Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors

Musaffe Tuna; Christopher I. Amos; Gordon B. Mills

doi:10.18632/oncotarget.26777

Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors

Musaffe Tuna, Christopher I. Amos, Gordon B. Mills

Cell Developmental and Cancer Biology

Research output: Contribution to journal › Review article › peer-review

22 Scopus citations

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 language	English (US)
Pages (from-to)	2095-2111
Number of pages	17
Journal	Oncotarget
Volume	10
Issue number	21
DOIs	https://doi.org/10.18632/oncotarget.26777
State	Published - 2019

Keywords

Epithelial tumors
Fusion genes
Fusion transcripts
Mechanisms
Pathobiology

ASJC Scopus subject areas

Oncology

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10.18632/oncotarget.26777

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title = "Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors",

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.",

keywords = "Epithelial tumors, Fusion genes, Fusion transcripts, Mechanisms, Pathobiology",

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AU - Amos, Christopher I.

AU - Mills, Gordon B.

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PY - 2019

Y1 - 2019

N2 - 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.

AB - 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.

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KW - Fusion transcripts

KW - Mechanisms

KW - Pathobiology

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Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors

Abstract

Keywords

ASJC Scopus subject areas

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