Evidence map›Paper›PMID 41160109›Full record

ArticleVirchows Archiv : an international journal of pathology2026

Multi-institutional study of mesonephric-like adenocarcinoma: its clinicopathological characteristics and histogenetic association with ectopic endometrium.

Yu Miyama, Kousuke Uranishi, Masataka Hirasaki, Akiko Tonooka, Fumi Kawakami, Yoshiki Mikami, Takako Kiyokawa, Hiroshi Kajiwara, Junichi Shiraishi, Eiji Kudo and 12 more

Abstract readMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Virchows Archiv : an international journal of pathology, 2026. 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. 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

22 authors.

Yu MiyamaDepartment of Pathology, Saitama Medical University International Medical Center, Yamane 1397-1,, Hidaka, 350-1298, Saitama, Japan.ORCID http://orcid.org/0000-0001-5901-6961
Kousuke UranishiDivision of Biomedical Sciences, Research Center for Genomic Medicine, Saitama Medical University, Hidaka, Saitama, Japan.
Masataka HirasakiDepartment of Clinical Cancer Genomics, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Akiko TonookaDivision of Pathology, Cancer Institute, Japanese Foundation for Cancer Research, Koto, Tokyo, Japan.
Fumi KawakamiDepartment of Diagnostic Pathology, Kumamoto University Hospital, Kumamoto, Kumamoto, Japan.
Yoshiki MikamiDepartment of Diagnostic Pathology, Kumamoto University Hospital, Kumamoto, Kumamoto, Japan.
Takako KiyokawaDepartment of Pathology, The Jikei University School of Medicine, Minato, Tokyo, Japan.
Hiroshi KajiwaraDepartment of Pathology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Junichi ShiraishiDepartment of Pathology, National Hospital Organization Tokyo Medical Center, Meguro, Tokyo, Japan.
Eiji KudoDepartment of Pathology, Tokushima Prefectural Central Hospital, Tokushima, Tokushima, Japan.
Kozue ItoDepartment of Pathology, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan.
Morihiro HigashiDepartment of Pathology, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan.
Sachiko MinamiguchiDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Kyoto, Japan.
Nasa OkazakiDepartment of Diagnostic Pathology, Japanese Red Cross Kumamoto Hospital, Kumamoto, Kumamoto, Japan.
Yuzuru KondoDepartment of Pathology, National Hospital Organization Kasumigaura Medical Center, Tsuchiura, Ibaraki, Japan.
Tetsuya ShimadaNational Hospital Organization Nishisaitama-Chuo National Hospital, Tokorozawa, Saitama, Japan.
Yoshinobu MaedaDepartment of Diagnostic Pathology, Toyama Red Cross Hospital, Toyama, Toyama, Japan.
Yumiko YasuharaDepartment of Pathology, Sakai City Medical Center, Sakai, Osaka, Japan.
Yoshiaki KawanoDepartment of Obstetrics and Gynecology, Japan Community Healthcare Organization Kyushu Hospital, Kitakyushu, Fukuoka, Japan.
Yohei KawasakiDepartment of Biostatistics, Graduate School of Medicine, Saitama Medical University, Iruma-Gun, Saitama, Japan.
Kosei HasegawaDepartment of Gynecologic Oncology, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Masanori YasudaDepartment of Pathology, Saitama Medical University International Medical Center, Yamane 1397-1,, Hidaka, 350-1298, Saitama, Japan. m_yasuda@saitama-med.ac.jp.ORCID http://orcid.org/0000-0002-0769-360X

Funding

Japan Society for the Promotion of Science 21K06928Japan Society for the Promotion of Science 24K18493Saitama Medical University internal grant 22-B-1-23
6 · The paper itself

Abstract

To explore the clinicopathological features and origin of mesonephric-like adenocarcinomas (MLAs), 83 cases diagnosed or suspected to be MLAs were collected from various institutions in Japan. We clearly classified 78 as MLAs (uterus: 47, ovary: 31) and 5 as non-MLAs (all ovary) based on our morphological and immunohistochemical criteria. In uterine MLAs (uMLAs), lymphovascular space invasion was an independent prognostic factor for progression-free survival (PFS) (P = 0.03). Patients with uMLAs had significantly shorter PFS and overall survival (OS) than those diagnosed with endometrial endometrioid carcinomas (EECs) (P < 0.0001 and P < 0.001, respectively) and comparable PFS and OS to those with copy number-high tumors. PFS and OS of ovarian MLAs (oMLAs) were similar to those of ovarian endometrioid carcinomas (OECs) overall but worse for patients with stage II-IV. Endometriosis was observed with oMLAs as often as with OECs (94% vs 93%, respectively). Adenomyosis was more frequently observed with uMLAs than with EECs (62% vs 28%, respectively, P = 0.0005). Six uMLAs were confined to the myometrium and adjacent to adenomyosis. In an analysis of molecularly speculated origin, among 29 oMLAs harboring a KRAS hotspot mutation, 23 (79%) instances of endometriosis in the background had the same mutation. Among 36 uMLAs carrying the KRAS hotspot mutation, common mutations were observed in 12 (33%) instances of adjacent adenomyosis (12/21 [67%] of adenomyosis). These findings suggest a histogenetic link between MLAs and ectopic endometrium, implicating both ovarian endometriosis and adenomyosis in MLA pathogenesis, with potential clinical significance.

Indexed as

AdenocarcinomaEndometrial NeoplasmsOvarian NeoplasmsUterine NeoplasmsAdenomyosisAdultAgedBiomarkers, TumorCarcinoma, EndometrioidEndometriosisFemaleHumansImmunohistochemistryJapanMiddle AgedMutationBiomarkers, TumorKRAS protein, humanProto-Oncogene Proteins p21(ras)AdenomyosisEndometriosisKRAS mutationsMesonephric-like adenocarcinoma

Identifiers

PMID41160109
PMCPMC13477489

What OpenQuestion holds

Textmetadata
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.