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Background: The causal role of human papilloma virus (HPV) in all cancers of the uterine cervix has been firmly established biologically and epidemiologically. HPV types 16 and 18 account for about 70 % of the cases worldwide. HPV has been recognized as a necessary cause of cervical cancer, meaning that in the absence of the persistent presence of HPV DNA in the cervical cells, cervical cancer will not occur. Thus preventive strategies based on HPV testing in screening programmes or HPV type-specific vaccination are based on solid ground. Most cancers of the vagina and anus are likewise caused by HPV 16, as are a siteable fraction of cancers of the vulva, the penis and the oropharynx. Cervical cancer screening can be a highly effective secondary intervention. In the developing countries these programmes are either not available or are ineffective. HPV vaccination represents the most effective intervention in that scenario. Prophylactic vaccination with human papillomavirus (HPV) virus-like particle (VPL) vaccines against HPV 16 and HPV 18, has transformed our prospects for reducing the in- cidence of cervical cancer on global scale. HPV vaccines are immunogenic, well tolerated and show remarkable efficacy. Screening will have to continue, as two of the 15 oncogenic HPV types are in the vaccines and for two to three decades at least unvaccinated sexually active women still remain at risk for the disease. Conclusions: If vaccination, screening and HPV testing are combined then the virtual elimination of cervical cancer is possible.

BACKGROUND HT should be considered only when an indication for therapy has been clearly identified,contraindications ruled out, and the potential individual benefits and risks adequatelydiscussed with the women so that an informed decision can be made.Breast cancer risk increases with EPT use beyond 5 years. In absolute terms, this increasedrisk are rare in the WHI, being 4 to 6 additional invasive cancers per 10.000 women peryear who used EPT for 5 or more years. Studies have not clarified whether the risk differsbetween continous or sequential use of progestogen. Women in the ET arm of the WHIdemonstrated no increase in risk of breast cancer after an average of 7.1 years of use, with8 fewer cases of invasive breast cancer per 10.000 women per year of ET use. There arelimited observational data suggesting that ET for more than 15 years may increase the riskof breast cancer. There are minimal data reporting any change in breast cancer mortalitywith HT. CONCLUSIONS It should be recognized that even in the absence of HT use, there is a risk of development ofbreast cancer. There are multiple risk factors for breast cancer, including alcohol intake,obesity and lack of exercise. These need to be included during counselling to put the magnitude of risk of HRT into an appropriate perspective