34 research outputs found
Epigenetic mechanisms in virus-induced tumorigenesis
About 15â20% of human cancers worldwide have viral etiology. Emerging data clearly indicate that several human DNA and RNA viruses, such as human papillomavirus, EpsteinâBarr virus, Kaposiâs sarcoma-associated herpesvirus, hepatitis B virus, hepatitis C virus, and human T-cell lymphotropic virus, contribute to cancer development. Human tumor-associated viruses have evolved multiple molecular mechanisms to disrupt specific cellular pathways to facilitate aberrant replication. Although oncogenic viruses belong to different families, their strategies in human cancer development show many similarities and involve viral-encoded oncoproteins targeting the key cellular proteins that regulate cell growth. Recent studies show that virus and host interactions also occur at the epigenetic level. In this review, we summarize the published information related to the interactions between viral proteins and epigenetic machinery which lead to alterations in the epigenetic landscape of the cell contributing to carcinogenesis
Prevalence of Chlamydia trachomatis and Oncogenic Human Papillomavirus Types in Cytologic Atypia of the Uterine Cervix
A history of having
substantial
Chlamydia trachomatis
exposure as detected by serum
antibodies is a cofactor of human papillomavirus (HPV) mediated cervical
carcinogenesis. In this study, we examined the concurrent
C. trachomatis
infections in cytologic atypia of the uterine cervix in order to evaluate the
impact of
C. trachomatis
infection in patients with high risk for
cervical intraepithelial neoplasia. Cervical scrapes form 707 patients were
subjected to PCR amplification with primer sets for HPV and
C. trachomatis
.
Based on negative beta-globin results, 10 specimens were not eligible for
further analysis. Oncogenic HPV types were detected in 278 specimens (39.8%).
C.
trachomatis
was found only in six specimens (0.9%). In conclusion,
concurrent
C. trachomatis
infection was uncommon and hence it was an
improbable risk factor in cytologic atypia