ArticleCancer letters2012
Effectiveness of a combination therapy using calcineurin inhibitor and mTOR inhibitor in preventing allograft rejection and post-transplantation renal cancer progression.
Article in Cancer letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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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.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Calcineurin Inhibitors: Current Role, Toxicity Management, and Future Frontiers in Immunosuppression.Molecular neurobiology · 2025Review
- Sirolimus-induced pulmonary toxicity without recurrence more than 8 years after everolimus replacement in a renal transplant patient with recurrent skin SCC: a case report.BMC nephrology · 2024Article
- Article
- Everolimus Reduces Cancer Incidence and Improves Patient and Graft Survival Rates after Kidney Transplantation: A Multi-Center Study.Journal of clinical medicine · 2022Article
- Article
- Honokiol inhibits c-Met-HO-1 tumor-promoting pathway and its cross-talk with calcineurin inhibitor-mediated renal cancer growth.Scientific reports · 2017Article
- Recessive nephrocerebellar syndrome on the Galloway-Mowat syndrome spectrum is caused by homozygous protein-truncating mutations of WDR73.Brain : a journal of neurology · 2015Article
- Prescription trends of immunosuppressive drugs in post-heart transplant recipients in Taiwan, 2000-2009.Pharmacoepidemiology and drug safety · 2014Article
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Calcineurin inhibitors (CNIs) may promote post-transplantation cancer through altered expression of cytokines and chemokines in tumor cells. We found that there is a potential cross-talk among CNI-induced signaling molecules and mTOR. Here, we utilized a murine model of post-transplantation cancer to examine the effect of a combination therapy (CNI + mTOR-inhibitor rapamycin) on allograft survival and renal cancer progression. The therapy prolonged allograft survival; and significantly attenuated CNI-induced post-transplantation cancer progression, with down-regulation of mTOR and S6-kinase phosphorylation. Also, rapamycin inhibited CNI-induced over-expression of the angiogenic cytokine VEGF, and the chemokine receptor CXCR3 and its ligands in post-transplantation tumor tissues.
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Registered trials
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