Evidence map›Paper›PMID 42263744›Full record

ArticleBiofabrication2026

Immune-driven stromal inflammation in pancreatic cancer within a microfluidic platform.

Mariana Viso, Karthik Rajkumar, Anna Bianchi, Bhumi Suthar, Neil Kumar, David Oliver, Mya Collins, Jashodeep Datta, Ashutosh Agarwal

Abstract read
In one paragraph

Article in Biofabrication, 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

9 authors.

Mariana VisoDepartment of Biomedical Engineering, University of Miami, Coral Gables, FL, United States of America.ORCID 0000-0002-1821-458X
Karthik RajkumarDivision of Surgical Oncology, Dewitt Daughtry Department of Surgery, University of Miami Miller School of Medicine, Miami, FL, United States of America.
Anna BianchiDivision of Surgical Oncology, Dewitt Daughtry Department of Surgery, University of Miami Miller School of Medicine, Miami, FL, United States of America.ORCID 0000-0001-7104-4180
Bhumi SutharDepartment of Biomedical Engineering, University of Miami, Coral Gables, FL, United States of America.
Neil KumarDepartment of Biomedical Engineering, University of Miami, Coral Gables, FL, United States of America.
David OliverDepartment of Biomedical Engineering, University of Miami, Coral Gables, FL, United States of America.
Mya CollinsDepartment of Neuroscience, Brown University, Providence, RI, United States of America.ORCID 0009-0003-5088-5820
Jashodeep DattaDivision of Surgical Oncology, Dewitt Daughtry Department of Surgery, University of Miami Miller School of Medicine, Miami, FL, United States of America.
Ashutosh AgarwalDepartment of Biomedical Engineering, University of Miami, Coral Gables, FL, United States of America.ORCID 0000-0002-2397-9886

Funding

Disrupting MDSC-fibroblast interactions to overcome chemoimmunotherapy resistance in pancreatic cancerR37CA292843 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Jashodeep Datta · 2024 to 2026
$1.1M
NCI NIH HHS R37 CA292843
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is defined by a highly fibrotic and immunosuppressive tumor microenvironment (TME). The inflammatory polarization of cancer-associated fibroblasts (CAFs), as well as the dense and early trafficking of myeloid-derived suppressor cells (MDSCs) contribute to tumor progression, immune exclusion, and therapy resistance. Yet, key mechanisms governing their interplay remain undefined. We developed a novel microfluidic platform that recapitulates the immuno-stromal PDAC microenvironment and enables controlled co-culture, high-resolution live imaging, and downstream molecular analyses. Spheroids composed of tumor cells, and dual reporter CAFs, were embedded in our engineered system and allowed to dynamically interact with MDSCs for 48 h. Dynamic interactions with MDSCs induce a significant increase in inflammatory CAF-specific reporter fluorescence compared to media controls. Gene set enrichment analysis demonstrated enrichment of inflammatory response pathways, and increased expression of iCAF related genes. RNA velocity, CellRank, and PAGA trajectory analyses collectively identify a constitutively fate-committed CAF progenitor population that is selectively expanded by MDSC exposure and preferentially transitions into an inflammatory iCAF state. Overall, our novel microfluidic platform recapitulated targeted MDSC-driven inflammatory CAF polarization and revealed a progenitor CAFs population as a potential precursor for iCAF differentiation, establishing its utility in mechanistic studies of stromal-immune interactions of the TME.

Indexed as

Carcinoma, Pancreatic DuctalInflammationLab-On-A-Chip DevicesMicrofluidicsPancreatic NeoplasmsAnimalsCancer-Associated FibroblastsCell Line, TumorCoculture TechniquesHumansMicrophysiological SystemsMyeloid-Derived Suppressor CellsStromal CellsTumor Microenvironmentcancer associated fibroblastcancer spheroidmicrofluidicsorgans on chipspancreatic cancertumor microenvironment

Identifiers

PMID42263744
PMCPMC13308500

What OpenQuestion 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 OpenQuestion graph.