BCR-ABL promotes PTEN downregulation in chronic myeloid leukemia.
basic_science · Level V
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- Record sourced from PubMed, PMID 25343485.
- Also identified by DOI 10.1371/journal.pone.0110682 and PMC identifier PMC3643208.
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Abstract
Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by the t(9;22) translocation coding for the chimeric protein p210 BCR-ABL. The tumor suppressor PTEN plays a critical role in the pathogenesis of CML chronic phase, through non genomic loss of function mechanisms, such as protein down-regulation and impaired nuclear/cytoplasmic shuttling. Here we demonstrate that BCR-ABL promotes PTEN downregulation through a MEK dependent pathway. Furthermore, we describe a novel not recurrent N212D-PTEN point mutation found in the EM2 blast crisis cell line.