Evidence map›Paper›PMID 39862711›Full record

ArticleNeoplasia (New York, N.Y.)2025

The chemokine CX3CL1 promotes intraperitoneal tumour growth despite enhanced T-cell recruitment in ovarian cancer.

Stefanie Seitz, Tobias F Dreyer, Christoph Stange, Katja Steiger, Dirk Wohlleber, Martina Anton, Thuý An Pham, Dominique Sauter-Peschke, Ute Reuning, Gabriele Multhoff and 4 more

Abstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. 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

14 authors.

Stefanie SeitzDepartment of Gynecology and Obstetrics, Technical University of Munich, 81675 Munich, Germany.
Tobias F DreyerDepartment of Gynecology and Obstetrics, Technical University of Munich, 81675 Munich, Germany.
Christoph StangeDepartment of Gynecology and Obstetrics, Technical University of Munich, 81675 Munich, Germany.
Katja SteigerComparative Experimental Pathology, Institute of Pathology, Technical University of Munich, 81675 Munich, Germany; Institute of Pathology, Technical University of Munich, 81675 Munich, Germany; German Cancer Consortium (DKTK), partner site Munich, and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Dirk WohlleberInstitute of Molecular Immunology, Klinikum rechts der Isar, Technical University of Munich, 81675 Munich, Germany.
Martina AntonInstitute of Molecular Immunology, Klinikum rechts der Isar, Technical University of Munich, 81675 Munich, Germany.
Thuý An PhamDepartment of Gynecology and Obstetrics, Technical University of Munich, 81675 Munich, Germany.
Dominique Sauter-PeschkeDepartment of Gynecology and Obstetrics, Technical University of Munich, 81675 Munich, Germany.
Ute ReuningDepartment of Gynecology and Obstetrics, Technical University of Munich, 81675 Munich, Germany.
Gabriele MulthoffDepartment of Radiation Oncology, Technical University of Munich, TranslaTUM, 81675 Munich, Germany.
Wilko WeichertInstitute of Pathology, Technical University of Munich, 81675 Munich, Germany; German Cancer Consortium (DKTK), partner site Munich, and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Marion KiechleDepartment of Gynecology and Obstetrics, Technical University of Munich, 81675 Munich, Germany.
Viktor MagdolenDepartment of Gynecology and Obstetrics, Technical University of Munich, 81675 Munich, Germany.
Holger BrongerDepartment of Gynecology and Obstetrics, Technical University of Munich, 81675 Munich, Germany; German Cancer Consortium (DKTK), partner site Munich, and German Cancer Research Center (DKFZ), Heidelberg, Germany. Electronic address: holger.bronger@tum.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-cell recruiting chemokines are required for a successful immune intervention in ovarian cancer, and also for the efficacy of modern anticancer agents such as PARP inhibitors. The chemokine CX3CL1 recruits tumour-suppressive T-cells into solid tumours, but also mediates cell-cell adhesions, e.g. of tumour cells, through its membrane-bound form. So far, its role in ovarian cancer has only been rudimentarily addressed. We show that high CX3CL1 expression significantly correlates with worsened survival in human high-grade serous ovarian cancer (n=219). In preclinical ovarian cancer, CX3CL1 plays a dual role, as it enhances the adaptive anti-tumour response, but overall still promotes tumour growth, the latter as a feature of the intraperitoneal environment. Moreover, PARP inhibitors are able to increase CX3CL1 release from human ovarian cancer cells. Collectively, our study shows that CX3CL1 is a driver of intraperitoneal tumour growth in ovarian cancer, a feature that may compromise the anticancer effect of CX3CL1-inducing PARP inhibitors.

Indexed as

Chemokine CX3CL1Ovarian NeoplasmsT-LymphocytesAnimalsCell Line, TumorCell ProliferationDisease Models, AnimalFemaleHumansLymphocytes, Tumor-InfiltratingMiceXenograft Model Antitumor AssaysChemokine CX3CL1CX3CL1 protein, humanChemokinesCX3CL1Mouse modelPARP inhibitionTumour-infiltrating lymphocytes

Identifiers

PMID39862711
PMCPMC11804824

What OpenQuestion holds

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Registered trials

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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.