ArticleProceedings of the National Academy of Sciences of the United States of America2024
Unconventional mechanism of action and resistance to rapalogs in renal cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Clinical Outcomes, Treatment Patterns, and Molecular Heterogeneity of TFE3-Rearranged Renal Cell Carcinoma: A Multicenter Real-World Study.Cancer medicine · 2026Article
- Overcoming mTOR Inhibitor Resistance: From Biological Basis to Therapeutic Strategies.Biomedicines · 2026Review
- Design, synthesis, and biological evaluation of procaine-based triazole-isoxazoline hybrids as selective PI3K/mTOR inhibitors for esophageal cancer therapy:RSC medicinal chemistry · 2026Article
- Machine learning-enhanced discovery of a basement membrane-related gene signature in glioblastoma via single-cell and Spatial transcriptomics.Journal of translational medicine · 2025Article
- Renal cell carcinoma organoids for precision medicine: bridging the gap between models and patients.Journal of translational medicine · 2025Review
- Review
- The role of cancer-associated fibroblasts in the tumour microenvironment of urinary system.Clinical and translational medicine · 2025Review
- Molecular dynamics and experimental evaluation of piperine as a potential mTOR inhibitor in colon cancer cells.In silico pharmacology · 2025Article
- Molecular docking and dynamics simulation of farnesol as a potential anticancer agent targeting mTOR pathway.In silico pharmacology · 2024Article
- Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
mTORC1 is aberrantly activated in renal cell carcinoma (RCC) and is targeted by rapalogs. As for other targeted therapies, rapalogs clinical utility is limited by the development of resistance. Resistance often results from target mutation, but mTOR mutations are rarely found in RCC. As in humans, prolonged rapalog treatment of RCC tumorgrafts (TGs) led to resistance. Unexpectedly, explants from resistant tumors became sensitive both in culture and in subsequent transplants in mice. Notably, resistance developed despite persistent mTORC1 inhibition in tumor cells. In contrast, mTORC1 became reactivated in the tumor microenvironment (TME). To test the role of the TME, we engineered immunocompromised recipient mice with a resistance mTOR mutation (S2035T). Interestingly, TGs became resistant to rapalogs in mTOR
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Registered trials
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