Article
Activating c-KIT mutations confer oncogenic cooperativity and rescue RUNX1/ETO-induced DNA damage and apoptosis in human primary CD34+ hematopoietic progenitors.
Leukemia - 1 Feb 2015
Wichmann C, Quagliano-Lo Coco I, Yildiz Ö, Chen-Wichmann L, Weber H, Syzonenko T, Döring C, Brendel C, Ponnusamy K, Kinner A, Brandts C, Henschler R, Grez M
Abstract excerpt
The RUNX1/ETO (RE) fusion protein, which originates from the t(8;21) chromosomal rearrangement, is one of the most frequent translocation products found in de novo acute myeloid leukemia (AML). In RE leukemias, activated forms of the c-KIT tyrosine kinase receptor are frequently found, thereby suggesting oncogenic cooperativity between these oncoproteins in the development and maintenance of t(8;21) malignancies....
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