: 10.1186/1472-6890-13-5
Department of Basic Pathology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan

1/15/2013 – Tsuda Y (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/23266186
Bioorg Med Chem. 2013 Jan 15;21(2):403-11. doi: 10.1016/j.bmc.2012.11.024. Epub 2012 Nov 29

1/2013 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/23202778
Int J Gynecol Pathol. 2013 Jan;32(1):26-30. doi: 10.1097/PGP.0b013e3182518533

10/2012 (1/13/2012) – Tsuda M (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/22244830
Eur J Cancer. 2012 Oct;48(15):2417-30. doi: 10.1016/j.ejca.2011.12.028. Epub 2012 Jan 13

8/2012 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/22537085
Dose-dependent mesothelioma induction by intraperitoneal administration of multi-wall carbon nanotubes in p53 heterozygous mice
Cancer Sci. 2012 Aug;103(8):1440-4. doi: 10.1111/j.1349-7006.2012.02318.x. Epub 2012 Jun 21
Division of Cellular and Molecular Toxicology, Biological Safety Research Center, National Institute of Health Sciences, Tokyo, Japan

4/2012 (5/12/2011) – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/21562709
Breast Cancer Res Treat. 2012 Apr;132(3):793-805. doi: 10.1007/s10549-011-1554-7. Epub 2011 May 12

2/2012 –
http://www.ncbi.nlm.nih.gov/m/pubmed/21512767
Mutational characterization of individual breast tumors: TP53 and PI3K pathway genes are frequently and distinctively mutated in different subtypes

12/2011 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/21683981
Hum Pathol. 2011 Dec;42(12):1823-32. doi: 10.1016/j.humpath.2011.02.015. Epub 2011 Jun 17

9/14/2011 – Tsuda A (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/21914223
Radiat Oncol. 2011 Sep 14;6:116. doi: 10.1186/1748-717X-6-116

7/2011 (2/11/1011) – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/21315415
Hum Pathol. 2011 Jul;42(7):998-1006. doi: 10.1016/j.humpath.2010.10.020. Epub 2011 Feb 11

5/2010 (3/5/2010) – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/20208478
p53 expression in tumor-stromal fibroblasts forming and not forming fibrotic foci in invasive ductal carcinoma of the breast
Mod Pathol. 2010 May;23(5):662-72. doi: 10.1038/modpathol.2010.47. Epub 2010 Mar 5
Pathology Consultation Service, Clinical Trials and Practice Support Division, Center for Cancer Control and Information Service, National Cancer Center, Chuo-ku, Tokyo, Japan

4/2010 (1/29/2010) – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/20118911
Mod Pathol. 2010 Apr;23(4):581-92. doi: 10.1038/modpathol.2010.3. Epub 2010 Jan 29

2/2010 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/19836055
p53 expression in tumor-stromal fibroblasts is closely associated with the nodal metastasis and outcome of patients with invasive ductal carcinoma who received neoadjuvant therapy
Hum Pathol. 2010 Feb;41(2):262-70. doi: 10.1016/j.humpath.2009.07.021
Clinical Trials and Practice Support Division, Pathology Consultation Service, Center for Cancer Control and Information Services, National Cancer Center, Tokyo 104-0045, Japan. thasebe@ncc.go.jp

11/2009 (8/6/2009) – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/19719774
p53 expression in tumor stromal fibroblasts is associated with the outcome of patients with invasive ductal carcinoma of the breast
Cancer Sci. 2009 Nov;100(11):2101-8. doi: 10.1111/j.1349-7006.2009.01307.x. Epub 2009 Aug 6
Pathology Consultation Service, Clinical Trials and Practice Support Division, Center for Cancer Control and Information Services, National Cancer Center, Tokyo, Japan. thasebe@ncc.go.jp

9/2009 (2/27/2009) – Tsuda M (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/19298529
J Cell Mol Med. 2009 Sep;13(9B):3251-9. doi: 10.1111/j.1582-4934.2009.00719.x. Epub 2009 Feb 27

