Foreword

The year 2006 was marked by an important event in cancer prevention: 30 years after Harald zur Hausen for the first time hypothesized that human papillomaviruses may be associated with the development of cervical cancer, a prophylactic vaccine against certain types of these viruses was launched to the market in Mexico, the US, Canada, Australia, and several European countries. Initially, the very rare malignant conversion of condylomata accuminata tempted zur Hausen to speculate that infectious genital warts and cervical cancer may have a similar infectious causes. These considerations were strongly supported by observations made by Alexander Meisels in Toronto who found that replicating HPV infections led to the formation of “koilocytes” that are found in condylomata but also in early cervical intraepithelial lesions (CIN 1), the early precursors of invasive cervical cancer. Shortly thereafter, the papillomavirus genotypes 6 and 11 were isolated from condylomata and were used as molecular probes to identify related viral genomes in cell lines and biopsies of cervical cancers. These experiments led to the successful detection of HPV 16 and 18 in the early 1980ies. Subsequent research revealed that oncogenic HPV genes are present in almost all cervical cancers, that the viral genes E6 and E7 are continuously expressed in all cancer cells, that these genes confer transforming activities once they are expressed in cultured human epithelial cells in vitro and, importantly, that the inhibition of the expression of these genes results in loss of the neoplastic growth of cervical cancer cells. Since then a tremendous amount of knowledge has been gathered by many scientists, including epidemiologists, pathologists, clinicians and public health physicians on the global distribution of oncogenic papillomaviruses and their disease causing role. It turned out that these virus-