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Cited by 121Lung Cancer Treatments and MutationsLung Cancer Research StudiesCancer Genomics and Diagnostics

ROS-1 Fusions in Non-Small-Cell Lung Cancer: Evidence to Date

Open access
Gendarme, Sébastien, Bylicki, Olivier, Chouaid, Christos, Guisier, Florian·2022·Current Oncology
DOI 10.3390/curroncol29020057PMC PMC8870726
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Abstract

The ROS-1 gene plays a major role in the oncogenesis of numerous tumors. ROS-1 rearrangement is found in 0.9–2.6% of non-small-cell lung cancers (NSCLCs), mostly lung adenocarcinomas, with a significantly higher rate of women, non-smokers, and a tendency to a younger age. It has been demonstrated that ROS-1 is a true oncogenic driver, and tyrosine kinase inhibitors (TKIs) targeting ROS-1 can block tumor growth and provide clinical benefit for the patient. Since 2016, crizotinib has been the first-line reference therapy, with two-thirds of the patients’ tumors responding and progression-free survival lasting ~20 months. More recently developed are ROS-1-targeting TKIs that are active against resistance mechanisms appearing under crizotinib and have better brain penetration. This review summarizes current knowledge on ROS-1 rearrangement in NSCLCs, including the mechanisms responsible for ROS-1 oncogenicity, epidemiology of ROS-1-positive tumors, methods for detecting rearrangement, phenotypic, histological, and molecular characteristics, and their therapeutic management. Much of this work is devoted to resistance mechanisms and the development of promising new molecules.

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Crossref · 10.3390/curroncol29020057

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  • Patients treated with first-generation ROS1 TKIs progress because of off-target bypass pathway activation, leading to refractory disease, development of on-target acquired resistance mutations such as G2032R, or brain metastases.

    “ROS1 tyrosine kinase inhibitors (TKIs) transformed clinical outcomes for ROS1+ NSCLC; however, patients treated with first-generation TKIs progress because of off-target bypass pathway activation, leading to refractory disease, development of on-target acquired resistance mutations such as G2032R, or brain metastases.1,6”

    From Taletrectinib in <i>ROS1</i> + Non–Small Cell Lung Cancer: TRUST (2025) · cites this paper as [1]

  • ROS1 gene fusions are oncogenic molecular alterations that drive persistent downstream signaling and dysregulated cell differentiation, proliferation, and survival.

    “Proto-oncogene tyrosine-protein kinase 1 (ROS1) gene fusions, first reported in 2007,1,2 are oncogenic molecular alterations resulting in constitutive activation of the ROS1 kinase domain and drive persistent downstream signaling and dysregulated cell differentiation, proliferation, and survival.”

    From Taletrectinib in <i>ROS1</i> + Non–Small Cell Lung Cancer: TRUST (2025) · cites this paper as [1]

  • Patients with ROS1+ NSCLC tend to be female, younger than patients without driver alterations, diagnosed at advanced stage (III-IV), have adenocarcinoma, and most are never smokers.

    “Patients with ROS1 fusion–positive (ROS1+) NSCLC tend to be female, are younger than patients without driver alterations, are diagnosed at an advanced stage (III-IV), have adenocarcinoma, and most are never smokers.1”

    From Taletrectinib in <i>ROS1</i> + Non–Small Cell Lung Cancer: TRUST (2025) · cites this paper as [1]

  • ROS1 fusions are rare genetic events reported in multiple solid tumors, including NSCLC, with prevalence 0.9% to 2.6%.

    “These ROS1 fusions are rare genetic events reported in multiple solid tumors, including non–small cell lung cancer (NSCLC), where the prevalence is 0.9% to 2.6%.1,3-5”

    From Taletrectinib in <i>ROS1</i> + Non–Small Cell Lung Cancer: TRUST (2025) · cites this paper as [1]

  • Approximately one third of patients with ROS1+ NSCLC have brain metastasis at diagnosis, which can be as high as 50% in previously treated patients.

    “Approximately one third of patients with ROS1+ NSCLC have a brain metastasis at diagnosis, which can be as high as 50% in previously treated patients.1,30”

    From Taletrectinib in <i>ROS1</i> + Non–Small Cell Lung Cancer: TRUST (2025) · cites this paper as [1]

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Authors
Gendarme, S., Bylicki, O., Chouaid, C., & Guisier, F.
Affiliations
  • Inserm (FR)
  • Hôpital d'Instruction des Armées Sainte-Anne (FR)
Corresponding author
Gendarme, Sébastien
ORCID
Venue
Current Oncology
Publisher
MDPI AG
Published
2022-01-28
Volume
29
Issue
2
Pages
641-658
ISSN
  • 1198-0052 (ISSN-L)
  • 1718-7729
DOI
10.3390/curroncol29020057
PMC
PMC8870726
OpenAlex
W4214668206
Cited by
121
References
131
Citations by year
2026: 13 · 2025: 44 · 2024: 30 · 2023: 29 · 2022: 5
FWCI
4.67
Type
journal article
Language
en
Open access
Licence
Locations
  • Current Oncology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • HAL (submittedVersion, other-oa)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
  • Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Keywords
non-small cell lung cancer, lung adenocarcinoma, tyrosine kinase inhibitors, crizotinib, crizotinib resistance, targeted therapy, brain penetration
MeSH terms
Anaplastic Lymphoma Kinase, Carcinoma, Non-Small-Cell Lung, Female, Humans, Lung Neoplasms, Gene Rearrangement, Reactive Oxygen Species, Protein Kinase Inhibitors

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