| Literature DB >> 27285855 |
Jiawei Yin1, Fan Zhang1, Huiquan Tao1, Xiao Ma2, Guangsong Su1, Xiaoli Xie1, Zhongjuan Xu1, Yanwen Zheng1, Hong Liu2, Chao He1, Zhengwei Jenny Mao3, Zhiwei Wang1, Weirong Chang2, Robert Peter Gale4, Depei Wu5, Bin Yin6.
Abstract
Chronic myeloid leukemia (CML) has chronic and acute phases. In chronic phase myeloid differentiation is preserved whereas in acute phase myeloid differentiation is blocked. Acute phase CML resembles acute myeloid leukemia (AML). Chronic phase CML is caused by BCR-ABL1. What additional mutation(s) cause transition to acute phase is unknown and may differ in different persons with CML. BCL11A encodes a transcription factor and is aberrantly-expressed in several haematological and solid neoplasms. We analyzed BCL11A mRNA levels in subjects with chronic and acute phase CML. BCL11A transcript levels were increased in subjects with CML in acute phase compared with those in normals and in subjects in chronic phase including some subjects studied in both phases. BCL11A mRNA levels were correlated with percent bone marrow blasts and significantly higher in lymphoid versus myeloid blast crisis. Differentiation of K562 with butyric acid, a CML cell line, decreased BCL11A mRNA levels. Cytology and flow cytometry analyses showed that ectopic expression of BCL11A in K562 cells blocked differentiation. These data suggest BCL11A may operate in transformation of CML from chronic to acute phase in some persons.Entities:
Keywords: BCL11A expression; Chronic myeloid leukemia; Differentiation; Leukemia
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Year: 2016 PMID: 27285855 DOI: 10.1016/j.leukres.2016.05.018
Source DB: PubMed Journal: Leuk Res ISSN: 0145-2126 Impact factor: 3.156