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Progresses Toward Precision Medicine in RET-altered Solid Tumors.

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The rearranged during transfection (RET) gene is crucial for normal functions but its alterations drive cancers. Selective RET inhibitors show promising results, overcoming limitations of older multikinase inhibitors.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The rearranged during transfection (RET) gene encodes a receptor tyrosine kinase vital for physiological processes.
  • RET aberrations, including loss-of-function mutations (Hirschsprung disease, CAKUT) and gain-of-function mutations/rearrangements, are implicated in various pathologies, notably cancer.
  • Multikinase inhibitors (MKIs) targeting RET have shown limited efficacy and significant side effects due to lack of specificity.

Purpose of the Study:

  • To review the oncogenic activation of RET and its role in tumorigenesis.
  • To discuss the clinical features and actionable genetic alterations of RET-altered tumors.
  • To evaluate the efficacy and safety of nonselective and selective RET-targeting agents.

Main Methods:

  • Literature review of studies on RET gene function, aberrations, and targeted therapies.
  • Analysis of clinical trial data for multikinase inhibitors and selective RET inhibitors.
  • Discussion of diagnostic approaches for RET alterations.

Main Results:

  • RET aberrations are key drivers in various cancers, with distinct clinical presentations.
  • Nonselective MKIs targeting RET have shown limited clinical activity and considerable toxicity.
  • Selective RET inhibitors, selpercatinib and pralsetinib, demonstrate promising efficacy and improved safety profiles in early trials.

Conclusions:

  • Targeting RET is a validated therapeutic strategy in oncology.
  • Selective RET inhibitors represent a significant advancement, offering improved outcomes and tolerability for RET-altered tumors.
  • Further research and clinical application of selective RET inhibitors are warranted.