Evidence map›Paper›PMID 41799185›Full record

ArticleTheranostics2026

Connective tissue growth factor contributes to resistance to anti-angiogenic therapies in renal cancer.

Manon Teisseire, Arthur Karaulic, Julien Parola, Maëva Totobesola, Delphine Borchiellini, Tanguy Pace-Loscos, Renaud Schiappa, Emmanuel Chamorey, Jérôme Durivault, Maëva Dufies and 6 more

Abstract read
In one paragraph

Article in Theranostics, 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

16 authors.

Manon TeisseireUniversité Côte d'Azur, Institute for research on cancer and aging of Nice, CNRS UMR 7284; INSERM U1081, Centre Antoine Lacassagne, France.
Arthur KaraulicUniversité Côte d'Azur, Institute for research on cancer and aging of Nice, CNRS UMR 7284; INSERM U1081, Centre Antoine Lacassagne, France.
Julien ParolaUniversité Côte d'Azur, Institute for research on cancer and aging of Nice, CNRS UMR 7284; INSERM U1081, Centre Antoine Lacassagne, France.
Maëva TotobesolaUniversité Côte d'Azur, Institute for research on cancer and aging of Nice, CNRS UMR 7284; INSERM U1081, Centre Antoine Lacassagne, France.
Delphine BorchielliniDepartment of medical oncology, Centre Antoine Lacassagne, Nice, France.
Tanguy Pace-LoscosDepartment of statistics, Centre Antoine Lacassagne, Nice, France.
Renaud SchiappaDepartment of statistics, Centre Antoine Lacassagne, Nice, France.
Emmanuel ChamoreyDepartment of statistics, Centre Antoine Lacassagne, Nice, France.
Jérôme DurivaultCentre Scientifique de Monaco, Biomedical Department, 8 quai Antoine Premier, 98000, Monaco, Monaco.
Maëva DufiesUniversité Côte d'Azur, Institute for research on cancer and aging of Nice, CNRS UMR 7284; INSERM U1081, Centre Antoine Lacassagne, France.
Damien AmbrosettiUniversité Côte d'Azur, Institute for research on cancer and aging of Nice, CNRS UMR 7284; INSERM U1081, Centre Antoine Lacassagne, France.
Frédéric LucianoUniversité Côte d'Azur, Institute for research on cancer and aging of Nice, CNRS UMR 7284; INSERM U1081, Centre Antoine Lacassagne, France.
Juan GaoDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden.
Yihai CaoDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden.
Gilles PagèsUniversité Côte d'Azur, Institute for research on cancer and aging of Nice, CNRS UMR 7284; INSERM U1081, Centre Antoine Lacassagne, France.
Sandy GiulianoUniversité Côte d'Azur, Institute for research on cancer and aging of Nice, CNRS UMR 7284; INSERM U1081, Centre Antoine Lacassagne, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Clear cell renal cell carcinoma (ccRCC) is predominantly treated with anti-angiogenic therapies (AATs), such as sunitinib and axitinib. While these therapies initially improve outcomes, resistance frequently emerges, limiting long-term efficacy. Understanding the molecular mechanisms underlying AAT resistance is essential to optimize treatment strategies. Methods: To identify factors involved in AAT resistance, we performed integrated transcriptomic and proteomic analyses on ccRCC cell lines subjected to either transient AAT treatment or with established acquired resistance. Functional validation was performed using Results: Connective Tissue Growth Factor (CTGF) was consistently upregulated following treatment and in resistant cell lines. CTGF, a secreted protein regulated by Yes-associated protein (YAP) in the Hippo pathway, is known to promote angiogenesis, fibrosis, and tumor progression. Functionally, CTGF enhanced tumor cell aggressiveness Conclusion: CTGF is a key mediator of resistance to AATs in ccRCC, by promoting tumor progression and remodeling the tumor microenvironment. CTGF may thus serve as both a predictive biomarker and a therapeutic target. These findings support further investigation of CTGF inhibition as a strategy to overcome AAT resistance and improve treatment outcomes in ccRCC patients.

Indexed as

Angiogenesis InhibitorsCarcinoma, Renal CellConnective Tissue Growth FactorDrug Resistance, NeoplasmKidney NeoplasmsAnimalsAxitinibCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansNeovascularization, PathologicSunitinibZebrafishAngiogenesis InhibitorsAxitinibCCN2 protein, humanConnective Tissue Growth FactorSunitinib

Identifiers

PMID41799185
PMCPMC12964018

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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.