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Chromosomal rearrangements with a common breakpoint at 6p23 in five cases of myeloid leukemia

E W Fleischman, E L Prigogina, G W Iljinskaja

    Human Genetics
    |January 1, 1983
    PubMed

    Insights

    Rearrangement at chromosome 6p23 is linked to myeloid leukemia, including acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). This specific breakpoint warrants further investigation in blood cancer development.

    Area of Science:

    • Hematology
    • Cytogenetics
    • Oncology

    Background:

    • Myeloid leukemias encompass a range of blood cancers.
    • Chromosomal abnormalities are frequently observed in leukemia and are crucial for diagnosis and prognosis.

    Observation:

    • Five patients with myeloid leukemia exhibited rearrangements on the short arm of chromosome 6, specifically at the 6p23 breakpoint.
    • Three patients had acute myeloid leukemia (AML) variants (M2, M3, M4), and two presented with blastic crisis of Philadelphia chromosome-negative or -positive chronic myeloid leukemia (CML).

    Findings:

    • A consistent translocation, t(6;9)(p23;q34), was identified in two patients, one with AML (M2) and another with blastic crisis of Ph1-negative CML.
    • The blast cells in the latter patient showed morphological similarities to AML M2.
    • This t(6;9)(p23;q34) translocation was previously reported in two other AML cases.

    Implications:

    • The breakpoint at 6p23 appears to play a significant role in the pathogenesis of myeloid malignancies.
    • Further research is necessary to elucidate the precise function of the 6p23 breakpoint in the development of these blood cancers.

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