Tumor suppressor promotes some acute myeloid leukemias, study reveals

3f3ff19d15460279cd9e094bdc487343Mutant hematopoietic stem cells in the bone marrow proliferate and fail to differentiate into white blood cells in Acute myeloid leukemia (AML). FLT3 is one of the most common genes mutated; however mutated FLT3 alone is not sufficient in leading to AML. Researchers have found that some patients with mutated FLT3 often have elevated levels of another protein RUNX1, which has been believed to be a tumor suppressor. Surprisingly, they reported that coexpression of RUNX1 with FLT3 blocks the differentiation of white blood cells by inducing another transcription factor Hhex. They proposed RUNX1 may suppress activation of AML initially; however, FLT3 inactivation may lead to RUNX1 activation that would promote tumor growth. Reducing RUNX1 in cancer stem cells may be deleterious but not in normal cells thus providing a selective target for potential interventions.

 

References:

1.https://www.sciencedaily.com/releases/2017/02/170217095930.htm

2.Kira Behrens, Katrin Maul, Nilgün Tekin, Neele Kriebitzsch, Daniela Indenbirken, Vladimir Prassolov, Ursula Müller, Hubert Serve, Jörg Cammenga, Carol Stocking. RUNX1 cooperates with FLT3-ITD to induce leukemia. The Journal of Experimental Medicine, 2017; jem.20160927 DOI

Article Summary Courtesy: Jennifer Lu and Waleed Khan

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