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Updated: Apr 6, 2026

Derivation of Thymic Lymphoma T-cell Lines from Atm-/- and p53-/- Mice
Published on: April 3, 2011
Haploinsufficiency of Bcl11b suppresses the progression of ATM-deficient T cell lymphomas
Kerice A Pinkney1,2, Wenxia Jiang3,4, Brian J Lee5
1Department of Pediatrics, Division of Hematology, Oncology and Stem Cell Transplantation, Columbia University, 1130 St Nicholas Ave, New York, NY, 10032, USA. kpinkney@mhs.net.
Abstract:
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.
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