Evidence map›Paper›PMID 23702733›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2013

No KRAS mutations found in gastrointestinal stromal tumors (GISTs): molecular genetic study of 514 cases.

Jerzy Lasota, Liqiang Xi, Tiffany Coates, RaShonda Dennis, Moses O Evbuomwan, Zeng-Feng Wang, Mark Raffeld, Markku Miettinen

Open access · bronzeAbstract read
In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Updated Asian consensus guidelines for the diagnosis and management of gastrointestinal stromal tumor (2025).Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. The Emerging Role of Succinate Dehyrogenase Genes (SDHx) in Tumorigenesis.International journal of hematology-oncology and stem cell research · 2019
    Article
  8. Article
  9. Article
  10. Observational
  11. Article
  12. Frequency and clinicopathologic profile of PIK3CA mutant GISTs: molecular genetic study of 529 cases.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. On the prevalence of KRAS mutations in GISTs.Virchows Archiv : an international journal of pathology · 2013
    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

8 authors at 1 institution in 1 country.

Jerzy LasotaLaboratory of Pathology, National Cancer Institute (NCI), Bethesda, MD, USA.
Liqiang Xi
Tiffany Coates
RaShonda Dennis
Moses O Evbuomwan
Zeng-Feng Wang
Mark Raffeld
Markku Miettinen
National Cancer Institute · US

Funding

Molecular Diagnostics Core LaboratoryZICBC011079 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI XI, LIQIANG · 2009 to 2025
$33.8M
Immunohistochemical and genomic analysis of tumorsZIABC011427 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MIETTINEN, MARKKU · 2012 to 2025
$24.0M
Intramural NIH HHS ZIA BC011427
6 · The paper itself

Abstract

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. A great majority of GISTs is driven by pathological activation of KIT or platelet-derived growth factor receptor-α (PDGFRA), two closely related receptor tyrosine kinases. However, other genetic changes including gain-of-function BRAF mutations and loss of succinate dehydrogenase (SDH) complex activity have been identified in the subsets of KIT-, PDGFRA-wild type tumors. Genetic mutations affecting KIT, PDGFRA, BRAF and SDH complex functions are believed to be mutually exclusive events. Recently, KRAS codon 12 and 13 mutations were reported in a small subset of KIT or PDGFRA mutant GISTs. Moreover, in in vitro experiments, KIT mutants with concurrent KRAS mutation showed resistance to imatinib, a receptor tyrosine kinase inhibitor used in GIST treatment. The aim of this study was to evaluate a large cohort of GISTs to define frequency and clinical significance of KRAS mutations in this type of cancer. A well-characterized cohort of 514 GISTs was screened for KRAS mutations using Sanger sequencing (n=450) and pyrosequencing (n=64). In all, 350 gastric, 100 intestinal and 64 primary disseminated GISTs were analyzed. No KRAS mutations were found. In GIST, KRAS mutations are extremely rare if they exist (<0.2%). Thus, mutational activation of KRAS does not seem to play any significant role in the development and progression of this type of cancer.

Indexed as

DNA Mutational AnalysisMutationDisease ProgressionGastrointestinal Stromal TumorsGene FrequencyGenetic Predisposition to DiseaseGenetic TestingHumansIntestinal NeoplasmsPhenotypePredictive Value of TestsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsRisk FactorsStomach NeoplasmsKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras Proteins

Identifiers

PMID23702733
PMCPMC7560948
OpenAlexW2092808333

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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.