Disease-associated SNPs at the 9p21 locus predominantly affect the expression of ANRIL. Overall, our results suggest that several CVD-associated SNPs in the 9p21 locus affect the expression of ANRIL, which, in turn modulate cell growth, possibly via CDKN2A/B regulation.

Cilostazol significantly reduces restenosis and target lesion revascularization rates after successful PTCA.

A new understanding of the genetic basis of coronary artery disease (CAD) has recently emerged from genome-wide association (GWA) studies of common single-nucleotide polymorphisms (SNPs), thus far performed mostly in European-descent populations. To identify novel susceptibility gene variants for CAD and confirm those previously identified mostly in populations of European descent, a multistage GWA study was performed in the Japanese. In the discovery phase, we first genotyped 806 cases and 1337 controls with 451 382 SNP markers and subsequently assessed 34 selected SNPs with direct genotyping (541 additional cases) and in silico comparison (964 healthy controls). In the replication phase, involving 3052 cases and 6335 controls, 12 SNPs were tested; CAD association was replicated and/or verified for 4 (of 12) SNPs from 3 loci: near BRAP and ALDH2 on 12q24 (P¼1.6Â10 À34 ), HLA-DQB1 on 6p21 (P¼4.7Â10 À7 ), and CDKN2A/B on 9p21 (P¼6.1Â10 À16 ). On 12q24, we identified the strongest association signal with the strength of association substantially pronounced for a subgroup of myocardial infarction cases (P¼1.4Â10 À40 ). On 6p21, an HLA allele, DQB1*0604, could show one of the most prominent association signals in an B8-Mb interval that encompasses the LTA gene, where an association with myocardial infarction had been reported in another Japanese study. CAD association was also identified at CDKN2A/B, as previously reported in different populations of European descent and Asians. Thus, three loci confirmed in the Japanese GWA study highlight the likely presence of risk alleles with two types of genetic effects -population specific and common -on susceptibility to CAD.

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'Pravastatin medicated' refers to patients in Groups I and IIa who took pravastatin for ≥ 75 % of the study period, and patients in Groups IIb and III who took pravastatin for >25% of the study period. 'Non-medicated' refers to the remaining subjects. Smoking habits were ascertained by interview at entry and in the follow-up period. 'Quit or start' refers to a subject who did not continuously smoke during the follow-up period. Person-years at risk were calculated from the date of entry until the date of the diagnosis of cancer, date of death, or closing date, i.e. 5 years after entry or the date of last contact, whichever occurred first. Site-specific sex, 5-year age group, and 5-year calendar period incidence rates for each type of cancer among the Osaka residents were applied to the appropriate person-years at risk to obtain the number of cancers to be expected. 26 A test of significance for the observed/expected (O/E) ratios was calculated using the exact Poisson probabilities and the 95% confidence interval (CI) of the O/E ratios was based on the formulation derived by Rothman. 26This study was approved by the ethics committee of the hospital.After 1255.5 person-years of follow-up, we documented 17 incident cases of cancer. Four cases, that is, one-quarter of the cancers were diagnosed in hospitals other than the Osaka Medical Center for Cancer and Cardiovascular Diseases. A past history of cancer before the entry was confirmed in 8 patients. These 8 cases were included in this analysis because the result was almost the Pravastatin and Cancer in Coronary Heart Disease Patients