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Abl1 deletion in gut stem cells suppresses p53 induction and promotes colitis-associated tumor formation 
Guo Yu1 , Jie Fu2 , Ana Romo3 , Baojie Li1 , Huijuan Liu1,*
1Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai 200240, China
2School of Basic Medical Science, Xinxiang Medical University, Xinxiang 453003, China
3Laboratory of Stem Cells and Gene Therapy, Instituto Tecnolo´gico de Chascomu´s (INTECH), CONICET-UNSAM, Chascomu´s, Buenos Aires, Argentina
*Correspondence to:Huijuan Liu , Email:liuhj@sjtu.edu.cn
J Mol Cell Biol, Volume 12, Issue 9, September 2020, 738-740,  https://doi.org/10.1093/jmcb/mjaa022

Dear Editor,

Abl1, when fused with BCR, expresses fusion protein BCR‒ABL that underlies the etiology of chronic myeloid leukemia and is therapeutically targeted by Imatinib Mesylate (Khatri et al., 2016). However, the function of proto-oncogene product Abl1 remains not fully understood. This non-receptor tyrosine kinase can be activated by growth factors, DNA damage, oxidative stress, and microbial pathogens (Wang, 2014). Cell-based studies suggest that Abl1 phosphorylates proteins in DNA damage response (DDR) and other signaling pathways, promoting p53 expression as well as cell cycle arrest and apoptosis (Gonfloni et al., 2009). Abl1 deletion leads to runtedness, osteoporosis, and other developmental defects in mice. Interestingly, it has been reported that Abl1 kinase is activated in many solid tumors and Abl1 is implicated in EphB2-mediated intestinal adenoma growth and colorectal cancer (CRC) invasion and metastasis (Kundu et al., 2015; Sonoshita et al., 2015). However, a recent study showed that Abl1 expression is reduced in most CRC patient samples (Uhlen et al., 2015). Thus, the function of Abl1 in CRC initiation warrants further investigation.