Selection for loss of p53 function in T-cell lymphomagenesis is alleviated by Moloney murine leukemia virus infection in myc transgenic mice.

ABSTRACT: Thymic lymphomas induced by Moloney murine leukemia virus (MMLV) have provided many examples of oncogene activation, but the role of tumor suppressor pathways in these tumors is less clear. These tumors display little evidence of loss of heterozygosity, and MMLV is only weakly synergistic with the Trp53 null genotype, suggesting that viral lymphomagenesis involves mechanisms which do not require mutational loss of Trp53 function. To explore this relationship in greater depth, we infected CD2-myc transgenic mice with MMLV and examined the role of Trp53 in the genesis of these tumors. Most (19 of 27) of the tumors from MMLV-infected, CD2-myc Trp53(+/-) mice retained the wild-type Trp53 allele in vivo while tumors of uninfected CD2-myc Trp53(+/-) mice invariably showed allele loss from a sign

SUBMITTER: Baxter EW 

PROVIDER: S-EPMC114551 | biostudies-literature | 2001 Oct

REPOSITORIES: biostudies-literature