Evidence map›Paper›PMID 32725342›Full record

ReviewCancer metastasis reviews2020

Molecular epidemiology and diagnostics of KRAS mutations in human cancer.

Jozsef Timar, Karl Kashofer

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed, 3 pooled it
11.7field-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

189 citing papers in PubMed, 3 syntheses or guidelines pooled it, 319 citations in OpenAlex.

  1. Pooled it
  2. Mucoepidermoid carcinoma (MEC) and adenosquamous carcinoma (ASC), the same or different entities?Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022
    Pooled it
  3. Pooled it
  4. Design, synthesis and biological evaluation of novel KRAS-G12D inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2026
    Article
  5. Article
  6. Discovery of TCR-like antibodies to the KRAS G12D neoantigen via in silico-in vitro workflow.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. KRAS-mediated CCDC6 degradation drives xCT upregulation and ferroptosis evasion.Apoptosis : an international journal on programmed cell death · 2026
    Article
  14. Article
  15. Renaissance of farnesyltransferase inhibitors in cancer.Journal of translational medicine · 2026
    Review
  16. Article
  17. RRAS and RRAS2 Mutations Are Recurrent Oncogenic Drivers in Lung Cancer and Are Sensitive to the Pan-RAS Inhibitor RMC-6236.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  18. Small-molecule degraders for oncogenic KRASNature communications · 2026
    Article
  19. Systematic and precise interventions for KRAS-mutant cancers.Experimental hematology & oncology · 2026
    Review
  20. Article

129 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Jozsef Timar2nd Department of Pathology, Semmelweis University, Budapest, Hungary. jtimar@gmail.com.
Karl KashoferDiagnostic and Research Institute of Pathology, Medical University of Graz, Auenbruggerpl. 2, 8036, Graz, Austria.
Medical University of Graz · ATSemmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RAS mutation is the most frequent oncogenic alteration in human cancers. KRAS is the most frequently mutated followed by NRAS. The emblematic KRAS mutant cancers are pancreatic, colorectal, lung adenocarcinomas and urogenital cancers. KRAS mutation frequencies are relatively stable worldwide in various cancer types with the one exception of lung adenocarcinoma. The frequencies of KRAS variant alleles appears cancer type specific, reflecting the various carcinogenic processes. In addition to point mutation KRAS, allelic imbalances are also frequent in human cancers leading to the predominance of a mutant allele. KRAS mutant cancers are characterized by typical, cancer-type-specific co-occurring mutations and distinct gene expression signatures. The heterogeneity of KRAS mutant primary cancers is significant, affecting the variant allele frequency, which could lead to unpredictable branching development in metastases. Selection of minute mutant subclones in the primary tumors or metastases during target therapies can also occur frequently in lung or colorectal cancers leading to acquired resistance. Ultrahigh sensitivity techniques are now routinely available for diagnostic purposes, but the proper determination of mutant allele frequency of KRAS in the primary or metastatic tissues may have larger clinical significance.

Indexed as

AnimalsGenes, rasHumansMolecular EpidemiologyMutationNeoplasmsProto-Oncogene Proteins p21(ras)KRAS protein, humanProto-Oncogene Proteins p21(ras)DiagnosticsEpidemiologyHuman cancerKRAS mutationTumor progression

Identifiers

PMID32725342
PMCPMC7680318
OpenAlexW3045897752

What OpenQuestion 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 OpenQuestion graph.