4.4 Review

Regulators of the RAS-ERK pathway as therapeutic targets in thyroid cancer

期刊

ENDOCRINE-RELATED CANCER
卷 26, 期 6, 页码 R319-R344

出版社

BIOSCIENTIFICA LTD
DOI: 10.1530/ERC-19-0098

关键词

thyroid cancer; RAS/ERK; GEF/GAP; scaffold; MKP

资金

  1. Asociacion Espanola Contra el Cancer (AECC) [GCB141423113]
  2. CIBERONC from the Instituto de Salud Carlos III (ISCIII)
  3. MINECO/FEDER, UE [SAF2016-75531-R, SAF-2015 63638R]
  4. Tironet2 (Comunidad de Madrid) [B2017/BMD-3724]
  5. RTICC from ISCIII [RD/12/0036/0030]
  6. RTICC [RD/12/0036/0033]

向作者/读者索取更多资源

Thyroid cancer is mostly an ERK-driven carcinoma, as up to 70% of thyroid carcinomas are caused by mutations that activate the RAS/ERK mitogenic signaling pathway. The incidence of thyroid cancer has been steadily increasing for the last four decades; yet, there is still no effective treatment for advanced thyroid carcinomas. Current research efforts are focused on impairing ERK signaling with small-molecule inhibitors, mainly at the level of BRAF and MEK. However, despite initial promising results in animal models, the clinical success of these inhibitors has been limited by the emergence of tumor resistance and relapse. The RAS/ERK pathway is an extremely complex signaling cascade with multiple points of control, offering many potential therapeutic targets: from the modulatory proteins regulating the activation state of RAS proteins to the scaffolding proteins of the pathway that provide spatial specificity to the signals, and finally, the negative feedbacks and phosphatases responsible for inactivating the pathway. The aim of this review is to give an overview of the biology of RAS/ERK regulators in human cancer highlighting relevant information on thyroid cancer and future areas of research.

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