REToma: a cancer subtype with a shared driver oncogene.


Journal

Carcinogenesis
ISSN: 1460-2180
Titre abrégé: Carcinogenesis
Pays: England
ID NLM: 8008055

Informations de publication

Date de publication:
22 04 2020
Historique:
received: 30 08 2019
revised: 17 10 2019
accepted: 07 11 2019
pubmed: 12 11 2019
medline: 1 9 2020
entrez: 12 11 2019
Statut: ppublish

Résumé

RET (REarranged during Transfection), which encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor, plays a role as driver oncogene in a variety of human cancers. Fusion of RET with several partner genes has been detected in papillary thyroid, lung, colorectal, pancreatic and breast cancers, and tyrosine kinase inhibitors (TKIs) for RET (particularly RET-specific inhibitors) show promising therapeutic effects against such cancers. Oncogenic mutations within the extracellular cysteine-rich and intracellular kinase domains of RET drive medullary thyroid carcinogenesis; the same mutations are also observed in a small subset of diverse cancers such as lung, colorectal and breast cancers. Considering the oncogenic nature of RET mutants, lung, colorectal and breast cancers are predicted to respond to RET TKIs in a manner similar to medullary thyroid cancer. In summary, cancers carrying oncogenic RET alterations as a driver mutation could be collectively termed 'REToma' and treated with RET TKIs in a tissue-agnostic manner.

Identifiants

pubmed: 31711124
pii: 5621476
doi: 10.1093/carcin/bgz184
doi:

Substances chimiques

Oncogene Proteins, Fusion 0
Protein Kinase Inhibitors 0
Pyrazoles 0
Pyridines 0
Pyrimidines 0
pralsetinib 0
selpercatinib CEGM9YBNGD
Proto-Oncogene Proteins c-ret EC 2.7.10.1
RET protein, human EC 2.7.10.1
Ret protein, mouse EC 2.7.10.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

123-129

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Auteurs

Takashi Kohno (T)

Division of Genome Biology, National Cancer Center Research Institute, Tsukiji, Chuo-ku, Tokyo, Japan.

Junya Tabata (J)

Division of Genome Biology, National Cancer Center Research Institute, Tsukiji, Chuo-ku, Tokyo, Japan.

Takashi Nakaoku (T)

Division of Genome Biology, National Cancer Center Research Institute, Tsukiji, Chuo-ku, Tokyo, Japan.

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Classifications MeSH