ABSTRACT
Objective: Describe for the first time the clinical, epidemiological features of vulvar cancer in southwest China. Identify risk factors and provide reference for the prevention of vulvar cancer. Method: We retrospectively analyzed 885 patients admitted to the West China Second University Hospital for vulvar diseases between 2006 and 2016. Vulvar cancer patients with previously diagnosed vulvar nonneoplastic epithelial disorders (n=132) were analyzed and compared to those without prior history of vulvar nonneoplastic epithelial disorders (n=219). Comparisons were also made among cancer patients and non-cancer patients with vulvar nonneoplastic epithelial disorders (n=288) and vulvar squamous intraepithelial lesions (n=246). The risk factors leading to vulvar cancer for the patients with vulvar nonneoplastic epithelial disorder were analyzed by univariate analysis. Furthermore, differences of the epidemiological features of vulvar nonneoplastic epithelial disorders, vulvar squamous intraepithelial lesion and vulvar cancer were identified. Results: According to the univariate analysis, age, first coital age, educational level, smoking, history of vaginal atrophy, HPV infection, lesion sites of the upper vulva and histo-pathological changes are strongly positively correlated with vulvar cancer. By comparing the features of vulvar cancer with those of the vulvar nonneoplastic epithelial disorder and vulvar squamous intraepithelial lesion, we found that on average patients with vulvar cancer had the highest age (ranged from 50 to 59), the lowest first coital age and the highest number of pregnancies and births. The incidences of vulvar nonneoplastic epithelial disorder and vulvar cancer were 1/1000 and 2.5/100,000 respectively with an increasing trend during last 10 years. Conclusion: Age, first coital age, educational level, smoking, atrophic vagina history, HPV infection, lesion sites of the upper vulva and histo-pathological changes are the risk factors that lead to vulvar cancer. Vulvar nonneoplastic epithelial disorder, vulvar squamous intraepithelial lesion and vulvar cancer each has distinct epidemiological features. Prompt surgical intervention and subsequent treatments are the key to a better outcome of vulvar cancer.
ABSTRACT
OBJECTIVES: We attempted to survey the inhibit effect of fisetin with human ovarian cancer cell line SKOV3 and the xenograft and the mechanism of the effect. METHODS: The ovarian cancer cell line SKOV3 treated by fisetin were observed directly under the transmission electronmicroscope (TEM);MTT assay was used to determine cell viability.Flow cytometry was used to analyze the apoptosis in ovarian cancer cell line SKOV3.In addition,we established an ovarian cancer athymicnude rat model.We observed the neoplasia and progression after fisetin treatment.The proliferation and apoptosis of athymic nude rat model were evaluated by testing Bcl-2,Bax and poly-ADP-ribose polyerase (PARP) expression through Western blot. RESULTS: The chromatin were brought together and the apoptotic bodies were detected in SKOV3 cells under transmission electron microscope after the treatment by fisetin.MTT assay indicated that fisetin inhibited ovarian cancer cell proliferation in a dose-dependent manner.The flow cytometry data demonstrated that the apoptosis might induct in SKOV3 cells after treatment by fisetin.In athymic rude rat model,under the influence of fisetin,tumor volume and tumor mass were significantly decreased.Western blot demonstrated that treatment with higher concentration of fisetin resulted in a significant decrease of Bcl-2 and a significant increase of Bax.The apoptosis proteins PARP was cut apparently. CONCLUSIONS: The results provided the first insight into antitumor anti-proliferative and the induction of apoptosis efficacy of fisetin against ovarian cancer in vitro and in vivo.All data suggested a safe promising therapeutic potential of fisetin in ovarian cancer treatment.
