Evidence map›Paper›PMID 41299036›Full record

ArticleNPJ precision oncology2025

KRAS-targeted therapies in colorectal cancer: a systematic analysis of mutations, inhibitors, and clinical trials.

Maria Navarro-Jiménez, Beatriz González, Nuria Mulet, Cinta Hierro, Sergio Alonso

Abstract read
In one paragraph

Article in NPJ precision oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Review
  2. Ultra-rare TP53 and KRAS variants predict survival in ICI-treated solid tumours.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. p53 and p21 Status Influences Cellular Response to Metformin inCurrent issues in molecular biology · 2026
    Article
  11. Review
  12. Review
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  14. 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

5 authors.

Maria Navarro-Jiménez *Cancer Genetics and Epigenetics Group (CGE), Translational Program in Cancer Research (CARE), Germans Trias i Pujol Research Institute (IGTP), Badalona, Spain.
Beatriz González *Cancer Genetics and Epigenetics Group (CGE), Translational Program in Cancer Research (CARE), Germans Trias i Pujol Research Institute (IGTP), Badalona, Spain.
Nuria MuletDepartment of Medical Oncology, Institut Català d'Oncologia (ICO) Badalona, Badalona, Spain.
Cinta HierroDepartment of Medical Oncology, Institut Català d'Oncologia (ICO) Badalona, Badalona, Spain.
Sergio AlonsoCancer Genetics and Epigenetics Group (CGE), Translational Program in Cancer Research (CARE), Germans Trias i Pujol Research Institute (IGTP), Badalona, Spain. salonsou@igtp.cat.

Funding

Fundación Mutua Madrileña AP174232020Fundació Olga Torres Beca Dionís Torres Segura 2024Instituto de Salud Carlos III Spanish Ministry of Science FIS PI21/01766Instituto de Salud Carlos III Spanish Ministry of Science FIS PI24/00824Sociedad Española de Oncología Médica Proyectos de Investigación 2024
6 · The paper itself

Abstract

KRAS mutations occur in over one-third of colorectal cancers (CRC), primarily affecting codons 12 and 13, and less frequently codons 61, 117, and 146. Rare mutations in other codons have been reported, but often lack clear functional significance. These mutations activate pathways that drive cell proliferation, impair differentiation, and suppress apoptosis. KRAS-mutant CRCs are associated with poorer prognosis, higher recurrence rates, reduced chemotherapy response, and resistance to EGFR-targeted therapies. Stratifying patients by KRAS mutation status is now standard for guiding treatment, though not all mutations confer the same oncogenicity or therapeutic response. Once considered undruggable, recent advances have led to the development of inhibitors targeting specific KRAS mutant isoforms. Consequently, precise characterization of KRAS mutational profiles is critical to optimize treatment strategies in CRC. This study provides a systematic analysis of KRAS mutation frequency and co-occurrence, reviews current targeted therapies, and examines ongoing clinical trials for the most prevalent KRAS alterations in CRC.

Identifiers

PMID41299036
PMCPMC12658183

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.