Evidence map›Paper›PMID 24510342›Full record

ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2015

Integrated analysis of cancer-related pathways affected by genetic and epigenetic alterations in gastric cancer.

Yukie Yoda, Hideyuki Takeshima, Tohru Niwa, Jeong Goo Kim, Takayuki Ando, Ryoji Kushima, Toshiro Sugiyama, Hitoshi Katai, Hirokazu Noshiro, Toshikazu Ushijima

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In one paragraph

Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 2 pooled it
5.6field-weighted citation impact, top 3% 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

73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 166 citations in OpenAlex.

  1. Pooled it
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  13. The methylation level of a single cancer risk marker gene reflects methylation burden in gastric mucosa.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023
    Article
  14. Article
  15. Big Data in Gastroenterology Research.International journal of molecular sciences · 2023
    Review
  16. Review
  17. Article
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  19. Influence of the Microbiome Metagenomics and Epigenomics on Gastric Cancer.International journal of molecular sciences · 2022
    Review
  20. Prediction of tissue origin of adenocarcinomas in the esophagogastric junction by DNA methylation.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022
    Article

13 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

10 authors at 4 institutions in 3 countries.

Yukie YodaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
Hideyuki Takeshima
Tohru Niwa
Jeong Goo Kim
Takayuki Ando
Ryoji Kushima
Toshiro Sugiyama
Hitoshi Katai
Hirokazu Noshiro
Toshikazu Ushijima
Tokyo National Hospital · JPUniversity of Toyama · JPNational Cancer Research Institute · GBSaga University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe profiles of genetic and epigenetic alterations in cancer-related pathways are considered to be useful for selection of patients likely to respond to specific drugs, including molecular-targeted and epigenetic drugs. In this study, we aimed to characterize such profiles in gastric cancers (GCs).

methodsGenetic alterations of 55 cancer-related genes were analyzed by a benchtop next-generation sequencer. DNA methylation statuses were analyzed by a bead array with 485,512 probes.

resultsThe WNT pathway was activated by mutations of CTNNB1 in 2 GCs and potentially by aberrant methylation of its negative regulators, such as DKK3, NKD1, and SFRP1, in 49 GCs. The AKT/mTOR pathway was activated by mutations of PIK3CA and PTPN11 in 4 GCs. The MAPK pathway was activated by mutations and gene amplifications of ERBB2, FLT3, and KRAS in 11 GCs. Cell-cycle regulation was affected by aberrant methylation of CDKN2A and CHFR in 13 GCs. Mismatch repair was affected by a mutation of MLH1 in 1 GC and by aberrant methylation of MLH1 in 2 GCs. The p53 pathway was inactivated by mutations of TP53 in 19 GCs and potentially by aberrant methylation of its downstream genes in 38 GCs. Cell adhesion was affected by mutations of CDH1 in 2 GCs.

conclusionsGenes involved in cancer-related pathways were more frequently affected by epigenetic alterations than by genetic alterations. The profiles of genetic and epigenetic alterations are expected to be useful for selection of the patients who are likely to benefit from specific drugs.

Indexed as

DNA MethylationEpigenesis, GeneticMutationAdultAgedAged, 80 and overCase-Control StudiesFemaleGene AmplificationGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMaleMetabolic Networks and PathwaysMiddle AgedPromoter Regions, GeneticMTOR protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID24510342
OpenAlexW1977977283

What OpenQuestion holds

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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.