Haploinsufficiency of Bcl11b suppresses the progression of ATM-deficient T cell lymphomas

J Hematol Oncol. 2015 Jul 30;8:94. doi: 10.1186/s13045-015-0191-8.


Bcl11b is a transcription factor important for T cell development and also a tumor-suppressor gene that is hemizygously inactivated in ~10% human T cell acute lymphoblastic leukemia (T-ALL) and several murine T-ALL models, including ATM(-/-) thymic lymphomas. Here we report that heterozygous loss of Bcl11b (Bcl11b(+/-)) unexpectedly reduced lethal thymic lymphoma in ATM(-/-) mice by suppressing lymphoma progression, but not initiation. The suppression was associated with a T cell-mediated immune response in ATM(-/-)Bcl11b(+/-) mice, revealing a haploid insufficient function of Bcl11b in immune modulation against lymphoma and offering an explanation for the complex relationship between Bcl11b status with T-ALL prognosis.

Publication types

  • Letter
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Disease Progression
  • Gene Expression Regulation
  • Haploinsufficiency / immunology*
  • Humans
  • Lymphoma, T-Cell / immunology*
  • Lymphoma, T-Cell / pathology
  • Mice
  • Repressor Proteins / metabolism*
  • Tumor Suppressor Proteins / metabolism*


  • Repressor Proteins
  • Tumor Suppressor Proteins