Discovering early molecular determinants of leukemogenesis

    Research output: Contribution to journalArticle

    10 Citations (Scopus)

    Abstract

    Truncating mutations of the G-CSF receptor are found during disease course in nearly half of all patients with severe congenital neutropenia. In this issue of the JCI, Liu et al. demonstrate that these mutations confer a competitive clonal advantage upon HSCs in mice and that the advantage is conditional because it is observed only in the presence of the ligand G-CSF (see the related article beginning on page 946). Once activated, the mutant receptor requires the function of Stat5 in order to effect clonal expansion of this stem cell population. The results support the notion that early molecular steps in this and other neoplastic processes represent adaptations in which, through somatic mutations, "unfit" stem cells gain a measure of fitness by altering their relationships with their microenvironment.

    Original languageEnglish (US)
    Pages (from-to)847-850
    Number of pages4
    JournalJournal of Clinical Investigation
    Volume118
    Issue number3
    DOIs
    StatePublished - Mar 2008

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    Mutation
    Stem Cells
    Granulocyte Colony-Stimulating Factor Receptors
    Neoplastic Processes
    Granulocyte Colony-Stimulating Factor
    Ligands
    Population
    Neutropenia, Severe Congenital, Autosomal Recessive 3

    ASJC Scopus subject areas

    • Medicine(all)

    Cite this

    Discovering early molecular determinants of leukemogenesis. / Bagby, Grover C.

    In: Journal of Clinical Investigation, Vol. 118, No. 3, 03.2008, p. 847-850.

    Research output: Contribution to journalArticle

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