Search

In this report, we present for the first time the coexistence of a conventional renal cell carcinoma (RCC) and an undefined Xp11 translocation renal neoplasm in distinct kidneys, which was difficult to definitively classify as either carcinoma or PEComa (perivascular epithelioid cell tumor). While one of the tumors showed the morphological and immunohistochemical features of clear RCC, the other had an unusual morphology with a prominent nested pattern. Microscopically this tumor showed nests of cells with clear and eosinophilic cytoplasm and nuclei with prominent nucleoli; some hyaline globules were evident. Immunohistochemical panel showed negativity for cytokeratin-pan, cytokeratin-7, PAX8, and CD10 but positive immunostaining for cathepsin K, racemase, Melan-A, and TFE3. A subsequent, metaphase, dual-color fluorescence in situ hybridization confirmed the Xp11 translocation. Attention should be paid to the routine immunohistochemical profile that, in case of negativity of specific RCC markers, may suggest an Xp11 translocation renal tumor. The addition of TFE3 can easily identify the specific subtype. [ABSTRACT FROM AUTHOR]

Pulmonary sarcomatoid carcinomas (PSCs) are currently defined as poorly differentiated non-small-cell carcinomas containing a component with sarcoma or sarcoma-like (spindle and/or giant cell) features. They consist of 5 major histological variants, namely pleomorphic carcinoma, spindle cell carcinoma, giant cell carcinoma, carcinosarcoma, and pulmonary blastoma. The segregation of PSCs into a distinct clinicopathologic entity seems justified on the basis of morphologic, behavioral, and genotypic/phenotypic attributes. As a group, PSCs generally run an aggressive clinical course and may cause major difficulties in the differential diagnosis with other primary and secondary malignancies of the lung. At present, PSCs are believed to represent a family of carcinomas "in transition," in which diverse pathways of clonal evolution account for histological differences of a common ancestor lesion. The sarcomatous or sarcomatoid component of these tumors is thought to derive from carcinoma cells during the progression of carcinogenesis through the activation of an epithelial-mesenchymal transition program leading to sarcomatous transformation or metaplasia (conversion paradigm). Conceivably, targeting the epithelial-mesenchymal transition program could become a valid therapeutic strategy for these life-threatening tumors, whose sensitivity to current medical manipulation is disappointing. [ABSTRACT FROM AUTHOR]

Studies the multicystic mesothelioma of the liver by researchers from Italy. Presentation of the condition with secondary involvement of peritoneum and inguinal region; Observation from the unusual location and peculiar biological behavior; Importance of the discovery to the development of treatment for liver diseases displaying the same pathogens.

In this report, we present for the first time the coexistence of a conventional renal cell carcinoma (RCC) and an undefined Xp11 translocation renal neoplasm in distinct kidneys, which was difficult to definitively classify as either carcinoma or PEComa (perivascular epithelioid cell tumor). While one of the tumors showed the morphological and immunohistochemical features of clear RCC, the other had an unusual morphology with a prominent nested pattern. Microscopically this tumor showed nests of cells with clear and eosinophilic cytoplasm and nuclei with prominent nucleoli; some hyaline globules were evident. Immunohistochemical panel showed negativity for cytokeratin-pan, cytokeratin-7, PAX8, and CD10 but positive immunostaining for cathepsin K, racemase, Melan-A, and TFE3. A subsequent, metaphase, dual-color fluorescence in situ hybridization confirmed the Xp11 translocation. Attention should be paid to the routine immunohistochemical profile that, in case of negativity of specific RCC markers, may suggest an Xp11 translocation renal tumor. The addition of TFE3 can easily identify the specific subtype., (© The Author(s) 2015.)

Pulmonary sarcomatoid carcinomas (PSCs) are currently defined as poorly differentiated non-small-cell carcinomas containing a component with sarcoma or sarcoma-like (spindle and/or giant cell) features. They consist of 5 major histological variants, namely pleomorphic carcinoma, spindle cell carcinoma, giant cell carcinoma, carcinosarcoma, and pulmonary blastoma. The segregation of PSCs into a distinct clinicopathologic entity seems justified on the basis of morphologic, behavioral, and genotypic/phenotypic attributes. As a group, PSCs generally run an aggressive clinical course and may cause major difficulties in the differential diagnosis with other primary and secondary malignancies of the lung. At present, PSCs are believed to represent a family of carcinomas "in transition," in which diverse pathways of clonal evolution account for histological differences of a common ancestor lesion. The sarcomatous or sarcomatoid component of these tumors is thought to derive from carcinoma cells during the progression of carcinogenesis through the activation of an epithelial-mesenchymal transition program leading to sarcomatous transformation or metaplasia (conversion paradigm). Conceivably, targeting the epithelial-mesenchymal transition program could become a valid therapeutic strategy for these life-threatening tumors, whose sensitivity to current medical manipulation is disappointing.