p53 mutations in human lymphoid malignancies: association with Burkitt lymphoma and chronic lymphocytic leukemia.

Titlep53 mutations in human lymphoid malignancies: association with Burkitt lymphoma and chronic lymphocytic leukemia.
Publication TypeJournal Article
Year of Publication1991
AuthorsGaidano G, Ballerini P, Gong JZ, Inghirami G, Neri A, Newcomb EW, Magrath IT, Knowles DM, Dalla-Favera R
JournalProc Natl Acad Sci U S A
Volume88
Issue12
Pagination5413-7
Date Published1991 Jun 15
ISSN0027-8424
KeywordsBase Sequence, Burkitt Lymphoma, Electrophoresis, Polyacrylamide Gel, Humans, Leukemia, B-Cell, Leukemia, Lymphocytic, Chronic, B-Cell, Leukemia, T-Cell, Molecular Sequence Data, Mutation, Polymerase Chain Reaction, Polymorphism, Genetic, Tumor Suppressor Protein p53
Abstract

We have investigated the frequency of p53 mutations in B- and T-cell human lymphoid malignancies, including acute lymphoblastic leukemia, the major subtypes of non-Hodgkin lymphoma, and chronic lymphocytic leukemia. p53 exons 5-9 were studied by using genomic DNA from 197 primary tumors and 27 cell lines by single-strand conformation polymorphism analysis and by direct sequencing of PCR-amplified fragments. Mutations were found associated with (i) Burkitt lymphoma (9/27 biopsies; 17/27 cell lines) and its leukemic counterpart L3-type B-cell acute lymphoblastic leukemia (5/9), both of which also carry activated c-myc oncogenes, and (ii) B-cell chronic lymphocytic leukemia (6/40) and, in particular, its stage of progression known as Richter's transformation (3/7). Mutations were not found at any significant frequency in other types of non-Hodgkin lymphoma or acute lymphoblastic leukemia. In many cases, only the mutated allele was detectable, implying loss of the normal allele. These results suggest that (i) significant differences in the frequency of p53 mutations are present among subtypes of neoplasms derived from the same tissue; (ii) p53 may play a role in tumor progression in B-cell chronic lymphocytic leukemia; (iii) the presence of both p53 loss/inactivation and c-myc oncogene activation may be important in the pathogenesis of Burkitt lymphoma and its leukemic form L3-type B-cell acute lymphoblastic leukemia.

DOI10.1073/pnas.88.12.5413
Alternate JournalProc Natl Acad Sci U S A
PubMed ID2052620
PubMed Central IDPMC51883
Grant ListCA40236 / CA / NCI NIH HHS / United States
CA44029 / CA / NCI NIH HHS / United States
EY06337 / EY / NEI NIH HHS / United States
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Giorgio Inghirami, M.D.

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