Evidence map›Paper›PMID 40796139›Full record

ArticleJNCI cancer spectrum2025

TP53 gene and pathway alterations in gastric-type adenocarcinoma of the cervix.

Daiki Higuchi, Maiko Yamaguchi, Erisa Fujii, Mayumi Kobayashi Kato, Kengo Hiranuma, Yuka Asami, Hanako Ono, Takafumi Koyama, Masaaki Komatsu, Ryuji Hamamoto and 9 more

Abstract read
In one paragraph

Article in JNCI cancer spectrum, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

19 authors.

Daiki HiguchiDivision of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan.
Maiko YamaguchiDivision of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan.
Erisa FujiiDivision of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0009-0004-0782-0922
Mayumi Kobayashi KatoDivision of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0003-4065-0289
Kengo HiranumaDepartment of Obstetrics and Gynecology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Yuka AsamiDivision of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0009-0000-2047-5618
Hanako OnoDepartment of Clinical Genomics, National Cancer Center Research Institute, Tokyo, Japan.
Takafumi KoyamaDepartment of Experimental Therapeutics, National Cancer Center Hospital, Tokyo, Japan.ORCID 0000-0001-5807-8458
Masaaki KomatsuDivision of Medical AI Research and Development, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0003-0421-8085
Ryuji HamamotoDivision of Medical AI Research and Development, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0002-2632-1334
Yasuhisa TeraoDepartment of Obstetrics and Gynecology, Juntendo University Faculty of Medicine, Tokyo, Japan.ORCID 0000-0002-9126-3361
Koji MatsumotoDepartment of Obstetrics and Gynecology, Showa Medical University, Tokyo, Japan.ORCID 0000-0001-6184-618X
Akihiko SekizawaDepartment of Obstetrics and Gynecology, Showa Medical University, Tokyo, Japan.ORCID 0000-0003-2249-1333
Mitsuya IshikawaDepartment of Gynecology, National Cancer Center Hospital, Tokyo, Japan.ORCID 0000-0001-8855-2966
Takashi KohnoDivision of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0002-5371-706X
Hiroshi YoshidaDepartment of Diagnostic Pathology, National Cancer Center Hospital, Tokyo, Japan.ORCID 0000-0002-7569-7813
Hideki MakinoshimaTsuruoka Metabolomics Laboratory, National Cancer Center Tsuruoka, Yamagata, Japan.ORCID 0009-0001-8181-6241
Kouya ShiraishiDivision of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0002-5821-7400
Tomoyasu KatoDepartment of Gynecology, National Cancer Center Hospital, Tokyo, Japan.ORCID 0000-0001-9561-1522

Funding

BRIDGEGrant-in-Aid for Challenging Research Pioneering 25K21788Grant-in-Aid for Scientific Research (B) 20H03695Grant-in-Aid for Scientific Research (C) 19K16572Grant-in-Aid for Scientific Research (C) 20K09636Grant-in-Aid for Scientific Research (C) 22K09563Grant-in-Aid for Young Scientists (B) 20K18207National Cancer Center Research and Development Fund 2023-JNCC BiobankNCC Core Facility
6 · The paper itself

Abstract

backgroundHuman papillomavirus infection contributes to the development of almost all cervical malignancies, aside from gastric-type adenocarcinoma of the cervix, a rare aggressive subtype without human papillomavirus infection.

methodsTo address the carcinogenic mechanism of this disease, we performed a comparative multi-omics analysis of gastric-type adenocarcinoma of the cervix and usual-type endocervical adenocarcinoma in 3 independent cohorts of patients with gastric-type adenocarcinoma of the cervix and usual-type endocervical adenocarcinoma. The first cohort comprised 8 gastric-type adenocarcinoma of the cervix and 22 patients with usual-type endocervical adenocarcinoma treated at the National Cancer Center Hospital between 2002 and 2020, who were examined by targeted and whole transcriptome sequencing. The other 2 cohorts comprised 52 patients with gastric-type adenocarcinoma of the cervix and 109 patients with usual-type endocervical adenocarcinoma and 39 patients with gastric-type adenocarcinoma of the cervix and 232 patients with usual-type endocervical adenocarcinoma, whose mutational data were obtained from the Center for Cancer Genomics and Advanced Therapeutics (Japanese patients) and Genomics Evidence Neoplasia Information Exchange (US patients) public databases, respectively. Metabolomic analysis was performed in 8 patients, including 5 with gastric-type adenocarcinoma of the cervix.

resultsTP53 mutations were more prevalent in gastric-type adenocarcinoma of the cervix than in usual-type endocervical adenocarcinoma in all 3 cohorts. Transcriptome analysis consistently revealed frequent suppression of TP53-related pathways in gastric-type adenocarcinoma of the cervix. Metabolites preferentially detected in gastric-type adenocarcinoma of the cervix tissues suggest TP53 alterations are implicated in intratumoral metabolic properties.

conclusionThe development of gastric-type adenocarcinoma of the cervix is likely driven by TP53 mutations, which play a large role in shaping intracellular signaling and metabolic profiles within tumor cells.

Indexed as

AdenocarcinomaGenes, p53Stomach NeoplasmsTumor Suppressor Protein p53Uterine Cervical NeoplasmsAdultAgedCohort StudiesFemaleHumansMetabolomicsMiddle AgedMutationTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID40796139
PMCPMC12459095

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LicenceCC BY-NC-ND
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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.