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Oncogenic Gene Fusion Detection Using Anchored Multiplex Polymerase Chain Reaction Followed by Next Generation Sequencing
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RET fusions in solid tumors.

Andrew Y Li1, Michael G McCusker2, Alessandro Russo3

  • 1Department of Medicine, Division of General Internal Medicine, University of Maryland Medical Center, Baltimore, United States.

Cancer Treatment Reviews
|November 13, 2019
PubMed
Summary
This summary is machine-generated.

RET alterations drive various cancers, including thyroid and lung. Targeted therapies like tyrosine kinase inhibitors show promise, with new selective RET inhibitors in clinical trials offering hope for RET-driven diseases.

Keywords:
BLU-667FusionLOXO-292NSCLCPralsetinibRETRearrangementSelpercatinibSolid

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The RET proto-oncogene plays critical roles in development and physiology.
  • RET alterations, including mutations and rearrangements, are implicated in diverse cancers such as papillary thyroid carcinoma (PTC) and non-small cell lung cancer (NSCLC).
  • RET alterations are also found in breast, pancreatic, colorectal cancers, melanoma, neuroblastoma, and small intestine neuroendocrine tumors, correlating with tumor progression.

Purpose of the Study:

  • To review the role of RET alterations in oncogenesis.
  • To discuss the therapeutic implications of targeting RET in cancer.
  • To highlight the development and efficacy of tyrosine kinase inhibitors (TKIs) against RET-driven malignancies.

Main Methods:

  • Literature review of studies on RET proto-oncogene, its mutations, and fusions in various cancers.
  • Analysis of the prevalence of RET alterations in different tumor types.
  • Examination of the mechanisms of action and clinical outcomes of existing and novel TKIs targeting RET.

Main Results:

  • RET alterations, particularly fusions (e.g., KIF5B-RET in NSCLC, CCDC6-RET and NCOA4-RET in PTC), are significant drivers in specific cancers.
  • RET alterations are found in a notable percentage of sporadic PTC (2.5-73%) and NSCLC (1-3%).
  • Emerging selective RET inhibitors (selpercatinib, pralsetinib) demonstrate promising efficacy with manageable safety profiles in early clinical trials.

Conclusions:

  • RET fusions represent a validated therapeutic target in oncologic treatment.
  • Further research into RET fusion prevalence, pathogenesis, and the development of advanced TKIs is crucial.
  • Targeting RET offers a promising strategy for patients with RET-driven cancers.