摘要:Cervical cancer, a well-characterized virus-induced malignancy, is the second most common cause of cancer-related death in women [1, 2]. While the link between the formation of genital warts and their inherent propensity to progress to cancer was suspected more then a century ago [1], the connection between cervical cancer and the human papillomavirus (HPV) was demonstrated only two decades ago. During the early 1980’s the zur Hausen laboratory provided the first experimental proof that the genome of malignant genital warts was integrated with DNA from the HPV subtypes 16 and 18 [3-5]. In addition to stimulating significant progress in delineating the molecular mechanisms causing cervical cancer, this observation led to the development of an effective vaccine that is now widely used in many countries [2]. However, while this vaccine prevents cervical cancer in ~ 70% of the population [6-10], it is not effective in individuals previously exposed to the virus [2]. Therefore, in order to develop effective strategies to eradicate cervical cancer, additional studies are needed to identify and characterize novel factors and cellular mechanisms involved in HPV-induced malignancy.
关键词:cervical cancer; human papillomavirus; mRNA decay; Tristetraprolin; senescence