Evidence map›Paper›PMID 40249206›Full record

ArticleCancer medicine2025

Genomic Differences and Distinct TP53 Mutation Site-Linked Chemosensitivity in Early- and Late-Onset Gastric Cancer.

Tomohiro Kamio, Yoshiyasu Kono, Kensuke Hirosuna, Toshiki Ozato, Hideki Yamamoto, Akira Hirasawa, Daisuke Ennishi, Shuta Tomida, Shinichi Toyooka, Motoyuki Otsuka

Abstract read
In one paragraph

Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

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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

10 authors.

Tomohiro KamioDepartment of Gastroenterology and Hepatology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Yoshiyasu KonoDepartment of Gastroenterology and Hepatology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.ORCID https://orcid.org/0000-0002-4717-5196
Kensuke HirosunaDepartment of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Toshiki OzatoDepartment of Gastroenterology, Okayama University Hospital, Okayama, Japan.
Hideki YamamotoDepartment of Clinical Genomic Medicine, Okayama University Hospital, Okayama, Japan.
Akira HirasawaDepartment of Clinical Genomic Medicine, Okayama University Hospital, Okayama, Japan.ORCID https://orcid.org/0000-0003-4124-5488
Daisuke EnnishiCenter for Comprehensive Genomic Medicine, Okayama University Hospital, Okayama, Japan.
Shuta TomidaCenter for Comprehensive Genomic Medicine, Okayama University Hospital, Okayama, Japan.
Shinichi ToyookaCenter for Comprehensive Genomic Medicine, Okayama University Hospital, Okayama, Japan.
Motoyuki OtsukaDepartment of Gastroenterology and Hepatology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.ORCID https://orcid.org/0000-0003-2869-2881

Funding

Foundation for Promotion of Cancer ResearchJapan Society for the Promotion of Science 22H02828Japan Society for the Promotion of Science 24K11153Mitsubishi Foundation
6 · The paper itself

Abstract

backgroundGastric cancer (GC) in younger patients often exhibits aggressive behavior and a poorer prognosis than that in older patients. Although the clinical differences may stem from oncogenic gene variations, it is unclear whether genetic differences exist between these groups. This study compared the genetic profiles of early- and late-onset GC and evaluated their impact on treatment outcomes.

methodsWe analyzed genetic data from 1284 patients with GC in the Japanese nationwide Center for Cancer Genomics and Advanced Therapeutics (C-CAT) database, comparing early-onset (≤ 39 years; n = 143) and late-onset (≥ 65 years; n = 1141) groups. The influence of TP53 mutations on the time to treatment failure (TTF) with platinum-based chemotherapy and the sensitivity of cancer cells with different TP53 mutation sites to oxaliplatin were assessed in vitro.

resultsEarly- and late-onset GC showed distinct genetic profiles, with fewer neoantigen-associated genetic changes observed in early-onset cases. In particular, TP53 has distinct mutation sites; R175H and R273 mutations are more frequent in early- and late-onset GC, respectively. The R175H mutation showed higher sensitivity to oxaliplatin in vitro, consistent with the longer TTF in early-onset patients (17.3 vs. 7.0 months, p = 0.013) when focusing on the patients with TP53 mutations.

conclusionGenomic differences, particularly in TP53 mutation sites, between early- and late-onset GC support the need for age-specific treatment strategies.

Indexed as

Drug Resistance, NeoplasmMutationStomach NeoplasmsTumor Suppressor Protein p53AdultAgedAged, 80 and overAge of OnsetFemaleGenomicsHumansMaleMiddle AgedOxaliplatinOxaliplatinTP53 protein, humanTumor Suppressor Protein p53comprehensive genomic profilingearly‐onset gastric canceroxaliplatinTP53

Identifiers

PMID40249206
PMCPMC12007182

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