Evidence map›Paper›PMID 41006303›Full record

ArticleNature communications2025

An injury-associated lobular microniche is associated with the classical tumor cell phenotype in pancreatic cancer.

Sara Söderqvist, Annika Viljamaa, Natalie Geyer, Anna-Lena Keller, Kseniya Ruksha, Carina Strell, Neda Hekmati, Alexandra Niculae, Jennie Engstrand, Ernesto Sparrelid and 14 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Novel Acinar Metaplastic States Uncovered in Exocrine Pancreas Disease.Cellular and molecular gastroenterology and hepatology · 2026
    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

24 authors.

Sara SöderqvistDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.
Annika ViljamaaDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.ORCID http://orcid.org/0009-0002-8511-8181
Natalie GeyerDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.
Anna-Lena KellerDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.
Kseniya RukshaDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.
Carina StrellCentre for Cancer Biomarkers - CCBIO, Department of Clinical Medicine, University of Bergen, Bergen, Norway.ORCID http://orcid.org/0000-0002-3783-7256
Neda HekmatiDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Alexandra NiculaeDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.
Jennie EngstrandDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.ORCID http://orcid.org/0000-0003-1123-7022
Ernesto SparrelidDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.
Caroline SalménDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.
Tânia D F CostaDepartment of Medicine, Huddinge - MedH, Karolinska Institutet, Huddinge, Sweden.ORCID http://orcid.org/0000-0002-6296-5225
Miao ZhaoDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.ORCID http://orcid.org/0000-0002-4895-1177
Staffan StrömbladDepartment of Medicine, Huddinge - MedH, Karolinska Institutet, Huddinge, Sweden.ORCID http://orcid.org/0000-0002-1236-6339
Argyro ZacharouliDepartment of Clinical Pathology and Cancer Diagnostics, Karolinska University Hospital, Stockholm, Sweden.
Poya GhorbaniDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.
Sara HarriziDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.
Yousra HamidiDepartment of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.
Olga KhorosjutinaCRISPR Functional Genomics, SciLifeLab and Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Solna, Sweden.ORCID http://orcid.org/0009-0001-0786-0260
Stefina MilanovaCRISPR Functional Genomics, SciLifeLab and Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Solna, Sweden.
Bernhard SchmiererCRISPR Functional Genomics, SciLifeLab and Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Solna, Sweden.ORCID http://orcid.org/0000-0002-9082-7022
Béla BozókyDepartment of Clinical Pathology and Cancer Diagnostics, Karolinska University Hospital, Stockholm, Sweden.
Carlos Fernández Moro *Department of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden.ORCID http://orcid.org/0000-0001-6863-5959
Marco Gerling *Department of Clinical Science, Intervention and Technology - CLINTEC, Karolinska Institutet, Huddinge, Sweden. marco.gerling@ki.se.ORCID http://orcid.org/0000-0002-1810-0662

Funding

Cancerfonden (Swedish Cancer Society) 22 2175 PjVetenskapsrådet (Swedish Research Council) 2018-02023Vetenskapsrådet (Swedish Research Council) 2024-03026
6 · The paper itself

Abstract

Pancreatic cancer is an aggressive disease with a dense fibrotic stroma and is often accompanied by chronic inflammation. Peritumoral inflammation is typically viewed as a reaction to nearby tumor growth. Here, we report that the inflamed pancreatic lobules are frequently invaded by tumor cells, forming a distinct, non-fibrotic tumor niche. Using a semi-supervised machine learning approach for annotations of clinical samples and multiplex protein profiling, we show that tumor cells at the invasion front are closely associated with acinar cells undergoing damage-induced changes, and with activated fibroblasts expressing markers of injury. The invaded lobules are linked to classical tumor phenotypes, in contrast to fibrotic areas where tumor cells display a more basal profile, highlighting microenvironment-dependent tumor subtype differences. In female mice, lobular invasion similarly aligns with the classical tumor phenotype. Together, our data reveal that pancreatic tumors colonize injured lobules, creating a unique niche that shapes tumor characteristics and contributes to disease biology.

Indexed as

PancreasPancreatic NeoplasmsAcinar CellsAnimalsCell Line, TumorFemaleHumansInflammationMaleMiceNeoplasm InvasivenessPhenotypeTumor Microenvironment

Identifiers

PMID41006303
PMCPMC12475445

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.