BACKGROUND We investigated the relationship of the polymorphisms of SET and MYND domain-containing protein 3 (SMYD3) with risk and prognosis of ovarian cancer. MATERIAL AND METHODS The polymerase chain reaction (PCR) amplification method was applied to detect the polymorphisms of variable number of tandem repeats (VNTR) in the SMYD3 gene promoter region for 156 patients with ovarian cancer (case group) and 174 healthy people (control group). Quantitative reverse transcription polymerase chain reaction and Western blot were applied to detect SMYD3 mRNA and protein expressions. RESULTS The frequencies of VNTR genotype 3/3 and allele genotype 3 in the case group were significantly higher than those in the control group, while the frequency of genotype 2/2 in the control group was significantly higher than that in case group (all P<0.05). The proportion of poorly differentiated patients carrying VNTR genotype 3/3 was significantly higher than the proportion of poorly differentiated patients carrying VNTR genotype 2/2+2/3, while the proportion of patients carrying genotype 3/3 with International Federation of Gynecology and Obstetrics (FIGO) stage III-IV disease was significantly higher than the proportion of patients carrying genotype 2/2 +2/3 with FIGO stage III-IV disease (all P<0.05). SMYD3 mRNA and protein expressions were higher in the patients carrying genotype 3/3 than they were in the patients with the 2/2+2/3 genotype (all P<0.05). The 5-year survival rate for patients carrying VNTR genotype 3/3 was significantly lower than that of patients carrying genotype 2/2+2/3, and Cox regression analysis showed that VNTR genotype 3/3 was an independent risk factor for ovarian cancer prognosis (all P<0.05). CONCLUSIONS VNTR genotype 3/3 of the SMYD3 gene was associated with the risk of ovarian cancer. The polymorphism of VNTR genotype could be recognized as an indicator for the poor prognosis of patients with ovarian cancer.
Background: Although cancer and its corresponding therapies are associated with increased ischemic heart disease, the temporal relationship between cancer and the development of coronary artery calcium (CAC), a marker of subclinical atherosclerosis, is unknown.
Methods and results: Among 3122 men and women free of cardiovascular disease and cancer in the Multi-Ethnic Study of Atherosclerosis trial, CAC scoring was performed at baseline (2000-2002) and at follow-up (2010-2012). Over this 10-year period, 85 men (age 63.6±8.3 years) and 50 women (age 62.1±9.8 years) were diagnosed with cancer (predominantly breast, lung, or uterine [52%] in women and prostate or colorectal [78%] in men). The other 2987 subjects (age 59.6±9.2 years for men, 59.7±9.4 years for women) remained cancer free. The incidence of new CAC (baseline Agatston score of zero converting to detectable CAC) was modeled with relative risk regression and compared for cancer versus no cancer. Increase in pre-existing CAC was compared in these groups using linear regression of log transformed CAC. The incidence of CAC was independently associated with cancer history (relative risk 1.32 [P=0.04] and 1.29 [P=0.01] for women and men, respectively). In participants with CAC at baseline, a clear difference of CAC progression was not observed between cancer and noncancer participants (P=0.6 for women, P=0.2 for men).
Conclusions: A diagnosis of cancer is associated with the development of CAC even after accounting for atherosclerotic risk factors. However, in individuals with pre-existing CAC, it is not clear whether the presence of cancer accelerates CAC over time.