C-MET is expressed in the majority of penile squamous cell carcinomas and correlates with polysomy-7 but is not associated with MET oncogene amplification, pertinent histopathologic parameters, or with cancer-specific survival
| Autor: | Matthias May, