Evidence map›Paper›PMID 38734764›Full record

ReviewCancer gene therapy2024

Targeting KRASG12D mutation in non-small cell lung cancer: molecular mechanisms and therapeutic potential.

Yining Tang, Xi Pu, Xiao Yuan, Zhonghao Pang, Feng Li, Xu Wang

Abstract readReview
In one paragraph

Review in Cancer gene therapy, 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. Design, synthesis and biological evaluation of novel KRAS-G12D inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2026
    Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Targeted therapeutic strategies forTranslational lung cancer research · 2026
    Review
  7. Article
  8. Article
  9. Loss of PIK3CA allowsbioRxiv : the preprint server for biology · 2026
    Article
  10. Article
  11. Article
  12. Review
  13. A KRASMolecular therapy. Oncology · 2025
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Biodistribution ofACS omega · 2025
    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

6 authors.

Yining TangDepartment of Radiation Oncology, Cancer Institute of Jiangsu University, Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, China.ORCID 0009-0006-5142-9538
Xi PuDepartment of Radiation Oncology, Cancer Institute of Jiangsu University, Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, China.
Xiao YuanDepartment of Radiation Oncology, Cancer Institute of Jiangsu University, Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, China.
Zhonghao PangDepartment of Thoracic Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, China.
Feng LiDepartment of Thoracic Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, China. 1000011360@ujs.edu.cn.ORCID 0009-0001-2819-7779
Xu WangDepartment of Radiation Oncology, Cancer Institute of Jiangsu University, Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, Jiangsu, China. wangxu@ujs.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung malignant tumors are a type of cancer with high incidence and mortality rates worldwide. Non-small cell lung cancer (NSCLC) accounts for over 80% of all lung malignant tumors, and most patients are diagnosed at advanced stages, leading to poor prognosis. Over the past decades, various oncogenic driver alterations associated with lung cancer have been identified, each of which can potentially serve as a therapeutic target. Rat sarcoma (RAS) genes are the most commonly mutated oncogenes in human cancers, with Kirsten rat sarcoma (KRAS) being the most common subtype. The role of KRAS oncogene in NSCLC is still not fully understood, and its impact on prognosis remains controversial. Despite the significant advancements in targeted therapy and immune checkpoint inhibitors (ICI) that have transformed the treatment landscape of advanced NSCLC in recent years, targeting KRAS (both directly and indirectly) remains challenging and is still under intensive research. In recent years, significant progress has been made in the development of targeted drugs targeting the NSCLC KRASG12C mutant subtype. However, research progress on target drugs for the more common KRASG12D subtype has been slow, and currently, no specific drugs have been approved for clinical use, and many questions remain to be answered, such as the mechanisms of resistance in this subtype of NSCLC, how to better utilize combination strategies with multiple treatment modalities, and whether KRASG12D inhibitors offer substantial efficacy in the treatment of advanced NSCLC patients.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsMutationProto-Oncogene Proteins p21(ras)AnimalsHumansMolecular Targeted TherapyKRAS protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID38734764
PMCPMC11257988

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.