Evidence map›Paper›PMID 27708434›Full record

ArticleScientific reports2016

Clinical Relevance and Molecular Phenotypes in Gastric Cancer, of TP53 Mutations and Gene Expressions, in Combination With Other Gene Mutations.

Sungjin Park, Jinhyuk Lee, Yon Hui Kim, Jaheun Park, Jung-Woog Shin, Seungyoon Nam

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. ATR-CHK1 Axis Inhibitors in Gastric Cancer Treatment.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
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  14. Article
  15. The Role of SliTrk5 in Central Nervous System.BioMed research international · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Article
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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

6 authors.

Sungjin ParkNew Experimental Therapeutics Branch, National Cancer Center, Goyang-si Gyeonggi-do, 10408, Korea.
Jinhyuk LeeKorean Bioinformation Center (KOBIC), Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Korea.
Yon Hui KimNew Experimental Therapeutics Branch, National Cancer Center, Goyang-si Gyeonggi-do, 10408, Korea.
Jaheun ParkDigital Information Computing Center, Inje University, Gimhae, Gyeongnam, 50834, Korea.
Jung-Woog ShinDepartment of Biomedical Engineering, Inje University, Gimhae, Gyeongnam, 50834, Korea.
Seungyoon NamNew Experimental Therapeutics Branch, National Cancer Center, Goyang-si Gyeonggi-do, 10408, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While altered TP53 is the most frequent mutation in gastric cancer (GC), its association with molecular or clinical phenotypes (e.g., overall survival, disease-free survival) remains little known. To that end, we can use genome-wide approaches to identify altered genes significantly related to mutated TP53. Here, we identified significant differences in clinical outcomes, as well as in molecular phenotypes, across specific GC tumor subpopulations, when combining TP53 with other signaling networks, including WNT and its related genes NRXN1, CTNNB1, SLITRK5, NCOR2, RYR1, GPR112, MLL3, MTUS2, and MYH6. Moreover, specific GC subpopulations indicated by dual mutation of NRXN1 and TP53 suggest different drug responses, according to the Connectivity Map, a pharmacological drug-gene association tool. Overall, TP53 mutation status in GC is significantly relevant to clinical or molecular categories. Thus, our approach can potentially provide a patient stratification strategy by dissecting previously unknown multiple TP53-mutated patient groups.

Indexed as

Mutationbeta CateninCalcium-Binding ProteinsCell Adhesion Molecules, NeuronalCell Line, TumorGene Expression Regulation, NeoplasticHumansNerve Tissue ProteinsNeural Cell Adhesion MoleculesPhenotypeStomach NeoplasmsTumor Suppressor Protein p53beta CateninCalcium-Binding ProteinsCell Adhesion Molecules, NeuronalCTNNB1 protein, humanNerve Tissue ProteinsNeural Cell Adhesion MoleculesNRXN1 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID27708434
PMCPMC5052597

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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.