Evidence map›Paper›PMID 39953623›Full record

ArticleJournal of experimental & clinical cancer research : CR2025

Soluble TIM-3, likely produced by myeloid cells, predicts resistance to immune checkpoint inhibitors in metastatic clear cell renal cell carcinoma.

Ivan Pourmir, Nadine Benhamouda, Thi Tran, Hugo Roux, Joséphine Pineau, Alain Gey, Andyara Munoz, Nesrine Mabrouk, Nicolas Epaillard, Virginie Verkarre and 3 more

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In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. Immune checkpoint TIM-3 in tumor immunotherapy.Acta biochimica et biophysica Sinica · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. 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

13 authors.

Ivan PourmirUniversité Paris Cité, INSERM U970, PARCC, Paris, France. ivan.pourmir@aphp.fr.
Nadine Benhamouda *Université Paris Cité, INSERM U970, PARCC, Paris, France.
Thi Tran *Université Paris Cité, INSERM U970, PARCC, Paris, France.
Hugo Roux *Institut Curie, PSL University, Inserm U932, Immunity and Cancer, Paris, France.
Joséphine PineauUniversité Paris Cité, INSERM U970, PARCC, Paris, France.
Alain GeyUniversité Paris Cité, INSERM U970, PARCC, Paris, France.
Andyara MunozImmunology Department, Georges Pompidou European Hospital, AP-HP Centre, Université Paris Cité, Paris, France.
Nesrine MabroukImmunology Department, Georges Pompidou European Hospital, AP-HP Centre, Université Paris Cité, Paris, France.
Nicolas EpaillardMedical Oncology Department, Clinique Kuindo Magnin, Nouméa, Nouvelle Calédonie, France.
Virginie VerkarrePathology Department, Georges Pompidou European Hospital, AP-HP Centre, Université Paris Cité, INSERM UMR970, Equipe Labellisée Ligue Contre Le Cancer, Paris, France.
Yann-Alexandre VanoMedical Oncology Department, Hôpital Foch, Suresnes, France.
Eric Tartour *Université Paris Cité, INSERM U970, PARCC, Paris, France. eric.tartour@inserm.fr.
Stéphane Oudard *Université Paris Cité, INSERM U970, PARCC, Paris, France. stephane.oudard@aphp.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmunotherapies targeting PD-1 and CTLA-4 are key components of the treatment of metastatic clear cell renal cell carcinoma (mccRCC). However, they have distinct safety profiles and resistance to treatment can occur. We assess soluble TIM-3 (sTIM-3) in the plasma of mccRCC patients as a potential theranostic biomarker, as well as its source and biological significance.

methodsWe analyzed the association between sTIM-3 and overall survival (OS), tumor response, and common clinical and biological factors in two mccRCC cohorts treated with anti-PD-1 (nivolumab, n = 27), anti-PD-1 or anti-PD-1 + anti-CTLA-4 (nivolumab + ipilimumab - N + I, n = 124). The origin and role of sTIM-3 are studied on tumor and blood samples, using multiplex immunohistochemistry and flow cytometry, as well as analyses of publicly available single-cell transcriptomic (scRNAseq) and mass cytometry data.

resultssTIM-3 is significantly elevated in the plasma of treatment-naive mccRCC. It shows distinct associations with survival on anti-PD-1 vs anti-PD-1 + anti-CTLA-4: under nivolumab monotherapy, sTIM-3-high patients have a significantly reduced survival compared to sTIM-3-low patients, while they have similar survival probabilities under N + I. sTIM-3 is independent from other clinical and biological factors. Myeloid immune cells appear as the prominent source of sTIM-3, which may indicate their dysfunctional role in the antitumor immune response.

conclusionssTIM-3 appears to be a promising biomarker for optimizing treatment strategies in ccRCC as well as a potential therapeutic target, linked with to the immune myeloid compartment. Future investigations are warranted in patients treated with anti-PD-1 + antiangiogenic therapies.

Indexed as

Biomarkers, TumorCarcinoma, Renal CellDrug Resistance, NeoplasmHepatitis A Virus Cellular Receptor 2Immune Checkpoint InhibitorsKidney NeoplasmsMyeloid CellsAgedFemaleHumansMaleMiddle AgedPrognosisBiomarkers, TumorHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2Immune Checkpoint InhibitorsBiomarkersClear cell renal cell carcinomaImmune checkpointsImmunotherapyIpilimumabMyeloid cellsNivolumabSoluble TIM-3

Identifiers

PMID39953623
PMCPMC11827183

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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.