Both clear cell renal carcinoma (ccRCC) and clear cell carcinoma of the ovary (CCOC) have a clear cytoplasmic morphological feature, hence it is difficult to identify metastatic ccRCC and CCOC by morphology alone. At present, there are no effective immunohistochemical markers to distinguish between these two tumors. Studies have shown that the clear cytoplasm of ccRCC is mainly caused by cholesterol-rich lipids in the cytoplasm, while that of CCOC is due to the accumulation of cytoplasmic glycogen. Objective: to hypothesize that the scavenger receptor class B-type 1 (SR-B1) protein responsible for HDL cholesterol uptake may be differentially expressed in ccRCC and CCOC, and high CD10 expression in the renal tubular epithelium may assist in distinguishing between ccRCC and CCOC. Methods: effective immunohistochemical markers were applied in 90 cases of renal clear cell carcinoma and 31 cases of ovarian cancer to distinguish between the two types of tumors.Result: SR-B1 and CD10 expression is significantly higher in ccRCC than CCOC. Both SR-B1 and CD10 exhibited focal weak-medium intensity staining in CCOC, and their staining extent and intensity were significantly lower than ccRCC. The sensitivity and specificity of SR-B1 for identifying ccRCC were 74.4% and 83.9%, respectively. The sensitivity and specificity of CD10 for identifying CCOC were 93.3% and 80.6%, respectively. The combined SR-B1( +) CD10( +) immunoprofile supports the diagnosis of ccRCC with a specificity of 93.5%. The combined SR-B1(-) CD10(-) immunoprofile supports the diagnosis of CCOC with a specificity of 93.3%. Conclusions: our findings demonstrate that the combination of SR-B1 and CD10 immunoprofiling is a valuable tool for differential diagnosis of ccRCC and CCOC.

Background: Medulloblastoma (MB) is a malignant intracranial tumor. Cisplatin is a broad-spectrum antitumor drug. It is important to study the cisplatin resistance of MB cells for the treatment of MB. In this article, we preliminarily studied the cisplatin resistance of microRNA (miR)-31 and the possible mechanism in DAOY and UW228 cells, laying a theoretical foundation for clinical treatment of MB. Methods: Following anti-miR-31 and pre-miR-31 transfections, cell viability, BrdU, CyclinD1, and apoptosis levels of DAOY and UW228 cell were detected by CCK8, BrdU, and western blot. Meanwhile, migration, invasion, and western blot assay were respectively used to detect the functions of miR-31 migration and invasion. miR-31 levels were changed by cell transfection and detected by RT-qPCR. Furthermore, the related-proteins of pathways were also detected by western blot. Results: Anti-miR-31 increased DAOY and UW228 cells viability, BrdU + numbers, and expression of CyclinD1. The migration/invasion rate and expression levels of MMP-9 and vimentin after anti-miR-31 transfection were increased. Furthermore, anti-miR-31 enhanced cells' cisplatin resistance and triggered PI3K/AKT and NF-κB pathways. Pre-miR-31 played opposite roles and promoted the apoptosis. Conclusion: miR-31 regulated cell growth, migration, invasion and cisplatin resistance of MB cells via PI3K/AKT and NF-κB pathways.

Background Myeloid Sarcoma with monocytic differentiation is rare and quite likely is missed by surgical pathologists. However it is frequently misdiagnosed because of its non-specific imaging and histological pattern. Case presentation We report the case of a 64-year-old woman with gastric primary myeloid sarcoma with monocytic differentiatio. Upper endoscopy revealed a neoplastic growth at the junction of the lesser curvature and gastric antrum. Except for a slightly increased peripheral monocyte count, no abnormalities were found on hematological and bone-marrow examination. Gastroscopic biopsy showed poorly differentiated atypical large cells with visible nucleoli and nuclear fission. Immunohistochemistry showed positive CD34, CD4, CD43, and CD56 expression, and weakly positive lysozyme expression. Immune markers for poorly differentiated adenocarcinoma, malignant melanoma, and lymphohematopoietic-system tumors were negative. The final diagnosis was myeloid sarcoma with monocytic differentiation. Chemotherapy did not shrink the tumor, so, radical surgery was performed. Although the tumor morphology did not change postoperatively, the immunophenotype did. CD68 and lysozyme expression (tumor tissue markers) changed from negative and weakly positive to strongly positive, AE1/3 expression (epithelial marker) changed from negative to positive, and CD34, CD4, CD43, and CD56 expression (common in naive hematopoietic cell-derived tumors) was greatly attenuated. Exome sequencing revealed missense mutations in FLT3 and PTPRB, which are associated with myeloid sarcoma, and in TP53, CD44, CD19, LTK, NOTCH2, and CNTN2, which are associated with lymphohematopoietic tumors and poorly differentiated cancers. Conclusion We diagnosed myeloid sarcoma with monocytic differentiation after excluding poorly differentiated adenocarcinoma, common lymphohematopoietic-system tumors, epithelioid sarcoma, and malignant melanoma. We identified that the immunophenotypic of patient had alterations after chemotherapy, and FLT3 gene mutations. We hope that the above results will improve our understanding of this rare tumor.

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