Cancer Research Cell Death Mechanisms and Cancer Therapy  Jordan
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

[Cancer Research 52, 4273-4276, August 1, 1992]
© 1992 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bhatia, K. G.
Right arrow Articles by Magrath, I. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bhatia, K. G.
Right arrow Articles by Magrath, I. T.

The Pattern of p53 Mutations in Burkitt's Lymphoma Differs from That of Solid Tumors

Kishor G. Bhatia1, Marina I. Gutiérrez2, Konrad Huppi, David Siwarski and Ian T. Magrath

Pediatric Branch [K. G. B., M. I. G., I. T. M.], Clinical Oncology Program, and Molecular Genetics Section [K. H., D. S.], Laboratory of Genetics, National Cancer Institute, Bethesda, Maryland 20892

Available evidence suggests that, among hematological malignancies, p53 is most often mutated in Burkitt's lymphoma (BL). However, much of the published data is based on cell lines. We have, therefore, analyzed BL biopsies to determine more accurately the frequency and pattern of p53 mutations in primary tumors and to determine whether there are differences among the various subtypes of BL. Among 27 BL biopsies from South America, we have observed mutations in the p53 gene (exons 5 through 8) in 37% of tumors. The higher frequency of mutations in cell lines (70%) suggests that mutation of p53 may be associated with tumor progression. Summarizing available data we conclude that the presence of mutated p53 in BL is independent of the geographic origin of the tumor, the 8;14 chromosomal breakpoint locations and Epstein-Barr virus association. We also find that the mutational spectrum of p53 in BL differs from that observed in nonlymphoid tumors. More than 50% of mutations in BL are clustered in a small stretch of 33 amino acids (codons 213 to 248). Interestingly, codon 213 appears to be as frequently mutated as codon 248. Conversely, codon 273, often mutated in solid tumors, is rarely involved in BL.

1 To whom requests for reprints should be addressed, at National Institutes of Health, National Cancer Institute-POB, Building 10, Room 13N240, Bethesda, MD 20892.

2 Supported by a Fellowship from the Cancer Research Foundation of America.

Received 4/15/92. Accepted 6/15/92.




This article has been cited by other articles:


Home page
Proc. Natl. Acad. Sci. USAHome page
K. T. Bieging, A. C. Amick, and R. Longnecker
Epstein-Barr virus LMP2A bypasses p53 inactivation in a MYC model of lymphomagenesis
PNAS, October 20, 2009; 106(42): 17945 - 17950.
[Abstract] [Full Text] [PDF]


Home page
BloodHome page
K. A. Blum, G. Lozanski, and J. C. Byrd
Adult Burkitt leukemia and lymphoma
Blood, November 15, 2004; 104(10): 3009 - 3020.
[Abstract] [Full Text] [PDF]


Home page
JNCI J Natl Cancer InstHome page
M. I. Gutierrez, M. M. Ibrahim, J. K. Dale, T. C. Greiner, S. E. Straus, and K. Bhatia
Discrete Alterations in the BZLF1 Promoter in Tumor and Non-Tumor-Associated Epstein-Barr Virus
J Natl Cancer Inst, December 4, 2002; 94(23): 1757 - 1763.
[Abstract] [Full Text] [PDF]


Home page
BloodHome page
R. M. Braziel, D. A. Arber, M. L. Slovak, M. L. Gulley, C. Spier, C. Kjeldsberg, J. Unger, T. P. Miller, R. Tubbs, C. Leith, et al.
The Burkitt-like lymphomas: a Southwest Oncology Group study delineating phenotypic, genotypic, and clinical features
Blood, June 15, 2001; 97(12): 3713 - 3720.
[Abstract] [Full Text] [PDF]


Home page
Clin. Cancer Res.Home page
R. E. Buller, T. A. Lallas, M. S. Shahin, A. K. Sood, M. Hatterman-Zogg, B. Anderson, J. I. Sorosky, and P. A. Kirby
The p53 Mutational Spectrum Associated with BRCA1 Mutant Ovarian Cancer
Clin. Cancer Res., April 1, 2001; 7(4): 831 - 838.
[Abstract] [Full Text]


Home page
BloodHome page
U. Klangby, I. Okan, K. P. Magnusson, M. Wendland, P. Lind, and K. G. Wiman
p16/INK4a and p15/INK4b Gene Methylation and Absence of p16/INK4a mRNA and Protein Expression in Burkitt's Lymphoma
Blood, March 1, 1998; 91(5): 1680 - 1687.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
M. N. Uittenbogaard, H. A. Giebler, D. Reisman, and J. K. Nyborg
Transcriptional Repression of p53 by Human T-cell Leukemia Virus Type I Tax Protein
J. Biol. Chem., December 1, 1995; 270(48): 28503 - 28506.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1992 by the American Association for Cancer Research.