Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors

Musaffe Tuna1,2, Christopher I Amos2,3, Gordon B Mills4,5,6

  • 1Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Oncotarget
|April 23, 2019
PubMed

Insights

Recurrent fusion transcripts, hallmarks of cancer, arise from DNA rearrangements or splicing errors. These oncogenic fusion genes create proteins that are key therapeutic targets and diagnostic biomarkers for epithelial tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Recurrent fusion transcripts are characteristic hallmarks of cancer.
  • They originate from chromosomal rearrangements (e.g., translocations, chromothripsis) or transcriptional errors like splicing errors and read-through transcription.
  • Fusion proteins derived from these transcripts can exhibit transforming activities.

Purpose of the Study:

  • To review the mechanisms of oncogenic fusion gene and transcript formation.
  • To discuss the impact of these fusions on the pathobiology of epithelial tumors.
  • To highlight fusion proteins as therapeutic targets and diagnostic biomarkers.

Main Methods:

  • Literature review of mechanisms generating fusion genes and transcripts.
  • Analysis of the pathobiological impact of fusion proteins in epithelial cancers.
  • Synthesis of current knowledge on therapeutic and diagnostic applications.

Main Results:

  • Fusion genes can form through various DNA rearrangements and transcriptional processes.
  • Chimeric proteins resulting from fusion transcripts possess oncogenic potential.
  • Fusion proteins serve as crucial biomarkers for cancer diagnosis, status, and progression.

Conclusions:

  • Understanding fusion gene formation is critical for cancer research.
  • Oncogenic fusion proteins offer promising avenues for targeted cancer therapies.
  • Fusion transcripts and proteins are valuable diagnostic and prognostic tools in oncology.

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