An imprinted locus epistatically influences Nstr1 and Nstr2 to control resistance to nerve sheath tumors in a neurofibromatosis type 1 mouse model.

摘要: Cancer is a complex disease in which cells acquire many genetic and epigenetic alterations. We have examined how three types of alterations, mutations tumor suppressor genes, changes an imprinted locus, polymorphic loci, interact to affect susceptibility mouse model neurofibromatosis type 1 (NF1). Mutations genes such as TP53 oncogenes KRAS major effects on tumorigenesis due the central roles these cell proliferation survival. Imprinted expressed from only one parental chromosome if their monoallelic expression lost or duplicated. Because loci are within regions deleted amplified cancer, origin genomic rearrangements could tumorigenesis. Gene polymorphisms can vary incidence by affecting rate-limiting steps surrounding stroma. In our NF1, tumors mutant for Nf1 Trp53 strongly modified linked locus acting epistatically two unlinked Nstr1 Nstr2. This interaction has profound implications human mapping studies where contribution alleles often unknown. (Cancer Res 2006; 66(1): 62-8)