Wip1 and p53 contribute to HTLV-1 Tax-induced tumorigenesis.

ABSTRACT:

Background

Human T-cell Leukemia Virus type 1 (HTLV-1) infects 20 million individuals world-wide and causes Adult T-cell Leukemia/Lymphoma (ATLL), a highly aggressive T-cell cancer. ATLL is refractory to treatment with conventional chemotherapy and fewer than 10% of afflicted individuals survive more than 5 years after diagnosis. HTLV-1 encodes a viral oncoprotein, Tax, that functions in transforming virus-infected T-cells into leukemic cells. All ATLL cases are believed to have reduced p53 activity although only a minority of ATLLs have genetic mutations in their p53 gene. It has been suggested that p53 function is inactivated by the Tax protein.

Results

Using genetically altered mice, we report here that Tax expression does not achieve a functional equivalence of p53 inact

SUBMITTER: Zane L 

PROVIDER: S-EPMC3532233 | biostudies-literature | 2012 Dec

REPOSITORIES: biostudies-literature