7/2009 (5/7/2009) – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/19423649
Carcinogenesis. 2009 Jul;30(7):1139-46. doi: 10.1093/carcin/bgp116. Epub 2009 May 7

2009 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/20104994
Asian Pac J Cancer Prev. 2009;10(5):939-60

2009 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/19472036
Breast Cancer. 2009;16(3):186-201. doi: 10.1007/s12282-009-0124-x. Epub 2009 May 27

12/1/2007 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/18056462
Cancer Res. 2007 Dec 1;67(23):11353-8

10/2007 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/17786323
Int J Oncol. 2007 Oct;31(4):899-906

7/2007 (6/27/2007) – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/17594113
Virchows Arch. 2007 Jul;451(1):27-35. Epub 2007 Jun 27

6/28/2007 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/17682140
Nihon Rinsho. 2007 Jun 28;65 Suppl 6:60-7. Article in Japanese

2/8/2006 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/15876486
Establishment of an apoptosis-sensitive rat mammary carcinoma cell line with a mutation in the DNA-binding region of p53
Cancer Lett. 2006 Feb 8;232(2):279-88
Second Department of Surgery, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie 514-0001, Japan

12/2005 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/16311351
J Clin Pathol. 2005 Dec;58(12):1299-304

12/1/2005 – Tsuda M (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/16103879
Oncogene. 2005 Dec 1;24(54):7984-90

8/25/2005 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/1429209
High incidence of p53 gene mutation in human ovarian cancer and its association with nuclear accumulation of p53 protein and tumor DNA aneuploidy
http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.1992.tb02010.x/full

6/2005 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/15958052
Cancer Sci. 2005 Jun;96(6):309-16

2005 – Aging: gene silencing or gene activation?
http://www.ncbi.nlm.nih.gov/m/pubmed/15533642
Med Hypotheses. 2005;64(1):201-8

9/2004 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/15289842
Oncol Rep. 2004 Sep;12(3):587-91

5/2004
http://www.lef.org/magazine/mag2004/may2004_report_mystery_02.htm

(4/2004 – Tsuda T (Japan))
http://www.ncbi.nlm.nih.gov/m/pubmed/15863843
J Dermatol. 2005 Apr;32(4):236-42

3/2004 – The present state of antineoplaston research (1)
http://www.ncbi.nlm.nih.gov/m/pubmed/15035876
Integr Cancer Ther. 2004 Mar;3(1):47-58

2/2004 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/14991533
Hum Pathol. 2004 Feb;35(2):165-75

2004 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/15557791
Oncology. 2004;67(3-4):291-9

12/5/2003 – Tsuda M (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/14607246
Life Sci. 2003 Dec 5;74(2-3):189-97

12/2003 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/14675665
Gynecol Oncol. 2003 Dec;91(3):476-85

4/2003 – Tsuda S (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/12679488
J Clin Endocrinol Metab. 2003 Apr;88(4):1889-96

3/2003 – Tsuda T (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/12619108
The TP53 gene, tobacco exposure, and lung cancer
Hum Mutat. 2003 Mar;21(3):229-39
Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8593, USA

3/2003 (2/24/2003) – Tsuda T (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/12619108
The TP53 gene, tobacco exposure, and lung cancer
Hum Mutat. 2003 Mar;21(3):229-39
Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8593, USA
PDF:
http://p53.free.fr/Database/p53_cancer/Human_Mutation_p53/p53_Lung.pdf
Toshihide Tsuda*
Article first published online: 24 FEB 2003
DOI: 10.1002/humu.10177
http://onlinelibrary.wiley.com/doi/10.1002/humu.10177/abstract

1/14/2003
http://wellnesswillpower.com/wellness/2010/09/17/antineoplastons-and-dr-burzynski
Blog
http://www.killermovies.com/forums/archive/index.php/t-552231-cure-for-cancer.html

http://www.killermovies.com/forums/f11/t552231.html

http://kanker-aktueel.nl/EN/interview-with-dr-burzynski-antineoplastons-from-lef-magazine-about-antineoplastontherapie-and-how-it-works.html

2003 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/12931023
Oncology. 2003;65(2):159-66

