ArticleBlood2009
A retroviral mutagenesis screen reveals strong cooperation between Bcl11a overexpression and loss of the Nf1 tumor suppressor gene.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Review
- The BCL11A transcription factor stimulates the enzymatic activities of the OGG1 DNA glycosylase.Biological chemistry · 2024Article
- Article
- 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
- RNA-seq analysis reveals candidate genes associated with proliferation, invasion, and migration in BCL11A knockdown B-NHL cell lines.Annals of hematology · 2023Article
- SWI/SNF complexes in hematological malignancies: biological implications and therapeutic opportunities.Molecular cancer · 2023Review
- The DNA repair function of BCL11A suppresses senescence and promotes continued proliferation of triple-negative breast cancer cells.NAR cancer · 2022Article
- Arginine Methyltransferase PRMT7 Deregulates Expression of RUNX1 Target Genes in T-Cell Acute Lymphoblastic Leukemia.Cancers · 2022Article
- BCL11A promotes myeloid leukemogenesis by repressing PU.1 target genes.Blood advances · 2022Article
- The Impact ofPharmacogenomics and personalized medicine · 2022Article
- Selective Inhibition of JAK1 Primes STAT5-Driven Human Leukemia Cells for ATRA-Induced Differentiation.Targeted oncology · 2021Article
- Molecular analysis of the erythroid phenotype of a patient with BCL11A haploinsufficiency.Blood advances · 2021Article
- High Expression ofFrontiers in oncology · 2021Article
- Development and validation of a prognostic nomogram for patients with lung adenocarcinoma based on a novel 6-DNA repair-related gene signature.American journal of translational research · 2021Article
- The transcriptional repressor BCL11A promotes breast cancer metastasis.The Journal of biological chemistry · 2020Article
- Proteome and Phosphoproteome Changes Associated with Prognosis in Acute Myeloid Leukemia.Cancers · 2020Article
- BCL11A: a potential diagnostic biomarker and therapeutic target in human diseases.Bioscience reports · 2019Review
- Systematic analysis of the frequently amplified 2p15-p16.1 locus reveals PAPOLG as a potential proto-oncogene in follicular and transformed follicular lymphoma.Turkish journal of biology = Turk biyoloji dergisi · 2019Article
- Bcl11a Deficiency Leads to Hematopoietic Stem Cell Defects with an Aging-like Phenotype.Cell reports · 2016Article
- Global Cell Proteome Profiling, Phospho-signaling and Quantitative Proteomics for Identification of New Biomarkers in Acute Myeloid Leukemia Patients.Current pharmaceutical biotechnology · 2016Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
NF1 inactivation occurs in specific human cancers, including juvenile myelomonocytic leukemia, an aggressive myeloproliferative disorder of childhood. However, evidence suggests that Nf1 loss alone does not cause leukemia. We therefore hypothesized that inactivation of the Nf1 tumor suppressor gene requires cooperating mutations to cause acute leukemia. To search for candidate genes that cooperate with Nf1 deficiency in leukemogenesis, we performed a forward genetic screen using retroviral insertion mutagenesis in Nf1 mutant mice. We identified 43 common proviral insertion sites that contain candidate genes involved in leukemogenesis. One of these genes, Bcl11a, confers a growth advantage in cultured Nf1 mutant hematopoietic cells and causes early onset of leukemia of either myeloid or lymphoid lineage in mice when expressed in Nf1-deficient bone marrow. Bcl11a-expressing cells display compromised p21(Cip1) induction, suggesting that Bcl11a's oncogenic effects are mediated, in part, through suppression of p21(Cip1). Importantly, Bcl11a is expressed in human chronic myelomonocytic leukemia and juvenile myelomonocytic leukemia samples. A subset of AML patients, who had poor outcomes, of 16 clusters, displayed high levels of BCL11A in leukemic cells. These findings suggest that deregulated Bcl11a cooperates with Nf1 in leukemogenesis, and a therapeutic strategy targeting the BCL11A pathway may prove beneficial in the treatment of leukemia.
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Registered trials
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