OBJECTIVE: The purpose of this study was to assess the role of HPV 16 and 18 in adenocarcinoma in situ(ACIS) of the uterine cervix. METHODS: Seventeen cases of primary cervical adenocarcinoma in situ were analyzed for HPV DNA by polymerase chain reaction. HPV 16 and 18 DNA extracted from formalin-fixed, paraffin-embedded histologic tissue sections by polymerase chain reaction. RESULTS: 35.3% and 23.5% of ACIS were positive for HPV 16 and HPV 18 DNA, respectively. From the normal tissue, 11.8% were positive for HPV 16. Human papillomavirus positive patients were younger than negative patients but statistically insignificant(mean age 42.1 vs 51.7 years). CONCLUSIONS: These results show that HPV type 16 and 18 were closely related to etiology of the ACIS of the uterine cervix.
Adenocarcinoma* ; Cervix Uteri* ; DNA ; Female ; Human papillomavirus 16 ; Human papillomavirus 18 ; Humans* ; Papilloma* ; Polymerase Chain Reaction

Autophagy is a process of cytoplasmic degradation of endogenous proteins and organelles. Although its primary role is protective, it can also contribute to cell death. Recently, autophagy was found to play a role in the activation of host defense against intracellular pathogens. The aims of our study was to investigate whether host cell autophagy influences Toxoplasma gondii proliferation and whether autophagy inhibitors modulate cell survival. HeLa cells were infected with T. gondii with and without rapamycin treatment to induce autophagy. Lactate dehydrogenase assays showed that cell death was extensive at 36-48 hr after infection in cells treated with T. gondii with or without rapamycin. The autophagic markers, LC3 II and Beclin 1, were strongly expressed at 18-24 hr after exposure as shown by Western blotting and RT-PCR. However, the subsequent T. gondii proliferation suppressed autophagy at 36 hr post-infection. Pre-treatment with the autophagy inhibitor, 3-methyladenine (3-MA), down-regulated LC3 II and Beclin 1. The latter was also down-regulated by calpeptin, a calpain inhibitor. Monodansyl cadaverine (MDC) staining detected numerous autophagic vacuoles (AVs) at 18 hr post-infection. Ultrastructural observations showed T. gondii proliferation in parasitophorous vacuoles (PVs) coinciding with a decline in the numbers of AVs by 18 hr. FACS analysis failed to confirm the presence of cell apoptosis after exposure to T. gondii and rapamycin. We concluded that T. gondii proliferation may inhibit host cell autophagy and has an impact on cell survival.
Anti-Bacterial Agents/pharmacology ; Apoptosis/drug effects/physiology ; Autophagy/drug effects ; HeLa Cells ; Humans ; Sirolimus/pharmacology ; Toxoplasma/*cytology/*physiology