Background: Vaginal intraepithelial neoplasia (VaIN) is a precursor of vaginal carcinoma that is often treated with CO2 laser therapy. However, recurrence after laser therapy is common, so new approaches are needed to enhance treatment effectiveness. The aim of this study was to investigate the efficacy and safety of combining 5- ami-nolevulinic acid photodynamic therapy (5-ALA-PDT) with CO2 laser therapy for the treatment of VaIN.Methods: Clinical data from 40 VaIN patients who received CO2 laser therapy with or without ALA-PDT were retrospectively analyzed. Cytology, human papillomavirus (HPV) status, colposcopic images, and histopathology before and after treatment were compared, and treatment efficacy, adverse reactions, and patient prognosis were assessed.Results: There was no significant difference in the cure rate between the CO2 laser group and the CO2 laser+5-ALA-PDT group after 12 months of follow-up. The difference in HPV clearance rate between the CO2 laser only group and the CO2 laser + 5-ALA-PDT group was significant at 6 and 12 months after treatment but not at 3 months after treatment. 10% patients in the CO2 laser only group experienced adverse events, while no serious adverse events were observed in the CO2 laser + 5-ALA-PDT group.Conclusions: 5-ALA-PDT combined with CO2 laser therapy appears to be a safe and effective treatment for VaIN that results in a high rate of HPV clearance with few side effects.

We aimed to study the function and mechanism of endothelial cell-specific molecule 1 (ESM1) in endometrial cancer (EC). The binding relationship between SPI1 and ESM1 was predicted by bioinformatics analysis and verified by the dual-luciferase reporter assay. The expressions and effects of SPI1 and ESM1 were determined using quantitative real-time PCR, immunohistochemistry, Western blot, and functional experiments. ESM1 was highly expressed in EC and was associated with the poor prognosis of patients. ESM1 silencing suppressed the viability, proliferation, invasion, and angiogenesis of EC cells, down-regulated expressions of PCNA, N-cadherin, Vimentin, VEGFR-1, VEGFR2, and EGFR, but upregulated E-cadherin level, while ESM1 overexpression did oppositely. Moreover, SPI1 bound to ESM1. Overexpressed SPI1 promoted the expression of ESM1 and induced malignant phenotype (viability, proliferation, and invasion), which were countervailed by ESM1 silencing. Collectively, ESM1 induced by SPI1 promotes the malignant phenotype of EC.