In the present study, BMI, the HDL/total cholesterol concentration ratio, and the use of QT-prolonging drugs were not significantly associated with risk of SCD. Interestingly, use of the QT-shortening drug digoxin was associated with an increased risk of SCD. This may be due to the fact that digoxin may have been prescribed to treat atrial fibrillation or heart failure, both of which are associated with SCD risk. Alternatively, digoxin use could be directly related to risk of SCD. This study explored the association of a wide selection of candidate SNPs with SCD in a large sample collection of four population cohorts and two series of forensic autopsies, including a total of 716 SCD events. A strength of the present study is the availability of large prospective population cohorts enabling more precise risk estimates than case-control studies. In addition, prospective studies enable exploration of the effects of covariate adjustment. The long-term follow-up of the study subjects was comprehensive covering all subjects living in Finland, the autopsy rate of SCD cases was high, and extensive information on the causes of death was gathered through several national registries. In Finland, autopsies are targeted on cases in which clinical information is insufficient to determine the cause of death. As the diagnoses in the death certificate are generally valid, including cases without autopsy can be considered sufficient for reliable classification of causes of death. Finns represent a genetically isolated population with significant substructure due to founder effects and bottlenecks during the settlement history. Significant East-West differences have previously been reported in the risk of SCD and we replicated this finding. To account for population stratification in the present study, geographic region was adjusted for in the statistical analyses of the population cohorts. A large proportion of SCDs in Western countries are unwitnessed and therefore the presence of an underlying fatal arrhythmia, and the time between onset of symptoms and death cannot be reliably determined in a population-based study. The inclusion of individuals with a wide age range increases the generalizability of the study but at the expense of increasing heterogeneity of the causes of death. Colorectal cancer ranks second to lung cancer in both incidence and mortality in developed countries. It is characterized by highly complex patterns of somatic genetic alterations of oncogenes and tumor suppressors that drive initiation and progression. Understanding the cellular and molecular mechanisms by which these genetic changes facilitate colon cancer formation is critical for development of targeted therapeutic strategies aimed at controlling disease progression while minimizing toxic side effects. One well-established genetic mechanism by which cancer cells alter the activity of oncogenes and tumor suppressors is through changes in gene dosage. Detailed characterization of DNA copy number aberrations have helped identify important oncogenes including ERBB2 and EGFR, as well as tumor suppressors such as TP53. Numerous studies have documented genome-wide somatic CNAs in CRC, some of which have been GANT61 Hedgehog inhibitor linked to clinical outcome or metastatic progression. However, many of these studies have been limited by modest sample size, low resolution assays, or lack of associated clinical annotation, particularly for early-stage colon cancer. Consequently, a comprehensive overview of CNAs and their association with outcome in stage II/III colon cancer has not been developed.