We are analyzing https://link.springer.com/article/10.1007/s12185-017-2241-1.

Title:
Somatic SETBP1 mutations in myeloid neoplasms | International Journal of Hematology
Description:
SETBP1 is a SET-binding protein regulating self-renewal potential through HOXA-protein activation. Somatic SETBP1 mutations were identified by whole exome sequencing in several phenotypes of myelodysplastic/myeloproliferative neoplasms (MDS/MPN), including atypical chronic myeloid leukemia, chronic myelomonocytic leukemia, and juvenile myelomonocytic leukemia as well as in secondary acute myeloid leukemia (sAML). Surprisingly, its recurrent somatic activated mutations are located at the identical positions of germline mutations reported in congenital Schinzel–Giedion syndrome. In general, somatic SETBP1 mutations have a significant clinical impact on the outcome as poor prognostic factor, due to downstream HOXA-pathway as well as associated aggressive types of chromosomal defects (-7/del(7q) and i(17q)), which is consistent with wild-type SETBP1 activation in aggressive types of acute myeloid leukemia and leukemic evolution. Biologically, mutant SETBP1 attenuates RUNX1 and activates MYB. The studies of mouse models confirmed biological significance of SETBP1 mutations in myeloid leukemogenesis, particularly associated with ASXL1 mutations. SETBP1 is a major oncogene in myeloid neoplasms, which cooperates with various genetic events and causes distinct phenotypes of MDS/MPN and sAML.
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Keywords {🔍}

setbp, mutations, pubmed, article, google, scholar, myeloid, leukemia, cas, neoplasms, cases, somatic, chronic, central, mutation, fig, acute, syndrome, protein, myelomonocytic, secondary, sequencing, patients, activation, prognostic, events, makishima, recurrent, schinzelgiedion, hoxa, med, poor, studies, genetic, disease, gene, myelodysplastic, csfr, genet, mdsmpn, clinical, germline, runx, asxl, neutrophilic, analysis, reported, wildtype, mutant, mutated,

Topics {✒️}

juvenile myelomonocytic leukaemia congenital schinzel–giedion syndrome cell lymphoblastic leukaemia gtp-binding gene rit1 myelodysplastic/myeloproliferative neoplasms schinzel–giedion syndrome caused set-binding protein regulating therapy-related myeloid neoplasms gene-expression profiles revealed germline ras-pathway mutations classical myeloproliferative neoplasms wild-type setbp1 belonged mds-related myeloid neoplasms shorter transplantation-free survival asxl1-mutated ancestral clone setbp1-mediated oncogenic potential tissue-specific events acquired mutated clone size primary myelodysplastic syndrome privacy choices/manage cookies wild-type setbp1 activation acute myeloid leukemia schinzel–giedion syndrome poor prognostic factors acute myelomonocytic leukemia acute undifferentiated leukemia patnaik mm chronic neutrophilic leukemia antecedent disease initiation taussig cancer institute chronic myelomonocytic leukemia article makishima chronic myelogenous leukemia poor prognostic factor initial disease presentation common primary mutations de novo mutations myeloproliferative neoplasms myeloid neoplasms progress murine myeloid progenitors distinct disease entity targeted resequencing analysis residue d868 led myeloproliferative potential therapy-related neoplasms including polycythemia vera serial time points de novo aml mouse transplantation model downstream hoxa-pathway

Schema {🗺️}

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         headline:Somatic SETBP1 mutations in myeloid neoplasms
         description:SETBP1 is a SET-binding protein regulating self-renewal potential through HOXA-protein activation. Somatic SETBP1 mutations were identified by whole exome sequencing in several phenotypes of myelodysplastic/myeloproliferative neoplasms (MDS/MPN), including atypical chronic myeloid leukemia, chronic myelomonocytic leukemia, and juvenile myelomonocytic leukemia as well as in secondary acute myeloid leukemia (sAML). Surprisingly, its recurrent somatic activated mutations are located at the identical positions of germline mutations reported in congenital Schinzel–Giedion syndrome. In general, somatic SETBP1 mutations have a significant clinical impact on the outcome as poor prognostic factor, due to downstream HOXA-pathway as well as associated aggressive types of chromosomal defects (-7/del(7q) and i(17q)), which is consistent with wild-type SETBP1 activation in aggressive types of acute myeloid leukemia and leukemic evolution. Biologically, mutant SETBP1 attenuates RUNX1 and activates MYB. The studies of mouse models confirmed biological significance of SETBP1 mutations in myeloid leukemogenesis, particularly associated with ASXL1 mutations. SETBP1 is a major oncogene in myeloid neoplasms, which cooperates with various genetic events and causes distinct phenotypes of MDS/MPN and sAML.
         datePublished:2017-04-26T00:00:00Z
         dateModified:2021-10-23T00:00:00Z
         pageStart:732
         pageEnd:742
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            Secondary acute myeloid leukemia
            Poor prognosis
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            Hematology
            Oncology
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      headline:Somatic SETBP1 mutations in myeloid neoplasms
      description:SETBP1 is a SET-binding protein regulating self-renewal potential through HOXA-protein activation. Somatic SETBP1 mutations were identified by whole exome sequencing in several phenotypes of myelodysplastic/myeloproliferative neoplasms (MDS/MPN), including atypical chronic myeloid leukemia, chronic myelomonocytic leukemia, and juvenile myelomonocytic leukemia as well as in secondary acute myeloid leukemia (sAML). Surprisingly, its recurrent somatic activated mutations are located at the identical positions of germline mutations reported in congenital Schinzel–Giedion syndrome. In general, somatic SETBP1 mutations have a significant clinical impact on the outcome as poor prognostic factor, due to downstream HOXA-pathway as well as associated aggressive types of chromosomal defects (-7/del(7q) and i(17q)), which is consistent with wild-type SETBP1 activation in aggressive types of acute myeloid leukemia and leukemic evolution. Biologically, mutant SETBP1 attenuates RUNX1 and activates MYB. The studies of mouse models confirmed biological significance of SETBP1 mutations in myeloid leukemogenesis, particularly associated with ASXL1 mutations. SETBP1 is a major oncogene in myeloid neoplasms, which cooperates with various genetic events and causes distinct phenotypes of MDS/MPN and sAML.
      datePublished:2017-04-26T00:00:00Z
      dateModified:2021-10-23T00:00:00Z
      pageStart:732
      pageEnd:742
      sameAs:https://doi.org/10.1007/s12185-017-2241-1
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         SETBP1
         Myelodysplastic/myeloproliferative neoplasms
         Secondary acute myeloid leukemia
         Poor prognosis
         Self-renewal potential
         Hematology
         Oncology
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      address:
         name:Department of Pathology and Tumor Biology, Kyoto University, Kyoto, Japan
         type:PostalAddress
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               type:PostalAddress
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            address:
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      name:Department of Pathology and Tumor Biology, Kyoto University, Kyoto, Japan
      name:Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, USA

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