[Cervical cancer in Poland and in the world--in the light of incidence and mortality data]. / Rak szyjki macicy w Polsce i na swiecie--w swietle danych o zapadalnosci i umieralnosci.

Cancer of the cervix uteri is a substantial problem of public health in Poland and some countries in the world. It develops within precancerous lesions of the cervix caused by oncogenic human papillomavirus (HPV) types. Epidemiology of precancerous cervical lesions and cervical cancer in Poland, Europe and selected countries in the world as well as 5-year survival rate of women diagnosed with cervical cancer is discussed.

[Risk factors of cervical cancer and possibilities of primary prevention]. / Czynniki ryzyka raka szyjki macicy i mozliwosci pierwotnej profilaktyki.

Cancer of the cervix uteri is one of the few malignancies with identified necessary etiological factor and described steps of its development. Sexually transmitted human papillomavirus (HPV) infections are the etiological factor of cervical cancer. Despite the fact that HPV infections are one of the most frequent in female reproductive tract, they rarely cause premalignant conditions which, if untreated, may lead to development of cervical cancer. Attempts of primary prevention of cervical cancer through reduction of HPV infections by propagation of proper sexual behaviour and use of condoms have limited efficacy. At present the most effective form of cervical cancer primary prevention are prophylactic vaccines against two most common HPV types: 16 and 18, which are responsible for approximately 70% of all cervical cancer cases in the world.

Worldwide human papillomavirus genotype attribution in over 2000 cases of intraepithelial and invasive lesions of the vulva.

BACKGROUND: Human papillomavirus (HPV) contribution in vulvar intraepithelial lesions (VIN) and invasive vulvar cancer (IVC) is not clearly established. This study provides novel data on HPV markers in a large series of VIN and IVC lesions. METHODS: Histologically confirmed VIN and IVC from 39 countries were assembled at the Catalan Institute of Oncology (ICO). HPV-DNA detection was done by polymerase chain reaction using SPF-10 broad-spectrum primers and genotyping by reverse hybridisation line probe assay (LiPA25) (version 1). IVC cases were tested for p16(INK4a) by immunohistochemistry (CINtec histology kit, ROCHE). An IVC was considered HPV driven if both HPV-DNA and p16(INK4a) overexpression were observed simultaneously. Data analyses included algorithms allocating multiple infections to calculate type-specific contribution and logistic regression models to estimate adjusted prevalence (AP) and its 95% confidence intervals (CI). RESULTS: Of 2296 cases, 587 were VIN and 1709 IVC. HPV-DNA was detected in 86.7% and 28.6% of the cases respectively. Amongst IVC cases, 25.1% were both HPV-DNA and p16(INK4a) positive. IVC cases were largely keratinising squamous cell carcinoma (KSCC) (N=1234). Overall prevalence of HPV related IVC cases was highest in younger women for any histological subtype. SCC with warty or basaloid features (SCC_WB) (N=326) were more likely to be HPV and p16(INK4a) positive (AP=69.5%, CI=63.6-74.8) versus KSCC (AP=11.5%, CI=9.7-13.5). HPV 16 was the commonest type (72.5%) followed by HPV 33 (6.5%) and HPV 18 (4.6%). Enrichment from VIN to IVC was significantly high for HPV 45 (8.5-fold). CONCLUSION: Combined data from HPV-DNA and p16(INK4a) testing are likely to represent a closer estimate of the real fraction of IVC induced by HPV. Our results indicate that HPV contribution in invasive vulvar cancer has probably been overestimated. HPV 16 remains the major player worldwide.