Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Mar 12;10(21):2095-2111.
doi: 10.18632/oncotarget.26777.

Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors

Musaffe Tuna  1   2 , Christopher I Amos  2   3 , Gordon B Mills  4   5   6
Affiliations
Review

Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors

Musaffe Tuna et al. Oncotarget. .

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.

PubMed Disclaimer

Conflict of interest statement

CONFLICTS OF INTEREST The authors declare that they have no conflicts of interest.

Figures

Figure 1
Figure 1. Schematic illustrations of formation of fusion genes
Formation of fusion gene via translocation (A), insertion (B), deletion (C), tandem duplication (D), inversion (E), chromothripsis (F).
Figure 2
Figure 2. Schematic illustration of formation of chimeric transcript
Figure 3
Figure 3. Schematic illustration of localization of parental and chimeric proteins
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Delattre O, Zucman J, Plougastel B, Desmaze C, Melot T, Peter M, Kovar H, Joubert I, de Jong P, Rouleau G, Aurias A, Thomas G. Gene fusion with an ets DNA-binding domain caused by chromosome translocation in human tumours. Nature. 1992;359:162–165. - PubMed
    1. Nowell PC, Hungerford DA. Chromosome studies on normal and leukemic human leukocytes. J Natl Cancer Inst. 1960;25:85–109. - PubMed
    1. Rowley JD. The critical role of chromosome translocations in human leukemias. Annu Rev Genet. 1998;32:495–519. - PubMed
    1. Fusco A, Grieco M, Santoro M, Berlingieri MT, Pilotti S, Pierotti MA, Della Porta G, Vecchio G. A new oncogene in human thyroid papillary carcinomas and their lymph-nodal metastases. Nature. 1987;328:170–172. - PubMed
    1. Grieco M, Santoro M, Berlingieri MT, Melillo RM, Donghi R, Bongarzone I, Pierotti MA, Della Porta G, Fusco A, Vecchio G. Ptc is a novel rearranged form of the ret proto-oncogene and is frequently detected in vivo in human thyroid papillary carcinomas. Cell. 1990;60:557–563. - PubMed

LinkOut - more resources