7/2002 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/12149146
Jpn J Cancer Res. 2002 Jul;93(7):798-806

6/2002 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/12094701
Nihon Geka Gakkai Zasshi. 2002 Jun;103(6):487-91. Article in Japanese

4/2002 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/12055672
Relationship between p53 pathway and estrogen receptor status in endometrioid-type endometrial cancer
Hum Pathol. 2002 Apr;33(4):386-91
Department of Obstetrics and Gynecology, Osaka City University Graduate School of Medicine, Japan

1 – 2/2002 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/11748457
Oncol Rep. 2002 Jan-Feb;9(1):65-8.

2002 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/12016392
Histological grade, p53, HER2 and hormone receptor status of synchronous bilateral breast carcinoma
Breast Cancer. 2002;9(2):127-33
Department of Surgical Oncology, National Cancer Center Hospital, 1-1, Tsukiji 5-chome, Chuo-ku, Tokyo 104-0045, Japan. tfukutom@ncc.go.jp

2002 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/12196721
Breast Cancer. 2002;9(1):43-9

9/2001 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/11567230
Combined analysis of p53 and RB pathways in epithelial ovarian cancer
Hum Pathol. 2001 Sep;32(9):988-96
Department of Obstetrics and Gynecology, Osaka City General Hospital, Osaka, Japan

5/2001 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/11344480
Differences in estrogen receptor status, HER2, and p53 comparing metachronous bilateral breast carcinoma
J Surg Oncol. 2001 May;77(1):31-4
Department of Surgical Oncology, National Cancer Center Hospital, Tokyo, Japan

2001 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/11180771
Breast Cancer. 2001;8(1):79-83

4/2000 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/11026026
[p53 as a prognostic factor of breast cancers]
Nihon Rinsho. 2000 Apr;58 Suppl:413-7. Article in Japanese
Pathology Division, National Cancer Center Research Institute

4/2000 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/10849311
Pathol Int. 2000 Apr;50(4):263-72

1/2000 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/10770566
Jpn J Clin Oncol. 2000 Jan;30(1):30-2

1/2000 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/10649273
c-erbB-2 protein overexpression and p53 immunoreaction in primary and recurrent breast cancer tissues
J Surg Oncol. 2000 Jan;73(1):17-20
Department of Surgical Oncology, National Cancer Center Hospital, Tokyo, Japan

5/24/1999 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/10395176
Heterozygous p53-deficient mice are not susceptible to 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) carcinogenicity
Cancer Lett. 1999 May 24;139(2):177-82
Experimental Pathology and Chemotherapy Division, National Cancer Center Research Institute, Tokyo, Japan. bpark@gan2.res.ncc.go.jp

4/25/1999 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/11091703
Breast Cancer. 1999 Apr 25;6(2):121-126

3/1999 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/10051471
Hepatology. 1999 Mar;29(3):703-9

11/1998 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9838905
Gan To Kagaku Ryoho. 1998 Nov;25(13):2043-8. Article in Japanese

9 – 10/1998 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9732224
The possible prognostic significance of p53 immunostaining status of the primary tumor in patients developing local recurrence after breast-conserving surgery
Oncology. 1998 Sep-Oct;55(5):450-5
Department of Surgery, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan

7/29/1998 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/11091655
Breast Cancer. 1998 Jul 25;5(3):251-254

7/1998 – Tsuda S (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9680114
Significance of chromosomal alterations and mutations of the N-RAS and TP53 genes in relation to leukemogenesis of acute myeloid leukemia
Leuk Res. 1998 Jul;22(7):631-7
Division of Hematology, Kyoto Prefectural Yosanoumi Hospital, Japan

4/25/1998 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/11091649
Breast Cancer. 1998 Apr 25;5(2):201-204

3/1998 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9541186
Breast Cancer Res Treat. 1998 Mar;48(1):21-32

1/1998 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9491142
Jpn J Clin Oncol. 1998 Jan;28(1):47-9

1/1998 – Tsuda H (Japan )
http://www.ncbi.nlm.nih.gov/m/pubmed/9491134
Jpn J Clin Oncol. 1998 Jan;28(1):5-11

