ReviewFrontiers in oncology2019
Towards a Better Understanding of Cohesin Mutations in AML.
Review in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Solubility based mechanistic profiling of combinatorial drug therapy.Nature communications · 2026Article
- Association of DNA damage response gene polymorphisms with treatment response and prognosis in acute myeloid leukemia.Journal of Cancer · 2026Article
- Down syndrome and leukemia: from basic mechanisms to clinical advances.Haematologica · 2023Review
- Epigenetic regulation by ASXL1 in myeloid malignancies.International journal of hematology · 2023Review
- Clinical and prognostic impact of STAG2 mutations in myeloid neoplasms: the Mayo Clinic experience.Blood advances · 2023Article
- An Updated Overview of the Role of CYP450 during Xenobiotic Metabolization in Regulating the Acute Myeloid Leukemia Microenvironment.International journal of molecular sciences · 2023Review
- Clinical, Mutational, and Transcriptomic Characteristics in Elderly Korean Individuals With Clonal Hematopoiesis Driver Mutations.Annals of laboratory medicine · 2023Article
- Novel Molecular Insights into Leukemic Evolution of Myeloproliferative Neoplasms: A Single Cell Perspective.International journal of molecular sciences · 2022Review
- Interpretation of the role of germline and somatic non-coding mutations in cancer: expression and chromatin conformation informed analysis.Clinical epigenetics · 2022Review
- ASXL1/2 mutations and myeloid malignancies.Journal of hematology & oncology · 2022Review
- Genetic variation as a long-distance modulator of RAD21 expression in humans.Scientific reports · 2022Article
- Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML.Cancer discovery · 2022Article
- The glucocorticoid receptor associates with the cohesin loader NIPBL to promote long-range gene regulation.Science advances · 2022Article
- Article
- Molecular Systems Architecture of Interactome in the Acute Myeloid Leukemia Microenvironment.Cancers · 2022Review
- Review
- Review
- Low tolerance for transcriptional variation at cohesin genes is accompanied by functional links to disease-relevant pathways.Journal of medical genetics · 2021Article
- Increased risk of leukaemia in children with Down syndrome: a somatic evolutionary view.Expert reviews in molecular medicine · 2021Article
- Characteristics of Cohesin Mutation in Acute Myeloid Leukemia and Its Clinical Significance.Frontiers in oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Classical driver mutations in acute myeloid leukemia (AML) typically affect regulators of cell proliferation, differentiation, and survival. The selective advantage of increased proliferation, improved survival, and reduced differentiation on leukemia progression is immediately obvious. Recent large-scale sequencing efforts have uncovered numerous novel AML-associated mutations. Interestingly, a substantial fraction of the most frequently mutated genes encode general regulators of transcription and chromatin state. Understanding the selective advantage conferred by these mutations remains a major challenge. A striking example are mutations in genes of the cohesin complex, a major regulator of three-dimensional genome organization. Several landmark studies have shown that cohesin mutations perturb the balance between self-renewal and differentiation of hematopoietic stem and progenitor cells (HSPC). Emerging data now begin to uncover the molecular mechanisms that underpin this phenotype. Among these mechanisms is a role for cohesin in the control of inflammatory responses in HSPCs and myeloid cells. Inflammatory signals limit HSPC self-renewal and drive HSPC differentiation. Consistent with this, cohesin mutations promote resistance to inflammatory signals, and may provide a selective advantage for AML progression. In this review, we discuss recent progress in understanding cohesin mutations in AML, and speculate whether vulnerabilities associated with these mutations could be exploited therapeutically.
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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.