ArticleProceedings of the National Academy of Sciences of the United States of America2017
Rhodium metalloinsertor binding generates a lesion with selective cytotoxicity for mismatch repair-deficient cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Ruthenium(ii) polypyridyl complexes and the DNA damage response: mechanisms and therapeutic implications.RSC medicinal chemistry · 2026Review
- Rhodium-based metallodrugs for biological applications: current status and future perspectives.Materials today. Bio · 2025Review
- Exploring Auger electron-emitting radionuclides for targeted DNA damage in mismatch repair-deficient cells: a theoretical study ofInternational journal of radiation biology · 2025Article
- Activation of the cGAS-STING pathway by a mitochondrial DNA-targeted emissive rhodium(iii) metallointercalator.Chemical science · 2023Article
- Cytotoxic sub-nanometer aqueous platinum clusters as potential antitumoral agents.Nanoscale advances · 2022Article
- In vivo anticancer activity of a rhodium metalloinsertor in the HCT116 xenograft tumor model.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- A Family of Rhodium Complexes with Selective Toxicity toward Mismatch Repair-Deficient Cancers.Journal of the American Chemical Society · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The DNA mismatch repair (MMR) pathway recognizes and repairs errors in base pairing and acts to maintain genome stability. Cancers that have lost MMR function are common and comprise an important clinical subtype that is resistant to many standard of care chemotherapeutics such as cisplatin. We have identified a family of rhodium metalloinsertors that bind DNA mismatches with high specificity and are preferentially cytotoxic to MMR-deficient cells. Here, we characterize the cellular mechanism of action of the most potent and selective complex in this family, [Rh(chrysi)(phen)(PPO)]
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Registered trials
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