Evidence map›Paper›PMID 42432797›Full record

ArticleJournal of experimental & clinical cancer research : CR2026

Suppression of the myofibroblastic cancer-associated fibroblast phenotype to enhance anti-PD-1 response.

Katherine A Johnson, Anna E L Lippert, Alec Cornelio, Yousef Gadalla, Xingqi Shen, Sean G Kraus, Philip B Emmerich, Anna M Field, Alyssa K Steimle, Cheri A Pasch and 4 more

Abstract read
PubMed Full text at PMC Publisher
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

14 authors.

Katherine A JohnsonDivision of Hematology, Medical Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Anna E L LippertDivision of Hematology, Medical Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Alec CornelioDivision of Hematology, Medical Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Yousef GadallaDivision of Hematology, Medical Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Xingqi ShenDivision of Hematology, Medical Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Sean G KrausDivision of Hematology, Medical Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Philip B EmmerichDivision of Hematology, Medical Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Anna M FieldDivision of Hematology, Medical Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Alyssa K SteimleDivision of Hematology, Medical Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Cheri A PaschUniversity of Wisconsin Carbone Cancer Center, Madison, WI, USA.
Huy Q DinhMcArdle Laboratory for Cancer Research, Department of Oncology, University of Wisconsin-Madison, Madison, WI, USA.
Wei ZhangUniversity of Wisconsin Carbone Cancer Center, Madison, WI, USA.
Kristina A MatkowskyjUniversity of Wisconsin Carbone Cancer Center, Madison, WI, USA.
Dustin A DemingDivision of Hematology, Medical Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA. ddeming@medicine.wisc.edu.

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Justine Yang Bruce · 1985 to 2026
$142.6M
Training in Cancer Biology Training GrantT32CA009135 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SUGDEN, WILLIAM M. · 1985 to 2024
$10.4M
Functional optical imaging for rapid, label-free predictions of treatment response and clonal evolution in patient-derived cancer organoidsR01CA272855 · NCI · MORGRIDGE INSTITUTE FOR RESEARCH, INC. · PI Dustin A Deming, Melissa Caroline Skala · 2023 to 2026
$3.1M
NCI NIH HHS P30 CA014520NCI NIH HHS R01 CA272855NCI NIH HHS T32 CA009135
6 · The paper itself

Abstract

backgroundCancer-associated fibroblasts (CAFs) are key modulators of tumor growth, the tumor immune context, and treatment response. CAFs take on diverse phenotypes with distinct functions. Myofibroblastic CAFs (myCAFs) regulate extracellular matrix remodeling, while inflammatory CAFs (iCAFs) modulate immune infiltration. Further studies are required to validate biomarkers of CAF phenotypes and to identify means to therapeutically manipulate CAFs.

methodsSingle-cell RNA sequencing analysis was used to identify markers of CAF phenotypes in CRC. CAF markers were validated and compared to clinical characteristics using patient-derived CAF cultures, fixed human CRC samples, and publicly available RNA sequencing data. Therapeutics were prioritized for their potential to inhibit the myCAF phenotype and nilotinib was selected for validation in patient-derived CAFs. Overall changes in CAFs were evaluated via RNA-seq, and results validated with in vitro experiments. Finally, the feasibility of altering CAF phenotypes to affect treatment response was evaluated in vivo.

resultsHere we identify disease-specific markers of colorectal CAFs that are functionally distinct, biologically identifiable, correlate with clinically relevant markers of disease, and can be therapeutically altered in vivo. High stromal expression of myCAF markers correlated with reduced infiltration of CD8

conclusionsThese results highlight the feasibility of targeting CAF functions to improve therapeutic response, and support the investigation of nilotinib and anti-PD-1 therapy clinically.

Indexed as

Cancer-Associated FibroblastsColorectal NeoplasmsImmune Checkpoint InhibitorsMyofibroblastsProgrammed Cell Death 1 ReceptorAnimalsFemaleHumansMicePhenotypePyrimidinesImmune Checkpoint InhibitorsnilotinibPDCD1 protein, humanProgrammed Cell Death 1 ReceptorPyrimidinesAnti-PD-1Cancer-associated fibroblastsColorectal cancerMyocardinNilotinibTumor microenvironment

Identifiers

PMID42432797
PMCPMC13640252

What OpenQuestion 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 OpenQuestion graph.