We are analyzing https://link.springer.com/article/10.1186/1471-2407-10-401.

Title:
Combined mutations of ASXL1, CBL, FLT3, IDH1, IDH2, JAK2, KRAS, NPM1, NRAS, RUNX1, TET2 and WT1 genes in myelodysplastic syndromes and acute myeloid leukemias | BMC Cancer
Description:
Background Gene mutation is an important mechanism of myeloid leukemogenesis. However, the number and combination of gene mutated in myeloid malignancies is still a matter of investigation. Methods We searched for mutations in the ASXL1, CBL, FLT3, IDH1, IDH2, JAK2, KRAS, NPM1, NRAS, RUNX1, TET2 and WT1 genes in 65 myelodysplastic syndromes (MDSs) and 64 acute myeloid leukemias (AMLs) without balanced translocation or complex karyotype. Results Mutations in ASXL1 and CBL were frequent in refractory anemia with excess of blasts. Mutations in TET2 occurred with similar frequency in MDSs and AMLs and associated equally with either ASXL1 or NPM1 mutations. Mutations of RUNX1 were mutually exclusive with TET2 and combined with ASXL1 but not with NPM1. Mutations in FLT3 (mutation and internal tandem duplication), IDH1, IDH2, NPM1 and WT1 occurred primarily in AMLs. Conclusion Only 14% MDSs but half AMLs had at least two mutations in the genes studied. Based on the observed combinations and exclusions we classified the 12 genes into four classes and propose a highly speculative model that at least a mutation in one of each class is necessary for developing AML with simple or normal karyotype.
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Keywords {🔍}

mutations, article, pubmed, tet, genes, asxl, google, scholar, idh, myeloid, cases, mutation, cas, amls, runx, mdss, cbl, gene, leukemia, npm, acute, aml, file, cancer, study, additional, flt, myelodysplastic, mds, syndromes, mutated, chronic, found, blood, jak, karyotype, frequent, authors, leukemias, birnbaum, gelsiboyer, case, primary, table, figure, central, including, mozziconacci, class, patients,

Topics {✒️}

hôpital de salon-de-provence internal tandem duplication marie-joelle mozziconacci laboratoire d'oncologie moléculaire acute myeloid leukaemia pre-publication history array-comparative genomic hybridization commission d'orientation scientifique chronic myelomonocytic leukaemia open access article phred/phrap/consed softwares prominent tyrosine-phosphorylated substrates pre-leukemic disorders jak2 v617f mutation article download pdf fondation de france salon-de-provence acute myeloid leukemias gelsi-boyer multi-hit model proposed acute myeloid leukemia centre hospitalier général privacy choices/manage cookies mansat-de mas authors’ original file myeloid malignant diseases van der heijden poor prognostic factor acute myelomonocytic leukemia table s3 summary institutional review board abdel-wahab cancer gene inactivation geurts van kessel biomed central mutational status impacts complete mutational status le beau mm table s1 mutations table s2 mutations constitute class ii bone marrow dysplasia bmc cancer bmc cancer 10 previous myeloid disease chronic myelomonocytic leukemia le couedic jp independent pcr product myeloid leukemogenesis european economic area

Questions {❓}

Acquaviva C, Gelsi-Boyer V, Birnbaum D: Myelodysplastic syndromes: lost between two states?
Random or ordered accumulation?

