Oral Candida colonisation is higher in tobacco smokers as compared to non-smokers; however, it remains unknown whether smokeless tobacco chewers are susceptible to increased oral Candida colonisation. The aim was to determine the oral Candida carriage and species prevalence amongst habitual gutka-chewers and non-chewers in a cohort from Karachi, Pakistan. Forty-five gutka-chewers and 45 non-chewers were included. Information regarding age, sex, duration of gutka-chewing habit, daily frequency of gutka consumption, duration of holding gutka in the mouth, daily frequency of tooth-brushing and tongue brushing was collected using a questionnaire. Oral yeast samples were collected by scraping the dorsum of the tongue and bilateral buccal mucosa with a sterile cotton swab. Identification of yeast species was performed using standard techniques. Tongue lesions were identified and recorded. Unstimulated whole salivary flow rate (UWSFR) was also measured. There was no significant difference in the mean age, UWSFR and oral Candida carriage among gutka-chewers and non-chewers. Individuals were chewing gutka since 4·4 years and were consuming five gutka sachets daily. Candida albicans (C. albicans) was the most common yeast species isolated from 57·8% gutka-chewers and 64.4% non-chewers. In 24.4% gutka-chewers and 22·2% non-chewers, two candidal strains (C. albicans and Candida tropicalis) were isolated. In conclusion, the present results indicated no significant difference in oral Candida carriage in habitual gutka-chewers and non-chewers.
Genome-wide association studies (GWAS) have identified 12 epithelial ovarian cancer (EOC) susceptibility alleles. The pattern of association at these loci is consistent in BRCA1 and BRCA2 mutation carriers who are at high risk of EOC. After imputation to 1000 Genomes Project data, we assessed associations of 11 million genetic variants with EOC risk from 15,437 cases unselected for family history and 30,845 controls and from 15,252 BRCA1 mutation carriers and 8,211 BRCA2 mutation carriers (3,096 with ovarian cancer), and we combined the results in a meta-analysis. This new study design yielded increased statistical power, leading to the discovery of six new EOC susceptibility loci. Variants at 1p36 (nearest gene, WNT4), 4q26 (SYNPO2), 9q34.2 (ABO) and 17q11.2 (ATAD5) were associated with EOC risk, and at 1p34.3 (RSPO1) and 6p22.1 (GPX6) variants were specifically associated with the serous EOC subtype, all with P < 5 × 10(-8). Incorporating these variants into risk assessment tools will improve clinical risk predictions for BRCA1 and BRCA2 mutation carriers.