The host cell has been generally considered a passive bystander in the infectious process. Recent developmentshowever point to the fact that there is a dynamic interaction between infectious agents and the hostcell, influencing each others physiological responses. Indeed, it has been now demonstrated that some nonviralinfectious disease agents modulate biological host cell processes such as apoptosis and may evencontribute to malignant transformation of the host cell. Interestingly, number of sexual contacts and inflammationhave been identified as contributing factor in cervical and prostate cancers.Cervical cancer is themost common gynecological malignancy and the second leading cause of death in women worldwide. Inmen, prostate cancer is the most common diagnosed cancer and second leading cause of death in the USA.Minority population bear an disproportinate burden of these cancers. Furthermore, the etiology of bothcancers have not been completely iluminated and epidemological studies suggest that STI such T. vaginalismay be co-factors in these malignancies. Our goal is to unravel the molecular basis of the association ofcervical and prostate cancers and trichomonosis.The hypothesis to be tested is that chronic infection of theprostate and cervical epithelium by trichomonad parasites initiates, augments, and/or maintains the type ofbiological alterations that promotes the development and progression of cervical/prostate cancer. The longtermobjective of this work is to demonstrate that trichomonad prostatitis and cervicitis in which trichomonadsalter the host environment contributes to neoplasia. To accomplish this goal and test the hypothesis fivespecific aims are proposed that examine the molecular alteration in the physiology and gene expressionpatterns of host cells due to the intimate contact with tricdhomonads. It is anticipated that ourfindings willprovide a new direction for screening and treatment of this STD, which will decrease the incidence of canceramong our citizens.
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