Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors.
epithelial tumors
fusion genes
fusion transcripts
mechanisms
pathobiology
Journal
Oncotarget
ISSN: 1949-2553
Titre abrégé: Oncotarget
Pays: United States
ID NLM: 101532965
Informations de publication
Date de publication:
12 Mar 2019
12 Mar 2019
Historique:
received:
14
11
2018
accepted:
22
02
2019
entrez:
23
4
2019
pubmed:
23
4
2019
medline:
23
4
2019
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 31007851
doi: 10.18632/oncotarget.26777
pii: 26777
pmc: PMC6459343
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
2095-2111Subventions
Organisme : NCI NIH HHS
ID : P30 CA016672
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA217842
Pays : United States
Déclaration de conflit d'intérêts
CONFLICTS OF INTEREST The authors declare that they have no conflicts of interest.
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