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Updated: Jun 8, 2026

Murine Full-thickness Skin Transplantation
Published on: January 2, 2017
[Skin cancer in renal transplant recipients]
Margherita Mangino1, Francesco Paolo Schena
1Unita' di Nefrologia Dialisi e Trapianto, Dipartimento dell'Emergenza e dei Trapianti d'Organo (DETO), Universita' degli Studi, Bari, Italy.
Abstract:
Kidney transplant is the best treatment option for renal failure. Over the years the 1-year patient survival has gradually increased, along with a reduction in acute rejection. The main causes of death in the late post-transplant period are cardiovascular disease, infections and malignancies. It is known that the incidence of cancer increases with the duration of post-transplant follow-up. Twenty years after transplantation, approximately 70% of patients on continuous immunosuppressive therapy present one or more tumor types. Some of the tumors that occur with a significantly higher frequency in transplant recipients compared with the general population are often associated with the reactivation of oncogenic viruses. Examples are herpes virus 8 (HHV8), implicated in Kaposi's sarcoma (KS), human papillomavirus (HPV), involved in squamous cell cancer of the skin, vulva, vagina and cervix, and Epstein-Barr virus (EBV), responsible for post-transplant lymphoproliferative disorder (PTLD). The type of drug used for the induction and maintenance of immunosuppression and the duration of treatment influence both the incidence and the type of cancer. For this reason, post-transplant malignancies often show a more aggressive behavior than tumors in the normal population. It is estimated that sarcomas occur 40 to 250 times more frequently in transplant recipients and are the leading cause of death from skin cancer after transplantation. The classic form of KS occurs in males and homosexuals. In the population of the Mediterranean area, KS is often associated with HHV8 infection that is reactivated by immunosuppression. The reduction or suspension of immunosuppressive therapy is the first step in the treatment of post-transplant KS. The second approach is chemotherapy. Since m-TOR, the target of sirolimus, is altered in many tumors, sirolimus may be an effective tool. Sirolimus inhibits not only cell proliferation but also tumor neovascularization by reducing VEGF production and inhibiting VEGF receptor signaling in endothelial cells. In conclusion, new strategies must be developed to reduce cancer mortality in transplant recipients while ensuring adequate immunosuppression to preserve the transplanted organ. One such strategy is the adoption of immunosuppressive regimens tailored to individual patients' medical history.
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