1INTRODUCTIONHuman B‐cell acute lymphoblastic leukemia (B‐ALL) is characterized by clonal expansion of developmentally arrested malignant B‐cell precursors, accounting for 83% of ALLs and 30–40% of all childhood cancers. Despite our current knowledge of the cytogenetics of this disease, obstacles to relapse‐free survival remain for up to 15% of children and the majority of adult with this disease. B‐cell chronic lymphocytic leukemia (CLL)/lymphoma 11 a (Bcl11a) is a krüppel transcription factor that was initially discovered as a retroviral insertion site (Evi9) in myeloid leukemia in the BXH‐2 mouse, and closely related to B‐cell proliferation and differentiation. Subsequently, Bcl11a was found to be associated with human malignant B cells, overexpression of which is primarily found in B‐cell lymphoma and B‐cell CLL.The Bcl11a transcription factor is also aberrantly‐expressed in some persons with acute myeloid leukemia, and increased in subjects with chronic myeloid leukemia in acute phase compared with those in normal and in subjects in chronic phase including some subjects studied in both phases. Our previous study also showed the expression levels of Bcl11a in B CLL and B‐cell lymphoma was significantly higher than those in the healthy control. However, the role of Bcl11a in B‐ALL patients has not been reported. Meanwhile,
Asia-Pacific Journal of Clinical Oncology – Wiley
Published: Jan 1, 2018
Keywords: ; ; ; ; ;
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