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

Overview of attention for article published in Journal of Hematology & Oncology, July 2015
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Title
Haploinsufficiency of Bcl11b suppresses the progression of ATM-deficient T cell lymphomas
Published in
Journal of Hematology & Oncology, July 2015
DOI 10.1186/s13045-015-0191-8
Pubmed ID
Authors

Kerice A. Pinkney, Wenxia Jiang, Brian J. Lee, Denis G. Loredan, Chen Li, Govind Bhagat, Shan Zha

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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Mendeley readers

The data shown below were compiled from readership statistics for 12 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 12 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 3 25%
Professor 2 17%
Other 2 17%
Student > Master 2 17%
Professor > Associate Professor 1 8%
Other 0 0%
Unknown 2 17%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 33%
Immunology and Microbiology 3 25%
Agricultural and Biological Sciences 1 8%
Arts and Humanities 1 8%
Medicine and Dentistry 1 8%
Other 1 8%
Unknown 1 8%