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OBJECTIVE: This study aimed to elucidate the diagnostic roles of PAX8 immunohistochemistry in various ovarian tumors. METHODS: We searched through the PubMed database and selected the eligible studies to perform the meta-analysis. The PAX8 immunohistochemical expression rates of various ovarian tumors, including primary and metastatic carcinomas, were analyzed. In addition, the subgroup analysis based on tumor behaviors was performed. RESULTS: The PAX8 expression rates were 0.056 (95% confidence interval [CI] 0.008-0.307), 0.400 (95% CI 0.228-0.600), 0.741 (95% CI 0.578-0.857), and 0.738 (95% CI 0.666-0.799) in normal ovary and benign, borderline, and malignant ovarian tumors, respectively. The PAX8 expression rates of serous and transitional cell carcinomas were 0.937 (95% CI 0.882-0.967) and 0.918 (95% CI 0.841-0.959). In addition, the PAX8 expression rate of mucinous carcinomas was 0.393 (95% CI 0.285-0.512). However, metastatic carcinomas showed a significantly lower PAX8 expression rate than primary ovarian cancers (P < 0.001 in the meta-regression test). In cytologic specimens, PAX8 expression rates of serous and endometrioid carcinomas were 0.905 (95% CI 0.832-0.948) and 0.714 (95% CI 0.327-0.928), respectively. CONCLUSION: PAX8 expression rate was significantly higher in serous ovarian tumors than in mucinous ovarian tumors. In addition, PAX8 expression rates were significantly higher in primary ovarian cancers than in metastatic carcinomas.
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A 45-year-old woman with a prior history of hysterectomy due to adenomyosis and leiomyomas was presented at our outpatient gynecology clinic 13 months later with sudden lower pelvic discomfort and vaginal bleeding symptoms. The patient underwent vaginal vault biopsy however diagnosis was still uncertain. Additional evaluation was required due to massive rebleeding incidents. After an emergent explorative laparoscopic operation with total excision of the vault, a diagnosis of vaginal vault endometriosis was made. Our theory is that a possible transplantation of endometrial cells during morcellation of the adenomyotic uterus which then may have progressed to iatrogenic endometriosis of the vaginal vault. Therefore, vault endometriosis must be considered in incidences of delayed massive bleeding occurring in post-hysterectomy patients when other diagnoses have been excluded.
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BACKGROUND: The class III histone deacetylase SIRT1 is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, and has been reported to serve diverse roles in various biological processes, such as caloric restriction, apoptosis, neuronal protection, cell growth, differentiation and tumourigenesis. With respect to tumourigenesis, there have been conflicting data supporting whether SIRT1 act as a tumour promoter or as a tumour suppressor. METHODS: SIRT1 protein expression, determined by immunohistochemistry, was investigated in human normal colonic mucosa, adenoma, adenocarcinoma and metastatic tissue samples. RESULTS: All normal colonic mucosa showed SIRT1 expression with no exception, and 42 (80.8%) of 52 adenomatous polyps were positive for SIRT1. However, only 208 (41.9%) of 497 colorectal adenocarcinomas were positive. Moreover, 45 (35.7%) of 126 metastatic tissues were positive. Collectively, the SIRT1 expression was gradually decreased during carcinogenesis and tumour progression. The associations between SIRT1 expression and clinicopathological parameters revealed that loss of SIRT1 expression was associated with proximal tumour location, mucinous histology and defective mismatch repair protein expression. This suggests that loss of SIRT1 expression is associated with the microsatellite instability phenotype of colorectal adenocarcinoma. In survival analyses, the loss of SIRT1 expression was significantly associated with overall survival (p=0.027, log-rank test) in univariable analysis, but multivariable analysis failed to achieve significance. CONCLUSIONS: SIRT1 expression was gradually decreased during the normal-adenoma-adenocarcinoma-metastasis sequence, suggesting a possible role of SIRT1 in tumour suppression in the colorectum, and a probable link to the microsatellite instability pathway.