Evidence map›Paper›PMID 36980522›Full record

ReviewCancers2023

Treatment Strategies for KRAS-Mutated Non-Small-Cell Lung Cancer.

Éabha O'Sullivan, Anna Keogh, Brian Henderson, Stephen P Finn, Steven G Gray, Kathy Gately

Open access · goldFull text readReview
In one paragraph

Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
15.0field-weighted citation impact, top 1% of its field
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

41 citing papers in PubMed, 65 citations in OpenAlex.

  1. Genomic alterations and their correlation with metabolic-related genes in lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. COPD-Lung Cancer Comorbidity: Mechanistic Insights and Precision Oncology Implications.International journal of chronic obstructive pulmonary disease · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Pathologica · 2025
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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

6 authors at 1 institution in 1 country.

Éabha O'SullivanThoracic Oncology Research Group, Department of Clinical Medicine, Trinity Translational Medicine Institute, St. James's Hospital, D08 W9RT Dublin, Ireland.ORCID 0009-0008-1069-7610
Anna KeoghThoracic Oncology Research Group, Laboratory Medicine and Molecular Pathology, Central Pathology Laboratory, St. James's Hospital, D08 RX0X Dublin, Ireland.
Brian HendersonThoracic Oncology Research Group, Department of Clinical Medicine, Trinity Translational Medicine Institute, St. James's Hospital, D08 W9RT Dublin, Ireland.
Stephen P FinnThoracic Oncology Research Group, Laboratory Medicine and Molecular Pathology, Central Pathology Laboratory, St. James's Hospital, D08 RX0X Dublin, Ireland.
Steven G GrayThoracic Oncology Research Group, Department of Clinical Medicine, Trinity Translational Medicine Institute, St. James's Hospital, D08 W9RT Dublin, Ireland.
Kathy GatelyThoracic Oncology Research Group, Department of Clinical Medicine, Trinity Translational Medicine Institute, St. James's Hospital, D08 W9RT Dublin, Ireland.ORCID 0000-0002-9616-424X
St. James's Hospital · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activating mutations in KRAS are highly prevalent in solid tumours and are frequently found in 35% of lung, 45% of colorectal, and up to 90% of pancreatic cancers. Mutated KRAS is a prognostic factor for disease-free survival (DFS) and overall survival (OS) in NSCLC and is associated with a more aggressive clinical phenotype, highlighting the need for KRAS-targeted therapy. Once considered undruggable due to its smooth shallow surface, a breakthrough showed that the activated G12C-mutated KRAS isozyme can be directly inhibited via a newly identified switch II pocket. This discovery led to the development of a new class of selective small-molecule inhibitors against the KRAS G12C isoform. Sotorasib and adagrasib are approved in locally advanced or metastatic NSCLC patients who have received at least one prior systemic therapy. Currently, there are at least twelve KRAS G12C inhibitors being tested in clinical trials, either as a single agent or in combination. In this study, KRAS mutation prevalence, subtypes, rates of occurrence in treatment-resistant invasive mucinous adenocarcinomas (IMAs), and novel drug delivery options are reviewed. Additionally, the current status of KRAS inhibitors, multiple resistance mechanisms that limit efficacy, and their use in combination treatment strategies and novel multitargeted approaches in NSCLC are discussed.

Indexed as

ACOX2adagrasibBRAFdrug resistanceG12C mutationIMAsKRASNSCLCsotorasib

Identifiers

PMID36980522
PMCPMC10046549
OpenAlexW4323572378

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read31
identifiers read22
Read underepoch 390

Registered trials

None linked

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.