Bone marrow failure as a risk factor for clonal evolution

prospects for leukemia prevention.

    Research output: Contribution to journalArticle

    23 Citations (Scopus)

    Abstract

    Patients with bone marrow failure syndromes are at risk for the development of clonal neoplasms, including paroxysmal nocturnal hemoglobinuria (PNH), myelodysplasia (MDS), and acute myelogenous leukemia (AML). Approximately 10% to 20% of those who survive acquired aplastic anemia will develop a clonal disease within the decade following their diagnosis. The relative risk of clonal neoplasms is very significantly increased in children and adults with inherited bone marrow failure syndromes as well. Until recently, the mechanisms underlying clonal evolution have been opaque, but a sufficient amount of evidence has now accumulated to support a model in which cells resistant to extracellular apoptotic cues are selected from the stem cell pool. Indeed, in the past two years this paradigm has been validated in preclinical models that are robust enough to reconsider new therapeutic objectives in aplastic states and to support the planning and development of rationally designed leukemia prevention trials.

    Original languageEnglish (US)
    Pages (from-to)40-46
    Number of pages7
    JournalHematology / the Education Program of the American Society of Hematology. American Society of Hematology. Education Program
    StatePublished - 2007

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    Clonal Evolution
    Leukemia
    Bone Marrow
    Paroxysmal Hemoglobinuria
    Aplastic Anemia
    Acute Myeloid Leukemia
    Cues
    Neoplasms
    Stem Cells
    Bone Marrow failure syndromes
    Therapeutics

    ASJC Scopus subject areas

    • Medicine(all)

    Cite this

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    title = "Bone marrow failure as a risk factor for clonal evolution: prospects for leukemia prevention.",
    abstract = "Patients with bone marrow failure syndromes are at risk for the development of clonal neoplasms, including paroxysmal nocturnal hemoglobinuria (PNH), myelodysplasia (MDS), and acute myelogenous leukemia (AML). Approximately 10{\%} to 20{\%} of those who survive acquired aplastic anemia will develop a clonal disease within the decade following their diagnosis. The relative risk of clonal neoplasms is very significantly increased in children and adults with inherited bone marrow failure syndromes as well. Until recently, the mechanisms underlying clonal evolution have been opaque, but a sufficient amount of evidence has now accumulated to support a model in which cells resistant to extracellular apoptotic cues are selected from the stem cell pool. Indeed, in the past two years this paradigm has been validated in preclinical models that are robust enough to reconsider new therapeutic objectives in aplastic states and to support the planning and development of rationally designed leukemia prevention trials.",
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