1998 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/18841336
Breast Cancer. 1998;5(3):251-4. doi: 10.1007/BF02966704

12/1997 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9437997
Prognostic indicators for breast cancer patients with one to three regional lymph node metastases, with special reference to alterations in expression levels of bcl-2, p53 and c-erbB-2 proteins
Jpn J Clin Oncol. 1997 Dec;27(6):371-7
Department of Clinical Oncology, National Cancer Center Hospital and Research Institute, Tokyo, Japan

11 – 12/1997 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9394843
Oncology. 1997 Nov-Dec;54(6):468-74

8/1997 – Tsuda T (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9262576
Ann Thorac Surg. 1997 Aug;64(2):363-7

6/1997 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9263537
Jpn J Cancer Res. 1997 Jun;88(6):590-9

3/1997 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9049201
Reduced p21(WAF1/CIP1) expression and p53 mutation in hepatocellular carcinomas
Hepatology. 1997 Mar;25(3):575-9
Pathology Division, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan

2/1997 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9119740
Demonstration of ras and p53 gene mutations in carcinomas in the forestomach and intestine and soft tissue sarcomas induced by N-methyl-N-nitrosourea in the rat
Jpn J Cancer Res. 1997 Feb;88(2):129-36
Second Department of Pathology, Fujita Health University School of Medicine, Toyoake

2/1997 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9070333
Histologic grade and p53 immunoreaction as indicators of early recurrence of node-negative breast cancer
Jpn J Clin Oncol. 1997 Feb;27(1):6-12
Pathology Division, National Cancer Center Research Institute, Tokyo, Japan

4/1996 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/8641970
Jpn J Cancer Res. 1996 Apr;87(4):385-94

3/1996 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/8702314
Gan To Kagaku Ryoho. 1996 Mar;23 Suppl 1:66-74. Article in Japanese

11/1995 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/8567395
Prognostic value of p53 protein accumulation in cancer cell nuclei in adenocarcinoma of the uterine cervix
Jpn J Cancer Res. 1995 Nov;86(11):1049-53
Pathology Division, National Cancer Center Research Institute and Hospital, Tokyo

10/31/1995 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/11091539
Breast Cancer. 1995 Oct 31;2(2):99-103

6/1995 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/7540234
Natural state of mutant p53 protein and heat shock protein 70 in breast cancer tissues
Lab Invest. 1995 Jun;72(6):707-14
Pathology Division, National Cancer Center Research Institute, Tokyo, Japan

4/14/1995 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/7736451
Cancer Lett. 1995 Apr 14;90(2):157-62

3/1995 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/9815981
Clin Cancer Res. 1995 Mar;1(3):261-7

12/30/1994 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/11091524
Bilateral Breast Cancer in a Patient with a Strong Family History of Cancer: Analysis of p53 Germ Line Mutations
Breast Cancer. 1994 Dec 30;1(2):151-155
Departments of Surgery, National Cancer Center Hospital, 5-1-1 Tsukiji, DChuo-ku, Tokyo 104, Japan

12/1/1994 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/7960232
Pathogenetic significance of p53 and c-Ki-ras gene mutations and human papillomavirus DNA integration in adenocarcinoma of the uterine cervix and uterine isthmus
Int J Cancer. 1994 Dec 1;59(5):601-6
Pathology Division, National Cancer Center Research Institute, Tokyo, Japan

8/15/1994 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/8062215
Different mutations of the p53 gene in nodule-in-nodule hepatocellular carcinoma as a evidence for multistage progression
Cancer Lett. 1994 Aug 15;83(1-2):197-200
http://www.science-direct.com/science/article/pii/0304383594903190

6/1994 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/7913600
Gan To Kagaku Ryoho. 1994 Jun;21 Suppl 2:172-7. Article in Japanese

5/15/1994 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/7910151
Association among p53 gene mutation, nuclear accumulation of the p53 protein and aggressive phenotypes in breast cancer
Tsuda H
Int J Cancer. 1994 May 15;57(4):498-503.
Pathology Division, National Cancer Center Research Institute, Tokyo, Japan

