ReviewLeukemia2013
B-lineage transcription factors and cooperating gene lesions required for leukemia development.
Review in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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.
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.
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Who cites it
45 citing papers in PubMed, 90 citations in OpenAlex.
- Common genetic variants associated with resting oxygenation in chronic obstructive pulmonary disease.American journal of respiratory cell and molecular biology · 2014Trial
- Loss of TBL1XR1 disrupts glucocorticoid receptor recruitment to chromatin and results in glucocorticoid resistance in a B-lymphoblastic leukemia model.The Journal of biological chemistry · 2014Trial
- Article
- SUMOylation inhibition potentiates the glucocorticoid receptor to program growth arrest of acute lymphoblastic leukemia cells.Oncogene · 2025Article
- Enhancer engagement sustains oncogenic transformation and progression of B-cell precursor acute lymphoblastic leukemia.Journal of experimental & clinical cancer research : CR · 2024Article
- B-cells absence in patients diagnosed as inborn errors of immunity: a registry-based study.Immunogenetics · 2024Article
- SIMBA: single-cell embedding along with features.Nature methods · 2024Article
- Spatial Transcriptomics Resolve an Emphysema-Specific Lymphoid Follicle B Cell Signature in Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2024Article
- Analyses of Genes Critical to Tumor Survival Reveal Potential 'Supertargets': Focus on Transcription.Cancers · 2023Article
- Epigenomic landscape exhibits interferon signaling suppression in the patient of myocarditis after BNT162b2 vaccination.Scientific reports · 2023Article
- Oncogenic TYK2 P760L kinase is effectively targeted by combinatorial TYK2, mTOR and CDK4/6 kinase blockade.Haematologica · 2023Article
- IRF4 deficiency vulnerates B-cell progeny for leukemogenesis via somatically acquired Jak3 mutations conferring IL-7 hypersensitivity.Cell death and differentiation · 2022Article
- The molecular hallmarks of primary and secondary vitreoretinal lymphoma.Blood advances · 2022Article
- Review
- P38 MAPK/AKT signalling is involved in IL-33-mediated anti-apoptosis in childhood acute lymphoblastic leukaemia blast cells.Annals of medicine · 2021Article
- Thyroid Hormone Receptor α1 Mutants Impair B Lymphocyte Development in a Mouse Model.Thyroid : official journal of the American Thyroid Association · 2021Article
- Genome-wide interference of ZNF423 with B-lineage transcriptional circuitries in acute lymphoblastic leukemia.Blood advances · 2021Article
- Recent Advances in Molecular Diagnosis and Prognosis of Childhood B Cell Lineage Acute Lymphoblastic Leukemia (B-ALL).Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2021Review
- Article
- A small molecular compound CC1007 induces cross-lineage differentiation by inhibiting HDAC7 expression and HDAC7/MEF2C interaction in BCR-ABL1Cell death & disease · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Differentiation of hematopoietic stem cells into B lymphocytes requires the concerted action of specific transcription factors, such as RUNX1, IKZF1, E2A, EBF1 and PAX5. As key determinants of normal B-cell development, B-lineage transcription factors are frequently deregulated in hematological malignancies, such as B-cell precursor acute lymphoblastic leukemia (BCP-ALL), and affected by either chromosomal translocations, gene deletions or point mutations. However, genetic aberrations in this developmental pathway are generally insufficient to induce BCP-ALL, and often complemented by genetic defects in cytokine receptors and tyrosine kinases (IL-7Rα, CRLF2, JAK2 and c-ABL1), transcriptional cofactors (TBL1XR1, CBP and BTG1), as well as the regulatory pathways that mediate cell-cycle control (pRB and INK4A/B). Here we provide a detailed overview of the genetic pathways that interact with these B-lineage specification factors, and describe how mutations affecting these master regulators together with cooperating lesions drive leukemia development.
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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.