Evidence map›Paper›PMID 42265884›Full record

ArticleMolecular oncology2026

Loss of proton-sensing TDAG8 increases tumor progression in mouse models of colon cancer.

Ermanno Malagola, Yasmine Illi, Anna Bircher, Marijn Wilmink, Rachele F Malagutti, Solenn Ottié, Cordelia Schuler, Pedro A Ruiz, Cheryl de Vallière, Klaus Seuwen and 2 more

Abstract read
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In one paragraph

Article in Molecular oncology, 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

12 authors.

Ermanno MalagolaDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.
Yasmine IlliDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.ORCID https://orcid.org/0009-0009-4904-1579
Anna BircherDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.
Marijn WilminkDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.
Rachele F MalaguttiDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.
Solenn OttiéDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.
Cordelia SchulerDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.
Pedro A RuizDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.
Cheryl de VallièreDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.
Klaus SeuwenDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.
Gerhard RoglerDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.
Martin HausmannDepartment of Gastroenterology and Hepatology, University Hospital of Zurich, University of Zurich, Switzerland.ORCID https://orcid.org/0000-0002-0696-0251

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 310030_172870Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 314730_153380Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 320030-231749
6 · The paper itself

Abstract

T-cell death-associated gene 8 (TDAG8) is a proton-sensing G-protein-coupled receptor that is activated by neutral to acidic extracellular pH. TDAG8 is primarily expressed in leukocytes and leukocyte-rich tissues, including the spleen, lymph nodes, and thymus. Genome-wide association studies have identified TDAG8 as a risk gene for inflammatory bowel disease (IBD). Patients with IBD have an increased risk of developing colorectal cancer (CRC), and TDAG8 has been implicated in regulating anti-tumor immunity. We used the MC38 and azoxymethane/dextran sodium sulfate (AOM/DSS) mouse models of CRC to evaluate the effect of TDAG8 deficiency on tumor growth. Tumor development was assessed by measuring size and weight, and tumor tissue was analyzed by immunohistochemistry (IHC), real-time quantitative polymerase chain reaction (qPCR), flow cytometry, and apurinic/apyrimidinic (AP) site quantification. In the MC38 model, Tdag8-deficient mice presented a significantly increased tumor burden together with significantly increased numbers of neutrophils and monocytes in tumor tissue compared with wild-type (WT) mice. In the AOM/DSS model of CRC, Tdag8-deficient mice exhibited significantly increased tumor size, weight, and number of AP sites compared with WT mice. Additionally, Tdag8-deficient mice showed a significantly increased number of macrophages in tumor tissue and an elevated CD4

Indexed as

colorectal cancerGPR65inflammatory bowel diseasepH‐sensing G‐protein‐coupled receptors

Identifiers

PMID42265884
PMCPMC13398714

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