10/1993 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/8254955
Rinsho Byori. 1993 Oct;41(10):1081-90. Article in Japanese

10/1993 – Tsuda H ( Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/7902882
Rinsho Byori. 1993 Oct;41(10):1092-8. Article in Japanese

4/1993 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/8099903
Jpn J Cancer Res. 1993 Apr;84(4):394-401
Pathology Division, National Cancer Center Research Institute and Hospital, Tokyo

1993 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/8280380
Mutations of the p53 tumor suppressor gene and the ras gene family in intrahepatic cholangiocellular carcinomas in Japan and Thailand
(PMID:8280380)
Mol Carcinog. 1993;8(4):312-8
Molecular Carcinogenesis [1993, 8(4):312-318]
http://europepmc.org/abstract/MED/8280380
Pathology Division, National Cancer Center Research Institute, Tokyo, Japan
Type: Journal Article, Research Support, Non-U.S. Gov’t, Comparative Study
DOI: 10.1002/mc.2940080415

11/1992 (8/25/2005) – Hitoshi Tsuda (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/1336492
Frequent Occurrence of p53 Gene Mutations in Uterine Cancers at Advanced Clinical Stage and with Aggressive Histological Phenotype
Jpn J Cancer Res. 1992 Nov;83(11):1184-91
Pathology Division, National Cancer Center Research Institute, Tokyo
http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.1992.tb02743.x/full
Article first published online: 25 AUG 2005
DOI: 10.1111/j.1349-7006.1992.tb02743.x

11/1992 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/1330291
p53 gene mutation spectrum in hepatocellular carcinoma
Cancer Res. 1992 Nov 15;52(22):6358-64

9/1992 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/1429209
High incidence of p53 gene mutation in human ovarian cancer and its association with nuclear accumulation of p53 protein and tumor DNA aneuploidy
Jpn J Cancer Res. 1992 Sep;83(9):978-84

7/1992 – Tsuda H ( Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/1319827
Mutation pattern of the p53 gene as a diagnostic marker for multiple hepatocellular carcinoma
Cancer Res. 1992 Jul 1;52(13):3674-8

6/1/1992 – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/1591722
Cancer Res. 1992 Jun 1;52(11):3099-102

7/1991 (8/25/2005) – Tsuda H (Japan)
http://www.ncbi.nlm.nih.gov/m/pubmed/1679056
Nuclear p53 immunoreaction associated with poor prognosis of breast cancer
Jpn J Cancer Res. 1991 Jul;82(7):835-40
Pathology Division, National Cancer Center Research Institute, Tokyo
http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.1991.tb02710.x/full
Article first published online: 25 AUG 2005
DOI: 10.1111/j.1349-7006.1991.tb02710.x
http://ci.nii.ac.jp/naid/80005999302

http://ci.nii.ac.jp/naid/80006541912/en

http://ci.nii.ac.jp/naid/80006541912

http://ci.nii.ac.jp/naid/80006656284

1/21/2013
http://helpwithcancer.org/2013/01/fine-line-between-cancer-therapy-and-cancer-quackery.html
2006 (2012)
http://www.canceractive.com/cancer-active-page-link.aspx?n=1268&Title=Antineoplastons,%20missing%20Peptides%20and%20Burzynski

http://www.canceractive.com/cancer-active-page-link.aspx?n=1268

http://www.canceractive.com/cancer-active-page-link.aspx?n=3081&Title=Antineoplastons

http://www.canceractive.com/cancer-active-page-link.aspx?n=2594
5/2004
http://www.vitaminb17.org/an_interview_with_dr_burzynski.htm
2004 (3/21/2012)
http://kanker-aktueel.nl/EN/interview-with-dr-burzynski-antineoplastons-from-lef-magazine-about-antineoplastontherapie-and-how-it-works.html
6/1995
http://www.karlloren.com/biopsy/p60.htm
1994
http://www.alternative-doctor.com/cancer/mossinterview.htm
1994
http://worldwithoutcancer.org.uk/ralphmoss.html

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