Li C C, O'Connell C D, Beckwith M, Longo D L
Biological Carcinogenesis and Development Program, Inc/Dyncorp, Frederick, MD, USA.
Leukemia. 1995 Apr;9(4):650-5.
The p53 tumor suppressor gene is frequently mutated within its evolutionarily conserved regions in a number of human cancers. Previous reports demonstrated mutations of this gene in both Burkitt's lymphoma and B cell chronic lymphocytic leukemia. However, dissimilar results were obtained in non-Hodgkin's lymphoma (NHL). In one study, no mutation was detected in 43 NHL tissues. A second study reported p53 mutations in eight (all with advanced stage disease) out of 48 tissues obtained from Japanese NHL patients. Using both immunoblotting and radio-immunoprecipitation, we detected mutant p53 proteins in nine out of 10 B cell lines established from NHL tissues. The mutations were confirmed by reverse transcription polymerase chain reaction-mediated single-strand conformational polymorphism (RT-PCR-SSCP) analysis in eight cell lines. The high frequency of p53 mutation in NHL B cell lines and the relatively low frequency of p53 mutations in fresh lymphoma tissue suggests that p53 gene alteration may play a role in lymphomagenesis and/or disease progression in a subset of B cell lymphomas and that the p53 mutation conveys a proliferative advantage on lymphoma cells that permits their in vitro growth.