Pathology, research and practice
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Pathol. Res. Pract. · Sep 2015
Multicenter StudyA switch from epithelial to mesenchymal properties correlates with lymphovascular invasion in squamous cell carcinoma of the penis.
The purpose of the study was to assess the incidence and prognostic role of epithelial-to-mesenchymal-transition (EMT) in squamous cell carcinoma of the penis (SCCP). Sixty tumor specimens of surgically treated SCCP patients characterized by a central histopathologic review were stained with antibodies against E-cadherin, N-cadherin, β-catenin, and vimentin. Staining profiles were scored by two independent raters, and correlated with pertinent clinical and pathological parameters and cancer-specific mortality (CSM; median follow-up: 34 months, interquartile range: 6-60 months). ⋯ Our data suggest that roughly half of surgically treated SCCP cases exhibit EMT, a parameter correlating with lymphovascular invasion. However, further studies are clearly needed to validate the so far unresolved possible role of cadherin switch in terms of predicting nodal spread in patients with SCCP. Moreover, the apparently complex mechanisms driving EMT in SCCP should be explored by future studies, as knowledge about these might provide a so far unexploited basis for the development of novel targeted therapies against SCCP with metastatic dissemination.
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Pathol. Res. Pract. · Jan 2007
Multicenter StudyProtein expression of KIT and gene mutation of c-kit and PDGFRs in Ewing sarcomas.
Ewing sarcoma is a highly malignant tumor of bone preferentially arising in children and young adults. Its 5-year survival rate is only 50% despite the use of multimodal therapeutic approaches, requiring a search for new therapeutic targets and the development of novel therapeutic modalities. KIT and PDGFRs are type III receptor tyrosine kinases, and activating mutations in c-kit (which encodes KIT) and PDGFRs have been reported as oncogenic events in many malignancies. ⋯ Our results for KIT protein expression agree with those of previous studies. This is the largest series of c-kit mutational analysis in Ewing sarcoma to date, and the results definitively show that c-kit activating mutations are not coincident with KIT protein expression in Ewing sarcoma in most samples. These findings imply other mechanisms for KIT activity and leave open the question of whether imatinib would be efficacious in the treatment of Ewing sarcoma.