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Updated: Aug 22, 2026

Structure-Guided Design and Development of Novel Cyclophilin A Inhibitors and Ganoderiol-F Derivatives: An In-Silico Approach
Published on: June 23, 2026
Molecular effects of cyclosporine and oncogenesis: a new model
N André1, B Roquelaure, J Conrath
1Pediatric Oncology Department, Children Hospital of "La Timone", Bd Jean Moulin, 13885 Marseille Cedex 5, France. nicolas.andre@ap-hm.fr
Abstract:
Cyclosporine A is the most commonly used immunosuppressive agent during organ transplantation. One of the most feared adverse effects of cyclosporine A is the appearance of de novo cancers. The mechanisms that lead to the genesis of such cancers are thought to be only related to a side effect of cyclosporine A: a depressed immune system. Here, we review different molecular effects induced by cyclosporine A (inhibition of DNA repair, synthesis of TGF Beta, induction of apoptosis of activated T cells, inhibition of apoptosis through the inhibition of the opening of the mitochondrial Permeability Transition Pore) and propose that cyclosporine A can promote the genesis and the spread of cancer not only because of immunosuppression but also because of its ability to facilitate DNA mutations accumulation, to diminish the clearance of altered cells and to transform cancer cells into aggressive cancer cells. This new insights into the mechanisms of genesis of cyclosporine A-related cancers should be taken into account to develop preventive strategies or new immunosuppressive strategies.
Insights
Cyclosporine A, an immunosuppressant, may increase cancer risk not just by weakening immunity but also by promoting DNA mutations and aggressive cancer cell behavior. New strategies are needed to prevent these adverse effects.
Area of Science:
- Immunology
- Oncology
- Pharmacology
Background:
- Cyclosporine A is a vital immunosuppressant in organ transplantation.
- A significant concern is the increased incidence of de novo cancers associated with its use.
- Current understanding attributes this risk primarily to immune suppression.
Purpose of the Study:
- To explore molecular mechanisms beyond immunosuppression by which Cyclosporine A may contribute to cancer.
- To propose a multifactorial model for Cyclosporine A-induced oncogenesis.
Main Methods:
- Review of existing literature on Cyclosporine A's molecular effects.
- Analysis of pathways including DNA repair, TGF-Beta signaling, and apoptosis regulation.
- Synthesis of evidence to link molecular effects to cancer development and progression.
Main Results:
- Cyclosporine A inhibits DNA repair mechanisms, potentially leading to increased mutations.
- It influences apoptosis pathways, affecting the clearance of potentially cancerous cells.
- The drug may also promote cancer cell aggressiveness and transformation.
Conclusions:
- Cyclosporine A's role in cancer genesis is likely multifactorial, involving direct molecular effects beyond immunosuppression.
- These include facilitating DNA mutations, reducing clearance of altered cells, and enhancing cancer cell aggression.
- Understanding these mechanisms is crucial for developing novel preventive and therapeutic strategies.
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