Interleukin-10, interleukin-6 and interferon-γ gene polymorphisms in melanoma patientsMartínez-Escribano, J. A.*; Moya-Quiles, M. R.; Muro, M.; Montes-Ares, O.; Hernández-Caselles, T.; Frías, J. F.; Álvarez-López, M. R.Melanoma Research: September 2002 - Volume 12 - Issue 5 - p 465-469 Original Articles Buy Abstract Author InformationAuthors The immune response against melanoma can be influenced by cytokines with potentially opposite effects on tumour cell growth, such as interleukin-10 (IL10), interleukin-6 (IL6) and interferon-γ (IFNγ). Our objective in this study was to investigate whether polymorphisms in the regulatory regions of IL10, IL6 and IFNγ genes are associated with the development of primary cutaneous melanoma and/or the prognosis of this tumour. We studied genotypic variations at positions −1082, −819 and −592 in the IL10 promoter, −174 in the IL6 promoter and +874 in the IFNγ intron 1 in 42 melanoma patients and 48 healthy controls. These two populations showed very similar genotypic frequencies for IL10, IL6 and IFNγ gene polymorphisms. There was a significant increase in the prevalence of IL10 low expression genotypes, specially the ACC/ATA genotype, among patients with a poorer prognosis. In contrast, IL6 promoter and IFNγ intron 1 gene polymorphisms did not correlate with melanoma prognosis. These data indicate that investigation of polymorphisms in the regulatory regions of IL10, IL6 and INFγ genes does not seem to be useful for predicting the risk of development of primary cutaneous melanoma. However, IL10 low expression genotypes may be associated with a poorer outcome in melanoma patients. Departments of Dermatology (J. A. Martínez-Escribano, J. F. Frías) and Immunology (M. R. Moya-Quiles, M. Muro, O. Montes-Ares, T. Hernández-Caselles, M. R. Álvarez-López), Virgen de la Arrixaca University Hospital, 30120 - El Palmar, Murcia, Spain. Tel: (+34) 968 369330; Fax: (+34) 968 369330; Email: email@example.com *To whom correspondence should be addressed (Received 28 January 2002;accepted in revised form 28 March 2002) © 2002 Lippincott Williams & Wilkins, Inc.