Although the fusion alone did not transform murine c-Kit+ bone marrow cells, 45.4% of 14q32 non-rearranged AML cases were also BCL11B-positive, suggesting a more general and complex mechanism of leukemogenesis associated with BCL11B expression.
Our genetic and functional data provide the first evidence that a reduction in the level of the BCL11B protein is a key event in the multistep progression of ATLL leukemogenesis.
This review describes phenotypes given by loss of Bcl11b and roles of Bcl11b in cell proliferation, differentiation and apoptosis, taking tissue development and lymphomagenesis into consideration.