Evidence map›Paper›PMID 16969076›Full record

ArticleCancer biology & therapy2006

Recurrent KRAS codon 146 mutations in human colorectal cancer.

Sarah Edkins, Sarah O'Meara, Adrian Parker, Claire Stevens, Marcelo Reis, Siân Jones, Chris Greenman, Helen Davies, Gillian Dalgliesh, Simon Forbes and 11 more

Abstract readMulticenter Study
In one paragraph

Article in Cancer biology & therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing 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

107 citing papers in PubMed.

  1. Trial
  2. Systematic and precise interventions for KRAS-mutant cancers.Experimental hematology & oncology · 2026
    Review
  3. Article
  4. Article
  5. Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024
    Review
  6. Article
  7. Review
  8. Characteristic Mutational Damages in Gastric and Colorectal Adenocarcinomas.Asian Pacific journal of cancer prevention : APJCP · 2023
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Mechanistic Differences of Activation of Rac1The journal of physical chemistry. B · 2021
    Article

47 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

21 authors.

Sarah EdkinsCancer Genome Project, Welcome Trust Sanger Institute, Hinxton, UK.
Sarah O'Meara
Adrian Parker
Claire Stevens
Marcelo Reis
Siân Jones
Chris Greenman
Helen Davies
Gillian Dalgliesh
Simon Forbes
Chris Hunter
Raffaella Smith
Philip Stephens
Peter Goldstraw
Andrew Nicholson
Tsun Leung Chan
Victor E Velculescu
Siu Tsan Yuen
Suet Yi Leung
Michael R Stratton
P Andrew Futreal

Funding

Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI LENNON, ANNE MARIE · 1993 to 2022
$54.6M
Large-Scale Genetic Analyses of Human CancerR01CA121113 · NCI · JOHNS HOPKINS UNIVERSITY · PI ANAGNOSTOU, VALSAMO, VELCULESCU, VICTOR E. · 2006 to 2022
$4.3M
NCI NIH HHS CA062924NCI NIH HHS CA121113NCI NIH HHS P50 CA062924NCI NIH HHS R01 CA121113Wellcome Trust 077012
6 · The paper itself

Abstract

An activating point mutation in codon 12 of the HRAS gene was the first somatic point mutation identified in a human cancer and established the role of somatic mutations as the common driver of oncogenesis. Since then, there have been over 11,000 mutations in the three RAS (HRAS, KRAS and NRAS) genes in codons 12, 13 and 61 reported in the literature. We report here the identification of recurrent somatic missense mutations at alanine 146, a highly conserved residue in the guanine nucleotide binding domain. In two independent series of colorectal cancers from Hong Kong and the United States we detected KRAS A146 mutations in 7/126 and 2/94 cases, respectively, giving a combined frequency of 4%. We also detected KRAS A146 mutations in 2/40 (5%) colorectal cell lines, including the NCI-60 colorectal cancer line HCC2998. Codon 146 mutations thus are likely to make an equal or greater contribution to colorectal cancer than codon 61 mutations (4.2% in our combined series, 1% in the literature). Lung adenocarcinomas and large cell carcinomas did not show codon 146 mutations. We did, however, identify a KRAS A146 mutation in the ML-2 acute myeloid leukemia cell line and an NRAS A146 mutation in the NALM-6 B-cell acute lymphoblastic leukemia line, suggesting that the contribution of codon 146 mutations is not entirely restricted to colorectal cancers or to KRAS.

Indexed as

AdenocarcinomaAmino Acid SequenceCarcinoma, Large CellCodonColorectal NeoplasmsDNA Mutational AnalysisDNA, NeoplasmGenes, rasHong KongHumansLeukemia, Myeloid, AcuteMolecular Sequence DataNeoplasm StagingPoint MutationPrecursor Cell Lymphoblastic Leukemia-LymphomaSequence Homology, Amino AcidCodonDNA, Neoplasm

Identifiers

PMID16969076
PMCPMC2714972

What OpenQuestion holds

Textmetadata
LicenceTDM
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.