Background: Mesonephric adenocarcinoma (MA) is a rare tumor believed to arise from mesonephric remnants occurring mostly in the uterine cervix and, to a lesser extent, the corpus. Since the first case report of MA in the corpus in 1995, only 16 cases have been reported in the English literature. A recent report suggested that MA originates in Müllerian tissue and exhibits the mesonephric differentiation phenotype. Case presentation: An asymptomatic 61-year-old woman was referred to our hospital because of elevated levels of tumor markers. Imaging revealed an intramural lesion of the uterine corpus exhibiting fluorodeoxyglucose uptake. A total hysterectomy and bilateral salpingo-oophorectomy were performed. The tumor was completely confined to the corpus wall and was composed of an intracystic bulky component and an invasive component in the myometrial layer. The tumor exhibited a variety of growth patterns, including a characteristic tubular pattern with dense eosinophilic secretion reminiscent of the thyroid, as well as a variety of morphologies, such as acinar, papillary, and ductal structures. The structures were immunoreactive for CK7, vimentin, CD10, calretinin, PAX8, and GATA3 and almost completely negative for ER/PgR. CA125 and CA19-9 antigen expression was also detected. Conclusion: A case of MA with a unique growth pattern of an intracystic mass within the corpus wall is presented. The histogenesis and differential diagnoses are discussed. The histogenesis of MA is not yet clear. We hypothesize two different pathways involved: 1) direct development from the mesonephric remnants and/or 2) mesonephric transformation of Müllerian adenocarcinoma.

We present 3 cases of extrapulmonary lymphangioleiomyomatosis (LAM) identified incidentally in the uterine corpus and pelvic nodes resected for other reasons. One patient, a 47-yr-old female with corpus cancer, underwent a total hysterectomy and nodal dissection; the other 2 patients, aged 44 and 49 yr, underwent simple hysterectomy for corpus leiomyomas. None of the patients had evidence of tuberous sclerosis complex or any significant lesions in other organs. An area of spindle cell proliferation, intimately associated with dilated and tortuous lymphatic vessels, was found in the myometrium of all 3 patients, and nodal involvement with spindle cell proliferation was observed in the patient with corpus cancer. The spindle cells had faintly eosinophilic cytoplasm and a bland appearance. They were immunoreactive for α-SMA, gp100 (HMB45), and Melan-A. Tumor cell clusters lined with a single layer of lymphatic endothelium were floating in the lymphatic vessel lumen. These lesions were diagnosed as lymphangioleiomyoma in the uterine corpus and associated lymph nodes. Two of the cases seemed to be the earliest manifestations of extrapulmonary LAM, and the other case represents early-phase metastasis of LAM from the uterus. The present cases support the speculation that the uterus is the primary source of LAM cells.

No abstract

Problem:The pathogenesis of endometriosis remains unclear. Endometrial cells in retrograde menstruation are considered the source of endometriosis; therefore, we hypothesized that the eutopic endometrium may provide clues regarding the pathogenesis. We aimed to clarify the role of eutopic endometrial cells in endometriosis development. Method of Study:Eutopic endometrial tissues were obtained from patients with or without endometriosis, and expression of cell surface molecules in eutopic endometrial stromal cells (ESCs) was evaluated via iTRAQ-based proteomic analysis. Based on the results, we focused on galectin-3. Galectin-3 expression in clinical samples was confirmed by immunohistochemistry and Western blot analysis. The concentration of secreted galectin-3 was measured using enzyme-linked immunosorbent assays. Adhesion and migration of ESCs were evaluated by in vitro adhesion and wound healing assays. The cytotoxicity of natural killer cells was measured via calcein release assays.Cell proliferation was measured using the CyQUANT Cell Proliferation Assay Kit.Results: iTRAQ analysis revealed that galectin-3 expression was specifically elevated in the ESCs from endometriosis patients. Immunohistochemistry confirmed galectin-3 overexpression in the eutopic endometrium of endometriosis, irrespective of the menstrual phase. Galectin-3 was overexpressed and secreted by the eutopic ESCs from patients with endometriosis compared to that from patients without endometriosis.Galectin-3 expression in ESCs increased adhesion and migration, whereas galectin-3 inhibitors impaired these processes. Galectin-3 reduced the cytotoxicity of natural killer cells toward ESCs, while not affecting cell proliferation. Conclusion:Galectin-3 promotes peritoneal engraftment of ESCs due to impaired immune surveillance in the peritoneal cavity and increases ESCs adhesion and migration to the peritoneum.