Comparison of overall and type-specific HPV prevalence between CIN1 and SCC, CIN2 and SCC, and CIN3 and SCC cases.

<p>95%CI = 95% confidence interval, RR =  relative risk, P =  probability.</p><p>**all HPV types detected (LR and HR).</p><p>***all HR HPV types detected.</p><p>****HR HPV types 16, 18, 31, 33, 45, 56, and 58.</p

Cumulative percentages of cancer cases of women and men in the Czech Republic.

<p>Cumulative percentages of cervical (A), vulvar (B) and anal (C) cancer cases in women and men occurring every year in the Czech Republic that are attributed to eight most prevalent HPV types (990, 189 and 121 incident cancer cases, respectively). (Sdapted from Munoz, 2004)[46].</p

HPV prevalence in precancerous lesions of different anatomical locations.

<p>CIN1 = cervical intraepithelial neoplasia grade 1, CIN2/3 =  cervical intraepithelial neoplasia grade 2 and 3, VIN = vulvar intraepithelial neoplasia.</p>#<p>samples HPV 16 and/or 18 positive.</p><p>*samples which do not contain HPV 16 and/or 18.</p><p>**samples which do not contain HPV 16 and/or 18 and/or 31 and/or 45.</p><p>***samples which do not contain HPV 16 and/or 18.</p

HPV prevalence in carcinomas of different anatomical locations.

<p>SCC = squamous cell cervical carcinoma, VC = vulvar carcinoma, AC = squamous cell anal carcinoma.</p>#<p>samples HPV 16 and/or 18 positive.</p><p>*samples which do not contain HPV 16 and/or 18.</p><p>**samples which do not contain HPV 16 and/or 18 and/or 31 and/or 45.</p><p>***samples which do not contain HPV 16 and/or 18.</p

HPV prevalence in condyloma acuminata of different anatomical locations.

<p>VCA  =  vulvar condyloma acuminatum, ACA  =  anal condyloma acuminatum.</p>#<p>samples HPV 16 and/or 18 positive.</p><p>*samples which do not contain HPV 16 and/or 18.</p><p>**samples which do not contain HPV 16 and/or 18 and/or 31 and/or 45.</p><p>***samples which do not contain HPV 16 and/or 18.</p

DataSheet_1_Complex molecular profile of DNA repair genes in epithelial ovarian carcinoma patients with different sensitivity to platinum-based therapy.pdf

Epithelial ovarian carcinoma (EOC) is known for high mortality due to diagnosis at advanced stages and frequent therapy resistance. Previous findings suggested that the DNA repair system is involved in the therapeutic response of cancer patients and DNA repair genes are promising targets for novel therapies. This study aimed to address complex inter-relations among gene expression levels, methylation profiles, and somatic mutations in DNA repair genes and EOC prognosis and therapy resistance status. We found significant associations of DUT expression with the presence of peritoneal metastases in EOC patients. The high-grade serous EOC subtype was enriched with TP53 mutations compared to other subtypes. Furthermore, somatic mutations in XPC and PRKDC were significantly associated with worse overall survival of EOC patients, and higher FAAP20 expression in platinum-resistant than platinum-sensitive patients was observed. We found higher methylation of RAD50 in platinum-resistant than in platinum-sensitive patients. Somatic mutations in BRCA1 and RAD9A were significantly associated with higher RBBP8 methylation in platinum-sensitive compared to platinum-resistant EOC patients. In conclusion, we discovered associations of several candidate genes from the DNA repair pathway with the prognosis and platinum resistance status of EOC patients, which deserve further validation as potential predictive biomarkers.</p