Trial reportBlood2011
The BCL11B tumor suppressor is mutated across the major molecular subtypes of T-cell acute lymphoblastic leukemia.
Trial report in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
116 citing papers in PubMed, 1 synthesis or guideline pooled it, 189 citations in OpenAlex.
- Pooled it
- Trial
- A De Novo heterozygous frameshift mutation identified in BCL11B causes neurodevelopmental disorder by whole exome sequencing.Molecular genetics & genomic medicine · 2019Trial
- SAMHD1 is recurrently mutated in T-cell prolymphocytic leukemia.Blood cancer journal · 2018Trial
- The role of epigenetic modifications in hematological cancers.Frontiers in oncology · 2026Review
- The transcription factor BCL11B drives NK cell cytotoxicity and antitumor activity.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Novel classification system and high-risk categories of pediatric acute myeloid leukemia.Haematologica · 2025Review
- Possible impacts of cosmic radiation on leukemia development during human deep space exploration.Leukemia · 2025Review
- Identification of novel genetic mutations for the treatment prognostication of canine lymphoma.NPJ precision oncology · 2025Article
- Impact of Tyrosine Kinase Inhibitors on the Expression Pattern of Epigenetic Regulators.Cancers · 2025Article
- Targeting BCL11B in CAR-engineered lymphoid progenitors drives NK-like cell development with prolonged anti-leukemic activity.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- DNA-binding affinity and specificity determine the phenotypic diversity in BCL11B-related disorders.American journal of human genetics · 2025Article
- ATM in immunobiology: From lymphocyte development to cancer immunotherapy.Translational oncology · 2025Review
- Dual role ofBlood science (Baltimore, Md.) · 2024Review
- Drive to survive: gene dependency in T-cell acute lymphoblastic leukemia.Haematologica · 2024Article
- Acute lymphoblastic leukaemia.Nature reviews. Disease primers · 2024Review
- Pivotal role of BCL11B in the immune, hematopoietic and nervous systems: a review of the BCL11B-associated phenotypes from the genetic perspective.Genes and immunity · 2024Review
- Immunophenotypic but Not Genetic Changes Reclassify the Majority of Relapsed/Refractory Pediatric Cases of Early T-Cell Precursor Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024Article
- The function of BCL11B in base excision repair contributes to its dual role as an oncogene and a haplo-insufficient tumor suppressor gene.Nucleic acids research · 2024Article
- Mutations atMolecular and cellular biology · 2024Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 7 institutions in 1 country.
Funding
Abstract
The BCL11B transcription factor is required for normal T-cell development, and has recently been implicated in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL) induced by TLX overexpression or Atm deficiency. To comprehensively assess the contribution of BCL11B inactivation to human T-ALL, we performed DNA copy number and sequencing analyses of T-ALL diagnostic specimens, revealing monoallelic BCL11B deletions or missense mutations in 9% (n = 10 of 117) of cases. Structural homology modeling revealed that several of the BCL11B mutations disrupted the structure of zinc finger domains required for this transcription factor to bind DNA. BCL11B haploinsufficiency occurred across each of the major molecular subtypes of T-ALL, including early T-cell precursor, HOXA-positive, LEF1-inactivated, and TAL1-positive subtypes, which have differentiation arrest at diverse stages of thymocyte development. Our findings provide compelling evidence that BCL11B is a haploinsufficient tumor suppressor that collaborates with all major T-ALL oncogenic lesions in human thymocyte transformation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.