Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add more filters

Database
Language
Affiliation country
Publication year range
1.
Proc Natl Acad Sci U S A ; 109(17): 6686-91, 2012 Apr 24.
Article in English | MEDLINE | ID: mdl-22496589

ABSTRACT

Copy number variants (CNVs) are a recently recognized class of human germ line polymorphisms and are associated with a variety of human diseases, including cancer. Because of the strong genetic influence on prostate cancer, we sought to identify functionally active CNVs associated with susceptibility of this cancer type. We queried low-frequency biallelic CNVs from 1,903 men of Caucasian origin enrolled in the Tyrol Prostate Specific Antigen Screening Cohort and discovered two CNVs strongly associated with prostate cancer risk. The first risk locus (P = 7.7 × 10(-4), odds ratio = 2.78) maps to 15q21.3 and overlaps a noncoding enhancer element that contains multiple activator protein 1 (AP-1) transcription factor binding sites. Chromosome conformation capture (Hi-C) data suggested direct cis-interactions with distant genes. The second risk locus (P = 2.6 × 10(-3), odds ratio = 4.8) maps to the α-1,3-mannosyl-glycoprotein 4-ß-N-acetylglucosaminyltransferase C (MGAT4C) gene on 12q21.31. In vitro cell-line assays found this gene to significantly modulate cell proliferation and migration in both benign and cancer prostate cells. Furthermore, MGAT4C was significantly overexpressed in metastatic versus localized prostate cancer. These two risk associations were replicated in an independent PSA-screened cohort of 800 men (15q21.3, combined P = 0.006; 12q21.31, combined P = 0.026). These findings establish noncoding and coding germ line CNVs as significant risk factors for prostate cancer susceptibility and implicate their role in disease development and progression.


Subject(s)
Chromosomes, Human, Pair 12 , Chromosomes, Human, Pair 15 , Gene Dosage , Genetic Predisposition to Disease , Prostatic Neoplasms/genetics , Case-Control Studies , Cell Line, Tumor , Cell Proliferation , Cohort Studies , Humans , Male , Polymerase Chain Reaction , Polymorphism, Single Nucleotide , Prostatic Neoplasms/pathology
SELECTION OF CITATIONS
SEARCH DETAIL