RESUMEN
Several susceptibility loci for classical Hodgkin lymphoma have been reported. However, much of the heritable risk is unknown. Here, we perform a meta-analysis of two existing genome-wide association studies, a new genome-wide association study, and replication totalling 5,314 cases and 16,749 controls. We identify risk loci for all classical Hodgkin lymphoma at 6q22.33 (rs9482849, P = 1.52 × 10-8) and for nodular sclerosis Hodgkin lymphoma at 3q28 (rs4459895, P = 9.43 × 10-17), 6q23.3 (rs6928977, P = 4.62 × 10-11), 10p14 (rs3781093, P = 9.49 × 10-13), 13q34 (rs112998813, P = 4.58 × 10-8) and 16p13.13 (rs34972832, P = 2.12 × 10-8). Additionally, independent loci within the HLA region are observed for nodular sclerosis Hodgkin lymphoma (rs9269081, HLA-DPB1*03:01, Val86 in HLA-DRB1) and mixed cellularity Hodgkin lymphoma (rs1633096, rs13196329, Val86 in HLA-DRB1). The new and established risk loci localise to areas of active chromatin and show an over-representation of transcription factor binding for determinants of B-cell development and immune response.
Asunto(s)
Predisposición Genética a la Enfermedad , Enfermedad de Hodgkin/genética , Alelos , Estudio de Asociación del Genoma Completo , Cadenas beta de HLA-DP/genética , Cadenas HLA-DRB1/genética , Humanos , Polimorfismo de Nucleótido SimpleRESUMEN
Ovarian cancer is a deadly disease, largely because of relapse and chemotherapy resistance. Common genetic mechanisms causing drug resistance have not been identified. A recent study unravels a novel and unexpected pathway involving the transfer of microvesicle-encapsulated miRNA from omental adipocytes and fibroblasts, to cancer cells.