Evidence map›Paper›PMID 42032842›Full record

ArticleCancer medicine2026

Simultaneous Establishment of Autologous Colorectal Cancer and Mesothelial Stromal Cell Lines from Malignant Ascites Reveals a Mesothelial-Stromal FGFR3 Axis as a Potential Vulnerability in Peritoneal Metastasis.

Yasuhiro Fukui, Hiroaki Kasashima, Zizhou Wang, Iguru Omori, Yukina Kusunoki, Kanae Echizen, Yoshiki Nonaka, Yuki Seki, Kenji Kuroda, Yuichiro Miki and 10 more

Abstract read
In one paragraph

Article in Cancer medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

20 authors.

Yasuhiro FukuiDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.ORCID https://orcid.org/0000-0001-8878-883X
Hiroaki KasashimaDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.ORCID https://orcid.org/0000-0001-5234-4030
Zizhou WangDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Iguru OmoriDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Yukina KusunokiDepartment of Pathophysiology, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Kanae EchizenDepartment of Pathophysiology, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Yoshiki NonakaDepartment of Pathophysiology, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Yuki SekiDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Kenji KurodaDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Yuichiro MikiDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.ORCID https://orcid.org/0000-0003-0116-0922
Mami YoshiiDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Tatsunari FukuokaDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Tatsuro TamuraDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Masatsune ShibutaniDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Takahiro ToyokawaDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Yu MutaDepartment of Gastroenterology and Hepatology, Kyoto University, Graduate School of Medicine, Kyoto, Japan.
Yuki NakanishiDepartment of Gastroenterology and Hepatology, Kyoto University, Graduate School of Medicine, Kyoto, Japan.
Masakazu YashiroMolecular Oncology and Therapeutics, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Naoko OhtaniDepartment of Pathophysiology, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Kiyoshi MaedaDepartment of Gastroenterological Surgery, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.

Funding

Japan Agency for Medical Research and Development S250264Japan Society for the Promotion of Science 21K16428Japan Society for the Promotion of Science 23K15480Kanae Foundation for the Promotion of Medical ScienceKobayashi Foundation for Cancer ResearchMochida Memorial Foundation for Medical and Pharmaceutical ResearchOsaka Community FoundationSGH cancer research grantsTakeda Science FoundationUehara Memorial FoundationYasuda Memorial Medical Foundation
6 · The paper itself

Abstract

Colorectal cancer (CRC) with peritoneal dissemination remains a major therapeutic challenge because of poor prognosis and limited treatment options. Experimental models that accurately recapitulate tumor-mesothelial interactions are scarce. Here, we report the establishment of a novel autologous paired model comprising a CRC cell line (OMUCR-1) and matched cancer-associated mesothelial cells (CAmeso), both simultaneously derived from the malignant ascites of the same patient. Lineage marker analysis using qPCR demonstrated that OMUCR-1 selectively expressed epithelial markers (EPCAM, KRT20), whereas CAmeso strongly expressed mesothelial-mesenchymal markers (ACTA2, MSLN) and lacked epithelial marker expression. These mutually exclusive expression patterns confirm that the two cell populations are phenotypically distinct and rule out cross-contamination. OMUCR-1 displayed strong tumorigenic capacity across multiple transplantation models. CAmeso enhanced CRC cell migration and invasion in vitro, and co-transplantation with OMUCR-1 resulted in larger tumors enriched with αSMA-positive stromal components. RNA sequencing of co-injected xenografts revealed increased expression of murine stromal Fgfr3. Treatment with the FGFR inhibitor BGJ398 reduced tumor growth and decreased stromal FGFR3-positive components, suggesting that stromal FGFR3 may represent a potential microenvironmental vulnerability in CRC with peritoneal dissemination. This autologous CRC-mesothelial system provides a physiologically relevant platform for dissecting tumor-stroma interactions in peritoneal metastasis and may advance stromal-targeted therapeutic strategies.

Indexed as

AscitesColorectal NeoplasmsPeritoneal NeoplasmsReceptor, Fibroblast Growth Factor, Type 3Stromal CellsAnimalsCell Line, TumorCell MovementEpitheliumFemaleHumansMiceReceptor, Fibroblast Growth Factor, Type 3cell line establishmentcolorectal cancermesothelial cellperitoneal disseminationtumor‐stroma interaction

Identifiers

PMID42032842
PMCPMC13109080

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.