Evidence map›Paper›PMID 42697413›Full record

ArticleCellular and molecular gastroenterology and hepatology2026

Comparative Analysis of Primary and Liver Fibroblasts Reveals MET as a Potent Target in Pancreatic Cancer Metastasis.

Rima Singh, Natalie Yousefian, Walker M Allen, Austin D Silva, Cecily Anaraki, Alica K Michels, Sabrina Calderon, Ian M Loveless, Daniella Rastelli, Ashley George and 10 more

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Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

5 · Who and what money

Authors and funding

20 authors.

Rima SinghDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California.
Natalie YousefianDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California.
Walker M AllenDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California.
Austin D SilvaDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California.
Cecily AnarakiDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California.
Alica K MichelsDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California.
Sabrina CalderonDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California.
Ian M LovelessPancreatic Cancer Center, Henry Ford Health System, Detroit, Michigan.
Daniella RastelliDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California.
Ashley GeorgeDivision of Digestive Diseases, Department of Internal Medicine, University of Cincinnati, Cincinnati, Ohio.
Mohammed AldakkakDepartment of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin; LaBahn Pancreatic Cancer Program, Medical College of Wisconsin, Milwaukee, Wisconsin.
Oliver G McDonaldDepartment of Pathology and Laboratory Medicine, University of Miami, Miami, Florida.
Nikki K LytleDepartment of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin; LaBahn Pancreatic Cancer Program, Medical College of Wisconsin, Milwaukee, Wisconsin.
Jennifer P MortonCancer Research UK Scotland Institute, Glasgow, United Kingdom; Institute of Cancer Sciences, University of Glasgow, Glasgow, United Kingdom.
Reed I AyabeDepartment of Surgery, University of California Irvine, Orange, California; Chao Family Comprehensive Cancer Center, University of California Irvine, Orange, California.
David ImagawaDepartment of Surgery, University of California Irvine, Orange, California; Chao Family Comprehensive Cancer Center, University of California Irvine, Orange, California.
Zeljka JutricDepartment of Surgery, University of California Irvine, Orange, California; Chao Family Comprehensive Cancer Center, University of California Irvine, Orange, California.
Thomas F MartinezChao Family Comprehensive Cancer Center, University of California Irvine, Orange, California; Department of Pharmaceutical Sciences, University of California Irvine, Irvine, California; Department of Biological Chemistry, University of California Irvine, Irvine, California.
Nina G SteelePancreatic Cancer Center, Henry Ford Health System, Detroit, Michigan; Division of Digestive Diseases, Department of Internal Medicine, University of Cincinnati, Cincinnati, Ohio.
Christopher J HalbrookDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California; Chao Family Comprehensive Cancer Center, University of California Irvine, Orange, California; Institute for Immunology, University of California Irvine, Irvine, California. Electronic address: chris.halbrook@uci.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsThe tumor microenvironment drives many malignant features of pancreatic ductal adenocarcinoma. The fibroblasts within pancreatic tumors promote tissue remodeling, immune suppression, and resistance to therapy. However, the interactions between stromal populations and pancreatic cancer cells are less understood in the liver, the most frequent site of pancreatic ductal adenocarcinoma metastasis.

methodsTo address this, we employed single-cell transcriptomics to compare primary pancreatic vs liver pancreatic ductal adenocarcinoma lesions. Using a ligand-receptor interaction tool, we assessed upregulated pathways in liver pancreatic ductal adenocarcinoma.

resultsHere, we identified that the expression of hepatocyte growth factor in fibroblasts and its receptor MET in cancer cells are both markedly increased in the pancreatic ductal adenocarcinoma liver niche. Using functional assays, we validated that mitogenic MET signaling is activated in pancreatic ductal adenocarcinoma cells by liver-derived fibroblasts. Importantly, the inhibition of MET signaling leads to reduced tumor growth in immune competent mouse models.

conclusionsCollectively, our data demonstrates that liver stromal-epithelial crosstalk networks engage in signaling pathways distinct from primary pancreatic tumors, highlighting opportunities to develop new treatments for metastatic disease.

Indexed as

DesmoplasiaHGFMETNRF2Redox MetabolismSingle-Cell Transcriptomics

Identifiers

PMID42697413

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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.