Evidence map›Paper›PMID 39177972›Full record

ReviewThe oncologist2024

Advances and future directions in ROS1 fusion-positive lung cancer.

Mary C Boulanger, Jaime L Schneider, Jessica J Lin

Abstract readReview
In one paragraph

Review in The oncologist, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed.

  1. Taletrectinib inJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025
    Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. AcquiredCurrent oncology (Toronto, Ont.) · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Frontiers in oncology · 2026
    Review
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Mary C BoulangerDepartment of Medicine and Cancer Center, Massachusetts General Hospital, Boston, MA 02114, United States.ORCID 0000-0002-1368-6350
Jaime L SchneiderDepartment of Medicine and Cancer Center, Massachusetts General Hospital, Boston, MA 02114, United States.ORCID 0000-0003-2591-2279
Jessica J LinDepartment of Medicine and Cancer Center, Massachusetts General Hospital, Boston, MA 02114, United States.ORCID 0000-0001-7373-3916

Funding

Project 3P50CA265826 · NCI · DANA-FARBER CANCER INST · PI David A Barbie · 2022 to 2026
$13.7M
Training Program in Cancer Biology and TherapeuticsT32CA071345 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI Daniel A. Haber, Lecia V. Sequist · 1997 to 2026
$10.6M
Overcoming Resistance Mechanisms to Anaplastic Lymphoma Kinase InhibitorsR01CA164273 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI Aaron N Hata, Jessica Jiyeong Lin · 2012 to 2026
$5.5M
NCI NIH HHS P50 CA265826NCI NIH HHS R01 CA164273NCI NIH HHS R01CA164273NCI NIH HHS T32 CA071345
6 · The paper itself

Abstract

ROS1 gene fusions are an established oncogenic driver comprising 1%-2% of non-small cell lung cancer (NSCLC). Successful targeting of ROS1 fusion oncoprotein with oral small-molecule tyrosine kinase inhibitors (TKIs) has revolutionized the treatment landscape of metastatic ROS1 fusion-positive (ROS1+) NSCLC and transformed outcomes for patients. The preferred Food and Drug Administration-approved first-line therapies include crizotinib, entrectinib, and repotrectinib, and currently, selection amongst these options requires consideration of the systemic and CNS efficacy, tolerability, and access to therapy. Of note, resistance to ROS1 TKIs invariably develops, limiting the clinical benefit of these agents and leading to disease relapse. Progress in understanding the molecular mechanisms of resistance has enabled the development of numerous next-generation ROS1 TKIs, which achieve broader coverage of ROS1 resistance mutations and superior CNS penetration than first-generation TKIs, as well as other therapeutic strategies to address TKI resistance. The approach to subsequent therapy depends on the pace and pattern of progressive disease on the initial ROS1 TKI and, if known, the mechanisms of TKI resistance. Herein, we describe a practical approach for the selection of initial and subsequent therapies for metastatic ROS1+ NSCLC based on these clinical considerations. Additionally, we explore the evolving evidence for the optimal treatment of earlier-stage, non-metastatic ROS1+ NSCLC, while, in parallel, highlighting future research directions with the goal of continuing to build on the tremendous progress in the management of ROS1+ NSCLC and ultimately improving the longevity and well-being of people living with this disease.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene ProteinsDrug Resistance, NeoplasmHumansOncogene Proteins, FusionOncogene Proteins, FusionProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene ProteinsROS1 protein, humandrug resistancenon–small cell lung cancerROS1targeted therapytyrosine kinase inhibitor

Identifiers

PMID39177972
PMCPMC11546726

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.