We are analyzing https://link.springer.com/article/10.1007/s12185-017-2257-6.

Title:
Epigenetic dysregulation of hematopoietic stem cells and preleukemic state | International Journal of Hematology
Description:
Recent genetic analyses have revealed that premalignant somatic mutations in hematopoietic cells are common in older people without an evidence of hematologic malignancies, leading to clonal hematopoietic expansion. This phenomenon has been termed clonal hematopoiesis of indeterminate potential (CHIP). Frequency of such clonal somatic mutations increases with age: in 5–10% of people older than 70 years and around 20% of people older than 90 years. The most commonly mutated genes found in individuals with CHIP were epigenetic regulators, including DNA methyltransferase 3A (DNMT3A), Ten–eleven-translocation 2 (TET2), and Additional sex combs-like 1 (ASXL1), which are also recurrently mutated in myeloid malignancies. Recent functional studies have uncovered pleiotropic effect of mutations in DNMT3A, TET2, and ASXL1 in hematopoietic stem cell regulation and leukemic transformation. Of note, CHIP is associated with an increased risk of hematologic malignancy and all-cause mortality, albeit the annual risk of leukemic transformation was relatively low (0.5–1%). These findings suggest that clonal hematopoiesis per se may not be sufficient to engender preleukemic state. Further studies are required to decipher the exact mechanism by which preleukemic stem cells originate and transform into a full-blown leukemic state.
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Keywords {🔍}

pubmed, article, mutations, google, scholar, cas, tet, central, clonal, dnmta, asxl, hematopoietic, myeloid, cells, dna, hematopoiesis, patients, loss, chip, leukemia, cell, stem, aml, epigenetic, studies, malignancies, blood, transformation, cancer, somatic, hematologic, individuals, disease, mice, mds, med, genetic, genes, mutant, study, vivo, human, functional, gene, mutation, modifiers, role, acute, fig, methylation,

Topics {✒️}

o-linked β-n-acetylglucosamine high-throughput genome-wide sequencing dnmt3a/dnmt3b double-knockout hscs c-terminal-truncating asxl1 mutant genome-wide profiling identifies mir-22/tet2 regulatory network lin− sca-1+ c-kit+ hematopoietic stem/progenitor cells full-blown leukemic state hematopoietic-specific conditional loss vega-rubín-de-celis hematopoietic-specific conditional deletion histone h2b o-glcnacylation age-related clonal skewing dnmt3a single-null cells targeted deep sequencing human t-cell lymphoma chronic myelomonocytic leukaemia activation-induced cytidine deaminase fully penetrant aml population-based cohorts revealed age-related clonal hematopoiesis dose-escalated induction therapy mediated base-excision repair aml1-eto leads active/passive dna demethylation sensitizing bap1-deficient mesothelioma α-kg-dependent oxygenases α-ketoglutarate-dependent dioxygenases normal t-cell compartment age-related prognostic impact tet2-mediated demethylation reactions wild-type cells long-term hsc compartment article kunimoto washington university analyzed chronic myelomonocytic leukemia human hematopoietic progenitors hematopoietic stem cells preleukemic stem cells asxl1-mutated clones tended prc2-mediated gene repression clonal hematopoiesis caused x-inactivation skewing drive hematopoietic transformation tdg-mediated ber pathway x-linked genes show disrupted hsc tet2-mutated myeloid malignancies blood-cancer risk inferred

Schema {🗺️}

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         headline:Epigenetic dysregulation of hematopoietic stem cells and preleukemic state
         description:Recent genetic analyses have revealed that premalignant somatic mutations in hematopoietic cells are common in older people without an evidence of hematologic malignancies, leading to clonal hematopoietic expansion. This phenomenon has been termed clonal hematopoiesis of indeterminate potential (CHIP). Frequency of such clonal somatic mutations increases with age: in 5–10% of people older than 70 years and around 20% of people older than 90 years. The most commonly mutated genes found in individuals with CHIP were epigenetic regulators, including DNA methyltransferase 3A (DNMT3A), Ten–eleven-translocation 2 (TET2), and Additional sex combs-like 1 (ASXL1), which are also recurrently mutated in myeloid malignancies. Recent functional studies have uncovered pleiotropic effect of mutations in DNMT3A, TET2, and ASXL1 in hematopoietic stem cell regulation and leukemic transformation. Of note, CHIP is associated with an increased risk of hematologic malignancy and all-cause mortality, albeit the annual risk of leukemic transformation was relatively low (0.5–1%). These findings suggest that clonal hematopoiesis per se may not be sufficient to engender preleukemic state. Further studies are required to decipher the exact mechanism by which preleukemic stem cells originate and transform into a full-blown leukemic state.
         datePublished:2017-05-29T00:00:00Z
         dateModified:2017-05-29T00:00:00Z
         pageStart:34
         pageEnd:44
         sameAs:https://doi.org/10.1007/s12185-017-2257-6
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            Clonal hematopoiesis
            CHIP
            Preleukemic state
            Epigenetic regulators
            Hematology
            Oncology
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ScholarlyArticle:
      headline:Epigenetic dysregulation of hematopoietic stem cells and preleukemic state
      description:Recent genetic analyses have revealed that premalignant somatic mutations in hematopoietic cells are common in older people without an evidence of hematologic malignancies, leading to clonal hematopoietic expansion. This phenomenon has been termed clonal hematopoiesis of indeterminate potential (CHIP). Frequency of such clonal somatic mutations increases with age: in 5–10% of people older than 70 years and around 20% of people older than 90 years. The most commonly mutated genes found in individuals with CHIP were epigenetic regulators, including DNA methyltransferase 3A (DNMT3A), Ten–eleven-translocation 2 (TET2), and Additional sex combs-like 1 (ASXL1), which are also recurrently mutated in myeloid malignancies. Recent functional studies have uncovered pleiotropic effect of mutations in DNMT3A, TET2, and ASXL1 in hematopoietic stem cell regulation and leukemic transformation. Of note, CHIP is associated with an increased risk of hematologic malignancy and all-cause mortality, albeit the annual risk of leukemic transformation was relatively low (0.5–1%). These findings suggest that clonal hematopoiesis per se may not be sufficient to engender preleukemic state. Further studies are required to decipher the exact mechanism by which preleukemic stem cells originate and transform into a full-blown leukemic state.
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      dateModified:2017-05-29T00:00:00Z
      pageStart:34
      pageEnd:44
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      keywords:
         Hematopoietic stem cells
         Clonal hematopoiesis
         CHIP
         Preleukemic state
         Epigenetic regulators
         Hematology
         Oncology
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                     type:PostalAddress
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               type:PostalAddress
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               type:PostalAddress
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            address:
               name:Center for Hematologic Malignancies, Memorial Sloan Kettering Cancer Center, New York, USA
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      name:Hideaki Nakajima
      affiliation:
            name:Yokohama City University Graduate School of Medicine
            address:
               name:Department of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, Yokohama, Japan
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      name:Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, USA
      name:Center for Epigenetics Research, Memorial Sloan Kettering Cancer Center, New York, USA
      name:Center for Hematologic Malignancies, Memorial Sloan Kettering Cancer Center, New York, USA
      name:Department of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine, Yokohama, Japan

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