Evidence map›Paper›PMID 39799325›Full record

ReviewMolecular cancer2025

Targeting KRAS: from metabolic regulation to cancer treatment.

Yanyan Shi, Huiling Zheng, Tianzhen Wang, Shengpu Zhou, Shiqing Zhao, Mo Li, Baoshan Cao

Abstract readReview
In one paragraph

Review in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing 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

50 citing papers in PubMed.

  1. Design, synthesis and biological evaluation of novel KRAS-G12D inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2026
    Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Targeted therapeutic strategies forTranslational lung cancer research · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Integrating multi-omics data for next-generation cancer research and precision medicine.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  14. Article
  15. Review
  16. CSIE: cancer subtyping via inference and ensemble.Briefings in bioinformatics · 2026
    Article
  17. Small-molecule degraders for oncogenic KRASNature communications · 2026
    Article
  18. Review
  19. Systematic and precise interventions for KRAS-mutant cancers.Experimental hematology & oncology · 2026
    Review
  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

7 authors.

Yanyan Shi *Research Center of Clinical Epidemiology, Peking University Third Hospital, Beijing, 100191, China.
Huiling Zheng *Department of Gastroenterology, Peking University Third Hospital, Beijing, 100191, China.
Tianzhen Wang *State Key Laboratory of Female Fertility Promotion, Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191, China.
Shengpu ZhouResearch Center of Clinical Epidemiology, Peking University Third Hospital, Beijing, 100191, China.
Shiqing ZhaoResearch Center of Clinical Epidemiology, Peking University Third Hospital, Beijing, 100191, China.
Mo LiState Key Laboratory of Female Fertility Promotion, Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191, China. limo@hsc.pku.edu.cn.
Baoshan CaoDepartment of Medical Oncology and Radiation Sickness, Peking University Third Hospital, Beijing, 100191, China. caobaoshan0711@aliyun.com.

Funding

Beijing Municipal Natural Science Foundation (Key program) Z220011National Natural Science Foundation of China T2225006National Natural Science Foundation of China (NSFC) 82272948
6 · The paper itself

Abstract

The Kirsten rat sarcoma viral oncogene homolog (KRAS) protein plays a key pathogenic role in oncogenesis, cancer progression, and metastasis. Numerous studies have explored the role of metabolic alterations in KRAS-driven cancers, providing a scientific rationale for targeting metabolism in cancer treatment. The development of KRAS-specific inhibitors has also garnered considerable attention, partly due to the challenge of acquired treatment resistance. Here, we review the metabolic reprogramming of glucose, glutamine, and lipids regulated by oncogenic KRAS, with an emphasis on recent insights into the relationship between changes in metabolic mechanisms driven by KRAS mutant and related advances in targeted therapy. We also focus on advances in KRAS inhibitor discovery and related treatment strategies in colorectal, pancreatic, and non-small cell lung cancer, including current clinical trials. Therefore, this review provides an overview of the current understanding of metabolic mechanisms associated with KRAS mutation and related therapeutic strategies, aiming to facilitate the understanding of current challenges in KRAS-driven cancer and to support the investigation of therapeutic strategies.

Indexed as

Antineoplastic AgentsEnergy MetabolismNeoplasmsProto-Oncogene Proteins p21(ras)AnimalsHumansMolecular Targeted TherapyMutationAntineoplastic AgentsKRAS protein, humanProto-Oncogene Proteins p21(ras)Cancer metabolismKRAS-driven cancersKRAS inhibitorsMetabolic reprogramming

Identifiers

PMID39799325
PMCPMC11724471

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.