Ontology highlight
ABSTRACT:
SUBMITTER: Qi J
PROVIDER: S-EPMC4636961 | biostudies-literature | 2015 Nov
REPOSITORIES: biostudies-literature
Qi Jing J Singh Sandeep S Hua Wei-Kai WK Cai Qi Q Chao Shi-Wei SW Li Ling L Liu Hongjun H Ho Yinwei Y McDonald Tinisha T Lin Allen A Marcucci Guido G Bhatia Ravi R Huang Wei-Jan WJ Chang Chung-I CI Kuo Ya-Huei YH
Cell stem cell 20150918 5
Acute myeloid leukemia (AML) is driven and sustained by leukemia stem cells (LSCs) with unlimited self-renewal capacity and resistance to chemotherapy. Mutation in the TP53 tumor suppressor is relatively rare in de novo AML; however, p53 can be regulated through post-translational mechanisms. Here, we show that p53 activity is inhibited in inv(16)(+) AML LSCs via interactions with the CBFβ-SMMHC (CM) fusion protein and histone deacetylase 8 (HDAC8). HDAC8 aberrantly deacetylates p53 and promotes ...[more]