Effects of immunosuppressive therapy on the induction of skin tumors by ultraviolet irradiation in hairless mice

Kelly, Graham; Manstein, Carl H.

doi:10.1097/00006534-198812000-00093

Cited by 34 publications

(51 citation statements)

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“…The risk of SCC in our cohort (SIR 28) was [7] and fivefold higher than that in patients with inflammatory bowel disease (SIR 5.5) [20]. The difference in SIR in different patient populations might be partially explained by (1) different intensity, regimen and duration of immunosuppression, (2) heterogeneity of different diseases and (3) different study time periods.…”

Section: Discussionmentioning

confidence: 64%

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Risk of Non-melanoma Skin Cancer in Autoimmune Hepatitis

et al. 2010

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Section: Discussionmentioning

confidence: 64%

“…Immunosuppression heightens NMSC risk through two distinct mechanisms: impairing immune surveillance against skin cancer and intrinsic carcinogenic properties [7]. One of the most studied examples is azathioprine, which enhances UV-induced tumorigenesis in mice [20] and photosensitizes human skin to UVA radiation [21,22].…”

Section: Discussionmentioning

confidence: 99%

Risk of Non-melanoma Skin Cancer in Autoimmune Hepatitis

et al. 2010

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“…116 In contrast, in C3Hf/HeN mice exposed to 1.79 Â 10 3 erg/cm 2 per UV for 10 minutes, 3 times per week, treatment with methotrexate (administered ip at a dose of 2 mg/kg for 23 weeks starting on day 0) had no effect on UV carcinogenesis. 117 And, in Skh-1 mice exposed to 2240 J/m 2 UVB, treatment with sirolimus (administered ip at a dose of 2 mg/kg daily for 9 weeks starting at 15 weeks) decreased the number and size of skin tumors.…”

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confidence: 96%

Critical Review of Preclinical Approaches to Evaluate the Potential of Immunosuppressive Drugs to Influence Human Neoplasia

Bugelski¹,

Volk²,

Walker³

et al. 2010

Int J Toxicol

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Many immunosuppressive drugs are associated with an increased risk of B-cell lymphoma, squamous cell carcinoma, and Kaposi sarcoma. Thirteen immunosuppressive drugs have been tested in 2-year carcinogenicity studies (abatacept; azathioprine; busulfan; cyclophosphamide; cyclosporine; dexamethasone; everolimus; leflunomide; methotrexate; mycophenolate mofetil; prednisone; sirolimus; and tacrolimus) and in additional models including neonatal and genetically modified mice; chemical, viral, ultraviolet, and ionizing radiation co-carcinogenesis, and in models with transplanted tumor cells. The purpose of this review is to outline the mechanisms by which immunosuppressive drugs can influence neoplasia, to summarize the available preclinical data on the 13 drugs, and to critically review the performance of the models. A combination of primary tumor and metastasis assays conducted with transplanted cells may provide the highest value for hazard identification and can be applied on a case-by-case basis. However, for both small molecules and therapeutic proteins, determining the relative risk to patients from preclinical data remains problematic. Classifying immunosuppressive drugs based on their mechanism of action and hazard identification from preclinical studies and a prospective pharmacovigilance program to monitor carcinogenic risk may be a feasible way to manage patient safety during the clinical development program and postmarketing.

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“…In our model, enhancement of BCC formation occurred in the absence of UV exposure, suggesting that continued UV is not essential for drug-enhanced BCC formation and that the effects of the ARD in this model were at a post-initiation stage of BCC development. A small number of publications have reported that ARD can enhance experimental mouse (mostly hairless) squamous cell photocarcinogenesis but the reported enhancement is far less impressive than is the increased incidence of SCC observed in human OTR (Koranda et al, 1975;Nathanson et al, 1976;Daynes et al, 1979;Reeve et al, 1985;Kelly et al, 1987Kelly et al, , 1989. These reported studies used UV photocarcinogenesis and mostly used mutant hairless mice, in which UV radiation primarily causes papillomas and carcinomas of the squamous cell lineage.…”

Section: Discussionmentioning

confidence: 99%

Anti-Rejection Drug Treatment Increases Basal Cell Carcinoma Burden in Ptch1+/- Mice

Vogt

Hebert

Hwang

et al. 2005

Journal of Investigative Dermatology

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The development of extensive and severe non-melanoma skin cancer is an extremely common complication of organ transplantation and is assumed to be caused by long-term treatment with anti-rejection drugs (ARD). Despite this florid clinical problem, ARD treatments have been reported to affect experimental murine skin carcinogenesis only weakly. We report here that treatment of cesium-137-irradiated Ptch1+/- mice with immunosuppressive doses of cyclosporine A plus prednisolone for 4-1/2 mo increased basal cell carcinoma burden by 2.5-fold. Thus, these mice provide a good model for study of the effects of long-term administration of ARD on at least one type of non-melanoma skin cancer.

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Effects of immunosuppressive therapy on the induction of skin tumors by ultraviolet irradiation in hairless mice

Cited by 34 publications

References 0 publications

Risk of Non-melanoma Skin Cancer in Autoimmune Hepatitis

Risk of Non-melanoma Skin Cancer in Autoimmune Hepatitis

Critical Review of Preclinical Approaches to Evaluate the Potential of Immunosuppressive Drugs to Influence Human Neoplasia

Anti-Rejection Drug Treatment Increases Basal Cell Carcinoma Burden in Ptch1+/- Mice

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