Anti-rejection drug treatment increases basal cell carcinoma burden in Ptch1+/- mice.
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.
Vogt
Annika
A
Department of Dermatology, University of California, San Francisco, California 94110, USA.
Hebert
Jennifer
J
Hwang
Jimmy
J
Lu
Ying
Y
Epstein
Ervin H
EH
D000818:Animals; D002280:Basal Cell Carcinoma / Q000276:immunology* / Q000473:pathology; D016572:Cyclosporine / Q000494:pharmacology*; D004195:Disease Models, Animal; D005938:Glucocorticoids / Q000494:pharmacology; D006084:Graft Rejection / Q000188:drug therapy; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D051379:Mice; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D000072079:Patched Receptors; D000072081:Patched-1 Receptor; D011239:Prednisolone / Q000494:pharmacology; D011506:Proteins / Q000235:genetics*; D011956:Receptors, Cell Surface; D012878:Skin Neoplasms / Q000276:immunology* / Q000473:pathology
D005938:Glucocorticoids; D007166:Immunosuppressive Agents; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D000072079:Patched Receptors; D000072081:Patched-1 Receptor; D011506:Proteins; C000606240:Ptch1 protein, mouse; D011956:Receptors, Cell Surface; D016572:Cyclosporine; D011239:Prednisolone