Evidence map›Paper›PMID 24774510›Full record

ArticleBMC research notes2014

Clinicopathological features and prognostic roles of KRAS, BRAF, PIK3CA and NRAS mutations in advanced gastric cancer.

Naoki Takahashi, Yasuhide Yamada, Hirokazu Taniguchi, Masaru Fukahori, Yusuke Sasaki, Hirokazu Shoji, Yoshitaka Honma, Satoru Iwasa, Atsuo Takashima, Ken Kato and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC research notes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Mutational Spectrum, Copy Number Changes, and Outcome: Results of a Sequencing Study of Patients With Newly Diagnosed Myeloma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015
    Trial
  3. Article
  4. International journal of molecular sciences · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Signaling pathways and therapeutic interventions in gastric cancer.Signal transduction and targeted therapy · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. GC1118, a novel anti-EGFR antibody, has potent KRAS mutation-independent antitumor activity compared with cetuximab in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2019
    Article
  19. Article
  20. HER2, NF-Disease markers · 2019
    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

12 authors at 1 institution in 1 country.

Naoki TakahashiGastrointestinal Oncology Division, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan. naoki19800623@gmail.com.
Yasuhide Yamada
Hirokazu Taniguchi
Masaru Fukahori
Yusuke Sasaki
Hirokazu Shoji
Yoshitaka Honma
Satoru Iwasa
Atsuo Takashima
Ken Kato
Tetsuya Hamaguchi
Yasuhiro Shimada
National Cancer Center Hospital East · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRAS-RAF-MEK-ERK and PI3K-AKT pathways form a significant cascade for potential molecular target therapy in advanced cancer. The clinical significance of mutations in these genes in advanced gastric cancer (AGC) is uncertain.

methodsWe collected formalin-fixed, paraffin-embedded and fresh frozen tumor samples from AGC patients and analyzed the KRAS, NRAS, BRAF and PIK3CA mutations by direct-sequencing. We retrospectively investigated the clinicopathological features of these mutations in AGC patients, and selected patients with metastatic gastric cancer.

resultsAmong 167 AGC patients, mutations of KRAS codons 12/13 (N = 8/164, 4.9%), PIK3CA (N = 9/163, 5.5%), and NRAS codon 12/13(N = 3/159, 1.9%) were detected. Comparison of the clinicopathological features of the mutated KRAS, PIK3CA, NRAS genes with an all-wild type of these genes showed that the frequency of the intestinal type was significantly higher in patients whose tumor tissue contained KRAS mutations (P = 0.014). Among 125 patients with metastatic gastric cancer, patients with NRAS codon 12/13 mutations in their tumors had shorter overall survival compared with NRAS wild-type patients (MST: 14.7 vs 8.8 months, P = 0.011). By multivariate analyses, NRAS codon 12/13 mutation was an indicator for poor prognosis in patients with metastatic gastric cancer (adjusted HR 5.607, 95% CI: 1.637-19.203).

conclusionsOur study indicated that mutations of KRAS, PIK3CA and NRAS were rare in AGC. NRAS mutations were likely to associate with poor prognosis in metastatic state of AGC patients, but further validation of other research is required.

Indexed as

Class I Phosphatidylinositol 3-KinasesCohort StudiesFemaleGTP PhosphohydrolasesHumansMaleMembrane ProteinsMiddle AgedMutationNeoplasm StagingPhosphatidylinositol 3-KinasesPrognosisProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)ras ProteinsBRAF protein, humanClass I Phosphatidylinositol 3-KinasesGTP PhosphohydrolasesKRAS protein, humanMembrane ProteinsNRAS protein, humanPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)ras Proteins

Identifiers

PMID24774510
PMCPMC4012089
OpenAlexW2041488531

What OpenQuestion holds

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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.