| Literature DB >> 14646348 |
Anita Boyapati1, Eiki Kanbe, Dong-Er Zhang.
Abstract
Although most solid tumors contain inactivating mutations of the p53 tumor suppressor, hematological malignancies do not contain frequent alterations in the p53 gene (<20%). How these tumors arise in the presence of a super tumor suppressor like p53 remains to be elucidated. Given the number of downstream effectors of p53, it is likely that critical targets of p53 are inactivated in leukemia, bypassing the requirement for p53 gene mutations in these tumors. This review describes new biochemical and transcriptional activities of p53 as well as the status of p53 in acute myelogenous leukemia and chronic myelogenous leukemia. Copyright 2004 S. Karger AG, BaselEntities:
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Year: 2004 PMID: 14646348 DOI: 10.1159/000074489
Source DB: PubMed Journal: Acta Haematol ISSN: 0001-5792 Impact factor: 2.195