ArticleJournal of hematology & oncology2015
Haploinsufficiency of Bcl11b suppresses the progression of ATM-deficient T cell lymphomas.
Article in Journal of hematology & oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Dual role ofBlood science (Baltimore, Md.) · 2024Review
- ATM-deficient murine thymic T-cell lymphoblastic lymphomas are PTEN-deficient and require AKT signaling for survival.PloS one · 2024Article
- The oncogenetic landscape and clinical impact ofHaematologica · 2023Article
- BCL11B suppresses tumor progression and stem cell traits in hepatocellular carcinoma by restoring p53 signaling activity.Cell death & disease · 2020Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
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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Registered trials
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