Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors

Musaffe Tuna, Christopher I. Amos, Gordon Mills

    Research output: Contribution to journalReview article

    Abstract

    Recurrent fusion transcripts, which are one of the characteristic hallmarks of cancer, arise either from chromosomal rearrangements or from transcriptional errors in splicing. DNA rearrangements include intrachromosomal or interchromosomal translocation, tandem duplication, deletion, inversion, or result from chromothripsis, which causes complex rearrangements. In addition, fusion proteins can be created through transcriptional read-through. Fusion genes can be transcribed to fusion transcripts and translated to chimeric proteins, with many having demonstrated transforming activities through multiple mechanisms in cells. Fusion proteins represent novel therapeutic targets and diagnostic biomarkers of diagnosis, disease status, or progression. This review focuses on the mechanisms underlying the formation of oncogenic fusion genes and transcripts and their impact on the pathobiology of epithelial tumors.

    Original languageEnglish (US)
    Pages (from-to)2095-2111
    Number of pages17
    JournalOncotarget
    Volume10
    Issue number21
    StatePublished - Jan 1 2019

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    Keywords

    • Epithelial tumors
    • Fusion genes
    • Fusion transcripts
    • Mechanisms
    • Pathobiology

    ASJC Scopus subject areas

    • Oncology

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