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WebPage:
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         headline:Combined mutations of ASXL1, CBL, FLT3, IDH1, IDH2, JAK2, KRAS, NPM1, NRAS, RUNX1, TET2 and WT1 genes in myelodysplastic syndromes and acute myeloid leukemias
         description:Gene mutation is an important mechanism of myeloid leukemogenesis. However, the number and combination of gene mutated in myeloid malignancies is still a matter of investigation. We searched for mutations in the ASXL1, CBL, FLT3, IDH1, IDH2, JAK2, KRAS, NPM1, NRAS, RUNX1, TET2 and WT1 genes in 65 myelodysplastic syndromes (MDSs) and 64 acute myeloid leukemias (AMLs) without balanced translocation or complex karyotype. Mutations in ASXL1 and CBL were frequent in refractory anemia with excess of blasts. Mutations in TET2 occurred with similar frequency in MDSs and AMLs and associated equally with either ASXL1 or NPM1 mutations. Mutations of RUNX1 were mutually exclusive with TET2 and combined with ASXL1 but not with NPM1. Mutations in FLT3 (mutation and internal tandem duplication), IDH1, IDH2, NPM1 and WT1 occurred primarily in AMLs. Only 14% MDSs but half AMLs had at least two mutations in the genes studied. Based on the observed combinations and exclusions we classified the 12 genes into four classes and propose a highly speculative model that at least a mutation in one of each class is necessary for developing AML with simple or normal karyotype.
         datePublished:2010-08-02T00:00:00Z
         dateModified:2010-08-02T00:00:00Z
         pageStart:1
         pageEnd:7
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         sameAs:https://doi.org/10.1186/1471-2407-10-401
         keywords:
            Acute Myeloid Leukemia
            JAK2 V617F
            Balance Translocation
            Internal Tandem Duplication
            Myeloid Malignancy
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
            Biomedicine
            general
            Medicine/Public Health
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ScholarlyArticle:
      headline:Combined mutations of ASXL1, CBL, FLT3, IDH1, IDH2, JAK2, KRAS, NPM1, NRAS, RUNX1, TET2 and WT1 genes in myelodysplastic syndromes and acute myeloid leukemias
      description:Gene mutation is an important mechanism of myeloid leukemogenesis. However, the number and combination of gene mutated in myeloid malignancies is still a matter of investigation. We searched for mutations in the ASXL1, CBL, FLT3, IDH1, IDH2, JAK2, KRAS, NPM1, NRAS, RUNX1, TET2 and WT1 genes in 65 myelodysplastic syndromes (MDSs) and 64 acute myeloid leukemias (AMLs) without balanced translocation or complex karyotype. Mutations in ASXL1 and CBL were frequent in refractory anemia with excess of blasts. Mutations in TET2 occurred with similar frequency in MDSs and AMLs and associated equally with either ASXL1 or NPM1 mutations. Mutations of RUNX1 were mutually exclusive with TET2 and combined with ASXL1 but not with NPM1. Mutations in FLT3 (mutation and internal tandem duplication), IDH1, IDH2, NPM1 and WT1 occurred primarily in AMLs. Only 14% MDSs but half AMLs had at least two mutations in the genes studied. Based on the observed combinations and exclusions we classified the 12 genes into four classes and propose a highly speculative model that at least a mutation in one of each class is necessary for developing AML with simple or normal karyotype.
      datePublished:2010-08-02T00:00:00Z
      dateModified:2010-08-02T00:00:00Z
      pageStart:1
      pageEnd:7
      license:https://creativecommons.org/licenses/by/2.0
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      keywords:
         Acute Myeloid Leukemia
         JAK2 V617F
         Balance Translocation
         Internal Tandem Duplication
         Myeloid Malignancy
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-10-401/MediaObjects/12885_2010_Article_2200_Fig1_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2407-10-401/MediaObjects/12885_2010_Article_2200_Fig2_HTML.jpg
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            address:
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            name:Institut Paoli-Calmettes
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            type:Organization
      name:Norbert Vey
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            name:Institut Paoli-Calmettes
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               name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
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               name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
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            name:Université de la Méditerranée
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               name:Faculté de Médecine, Université de la Méditerranée, Marseille, France
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      name:Marie-Joelle Mozziconacci
      affiliation:
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            address:
               name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
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      email:[email protected]
PostalAddress:
      name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
      name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
      name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
      name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
      name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
      name:Département de BioPathologie, Institut Paoli-Calmettes, Marseille, France
      name:Service de Médecine Interne, Centre Hospitalier Général, Martigues, France
      name:Service de Médecine Interne-Oncologie, Hôpital de Salon-de-Provence, Salon-de-Provence, France
      name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
      name:Département de BioPathologie, Institut Paoli-Calmettes, Marseille, France
      name:Faculté de Médecine, Université de la Méditerranée, Marseille, France
      name:Département d'Hématologie, Institut Paoli-Calmettes, Marseille, France
      name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
      name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
      name:Département de BioPathologie, Institut Paoli-Calmettes, Marseille, France
      name:Faculté de Médecine, Université de la Méditerranée, Marseille, France
      name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d'Oncologie Moléculaire; UMR891 Inserm; Institut Paoli-Calmettes, Marseille, France
      name:Département de BioPathologie, Institut Paoli-Calmettes, Marseille, France

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