Evidence map›Paper›PMID 41673768›Full record

ArticleJournal of experimental & clinical cancer research : CR2026

Patient-derived orthotopic xenograft models recapitulate the peritoneal dissemination of pancreatic cancer and delineate its transcriptional and regulatory programs.

Takaaki Furukawa, Kohei Kumegawa, Kenichi Miyata, Manabu Takamatsu, Asumi Iesato, Sumito Saeki, Liying Yang, Chikako Shibata, Tomoko Takahara, Kaoru Masuda and 11 more

Abstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 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

21 authors.

Takaaki Furukawa *Division of Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto, Tokyo, Japan.
Kohei Kumegawa *Cancer Cell Diversity Project, NEXT-Ganken Program, Japanese Foundation for Cancer Research, Tokyo, Japan.
Kenichi MiyataDivision of Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto, Tokyo, Japan.
Manabu TakamatsuDivision of Pathology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Asumi IesatoCancer Cell Diversity Project, NEXT-Ganken Program, Japanese Foundation for Cancer Research, Tokyo, Japan.
Sumito SaekiDivision of Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto, Tokyo, Japan.
Liying YangDivision of Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto, Tokyo, Japan.
Chikako ShibataDivision of Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto, Tokyo, Japan.
Tomoko TakaharaDivision of Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto, Tokyo, Japan.
Kaoru MasudaCancer Cell Diversity Project, NEXT-Ganken Program, Japanese Foundation for Cancer Research, Tokyo, Japan.
Takafumi MieDepartment of Hepato-Biliary-Pancreatic Medicine, Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Takeshi OkamotoDepartment of Hepato-Biliary-Pancreatic Medicine, Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Tsuyoshi TakedaDepartment of Hepato-Biliary-Pancreatic Medicine, Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Takashi SasakiDepartment of Hepato-Biliary-Pancreatic Medicine, Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Masato OzakaDepartment of Hepato-Biliary-Pancreatic Medicine, Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Miwa TanakaDivision of Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto, Tokyo, Japan.
Shunji TakahashiDepartment of Genomic Medicine, Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Tetsuo NodaDirector's room, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Ryoji YaoDepartment of Cell Biology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Naoki SasahiraDepartment of Hepato-Biliary-Pancreatic Medicine, Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Reo MaruyamaDivision of Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto, Tokyo, Japan. reo.maruyama@jfcr.or.jp.

Funding

AMED JP24ama221606JSPS JP24K02312JSPS JP 24K18499
6 · The paper itself

Abstract

BACKGROUND &

aimsThe mechanisms of peritoneal dissemination in pancreatic ductal adenocarcinoma (PDAC) remain unclear partly owing to the lack of patient-derived models that recapitulate this process. This study aimed to establish an orthotopic model of PDAC peritoneal dissemination and to uncover the transcriptional and regulatory programs underlying this process.

methodsOrganoids were established from primary pancreatic tumors and malignant effusions of patients with PDAC and orthotopically transplanted into the pancreas of immunodeficient mice to generate patient-derived orthotopic xenograft (PDOX) models. Subsequently, the organoids were rederived from pancreatic and peritoneal lesions of a representative model (PDOX12) and orthotopically reimplanted to assess the dissemination capacity. Single-nucleus RNA sequencing (snRNA-seq) and single-cell ATAC sequencing (scATAC-seq) were performed to analyze the tumors from these models.

resultsThe organoids that were derived from malignant effusions reproducibly generated peritoneal metastases after orthotopic implantation. To dissect this process more precisely, we focused on one representative model (PDOX12) and rederived organoids from its pancreatic and peritoneal lesions. These organoids generated matched PDOX models that differed only in dissemination potential when reimplanted orthotopically. The results of snRNA-seq revealed a distinct subpopulation enriched in the high-dissemination model, which was characterized by the coordinated activation of genes involved in cytoskeletal dynamics, extracellular matrix remodeling, and plasticity-related signaling—suggesting a dissemination-primed state. Integration with scATAC-seq identified STAT3, SMAD3, and SOX2 as potential upstream regulators of this gene program.

conclusionsThis study established PDOX models that isolate the peritoneal dissemination phenotype and reveal the transcriptional and regulatory programs driving this process.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsPeritoneal NeoplasmsAnimalsDisease Models, AnimalFemaleGene Expression Regulation, NeoplasticHeterograftsHumansMiceOrganoidsXenograft Model Antitumor AssaysPancreatic ductal adenocarcinomaPatient-derived organoidsPatient-derived orthotopic xenograft modelsPeritoneal disseminationSingle-cell multi-omics analyses

Identifiers

PMID41673768
PMCPMC12998334

What Socratic holds

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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 Socratic graph.