Evidence map›Paper›PMID 29337182›Full record

ArticleCell stem cell2018

Human Pancreatic Tumor Organoids Reveal Loss of Stem Cell Niche Factor Dependence during Disease Progression.

Takashi Seino, Shintaro Kawasaki, Mariko Shimokawa, Hiroki Tamagawa, Kohta Toshimitsu, Masayuki Fujii, Yuki Ohta, Mami Matano, Kosaku Nanki, Kenta Kawasaki and 9 more

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Cell stem cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05196334 (Pharmacotyping of Patient-derived Pancreatic Cancer Organoids From Endoscopic Ultrasound-guided Biopsy as a Tool for Predicting Oncological Response), which is not on this map. Cited by 376 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
376citing papers in PubMed, 1 pooled it
26.3field-weighted citation impact, top 1% of its field
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.

NCT05196334 recruitingnot on this mapstarted 2021, after this paper: background citation

Pharmacotyping of Patient-derived Pancreatic Cancer Organoids From Endoscopic Ultrasound-guided Biopsy as a Tool for Predicting Oncological Response

TypeobservationalSponsorHerlev HospitalRan2021 to 2025Enrolled88ConditionsPancreatic CancerArmsNo intervention
3 · Its place in the literature

Who cites it

376 citing papers in PubMed, 1 synthesis or guideline pooled it, 625 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. New developments and applications of human organoids.Nature reviews. Molecular cell biology · 2026
    Review
  9. Review
  10. Review
  11. Article
  12. Progress and challenges in the development of advanced pancreatic cancer organoids.Journal of experimental & clinical cancer research : CR · 2026
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

316 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 3 institutions in 1 country.

Takashi SeinoDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Shintaro KawasakiDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Mariko ShimokawaDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Hiroki TamagawaDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Kohta ToshimitsuDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Masayuki FujiiDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Yuki OhtaDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Mami MatanoDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Kosaku NankiDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Kenta KawasakiDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Sirirat TakahashiDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Shinya SugimotoDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Eisuke IwasakiDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Junichi TakagiLaboratory of Protein Synthesis and Expression, Institute for Protein Research, Osaka University, Suita 565-0871, Japan.
Takao ItoiDepartment of Gastroenterology, Tokyo Medical University, Tokyo 160-0023, Japan.
Minoru KitagoDepartment of Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Yuko KitagawaDepartment of Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Takanori KanaiDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Toshiro SatoDepartment of Gastroenterology, Keio University School of Medicine, Tokyo 160-8582, Japan. Electronic address: t.sato@keio.jp.
Keio University · JPOsaka University · JPTokyo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite recent efforts to dissect the inter-tumor heterogeneity of pancreatic ductal adenocarcinoma (PDAC) by determining prognosis-predictive gene expression signatures for specific subtypes, their functional differences remain elusive. Here, we established a pancreatic tumor organoid library encompassing 39 patient-derived PDACs and identified 3 functional subtypes based on their stem cell niche factor dependencies on Wnt and R-spondin. A Wnt-non-producing subtype required Wnt from cancer-associated fibroblasts, whereas a Wnt-producing subtype autonomously secreted Wnt ligands and an R-spondin-independent subtype grew in the absence of Wnt and R-spondin. Transcriptome analysis of PDAC organoids revealed gene-expression signatures that associated Wnt niche subtypes with GATA6-dependent gene expression subtypes, which were functionally supported by genetic perturbation of GATA6. Furthermore, CRISPR-Cas9-based genome editing of PDAC driver genes (KRAS, CDKN2A, SMAD4, and TP53) demonstrated non-genetic acquisition of Wnt niche independence during pancreas tumorigenesis. Collectively, our results reveal functional heterogeneity of Wnt niche independency in PDAC that is non-genetically formed through tumor progression.

Indexed as

Disease ProgressionStem Cell NicheCRISPR-Cas SystemsEpithelial CellsFibroblastsGATA6 Transcription FactorGene Expression Regulation, NeoplasticGenetic EngineeringHumansLigandsOrganoidsPancreatic NeoplasmsWnt Signaling PathwayGATA6 Transcription FactorLigandsCRISPR-Cas9GATA6organoidspancreatic cancerstem cell nicheWnt

Identifiers

PMID29337182
OpenAlexW2783122422

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.