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Updated: May 11, 2026

Oncogenic Gene Fusion Detection Using Anchored Multiplex Polymerase Chain Reaction Followed by Next Generation Sequencing
09:49

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Published on: July 5, 2019

Molecular pathways: ROS1 fusion proteins in cancer

Kurtis D Davies1, Robert C Doebele

  • 1Division of Medical Oncology, Department of Medicine, University of Colorado - Anschutz Medical Campus, Aurora, Colorado, USA.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|May 31, 2013
PubMed

Insights

Genetic rearrangements in ROS1 (receptor tyrosine kinase) lead to cancer growth. Inhibiting these ROS1 fusions, like with crizotinib in non-small cell lung cancer, shows therapeutic promise.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Constitutive kinase activation is a hallmark of cancer, driving tumor cell growth and survival.
  • ROS1 (receptor tyrosine kinase) rearrangements create constitutively active fusion proteins, implicated in various cancers.

Purpose of the Study:

  • To review recent preclinical and clinical findings on ROS1 gene fusions in human cancers.
  • To highlight the therapeutic potential of targeting ROS1 alterations.

Main Methods:

  • Literature review of preclinical studies.
  • Analysis of clinical trial data for ROS1-targeted therapies.

Main Results:

  • ROS1 gene fusions identified in glioblastoma, non-small cell lung cancer (NSCLC), cholangiocarcinoma, and other malignancies.
  • The small-molecule inhibitor crizotinib demonstrates efficacy against ROS1 fusion-positive NSCLC.
  • Targeting constitutively active ROS1 kinase domains offers a promising therapeutic strategy.

Conclusions:

  • ROS1 fusions are oncogenic drivers across a spectrum of cancers.
  • Targeted inhibition of ROS1 fusion proteins represents an effective therapeutic approach, particularly in NSCLC.

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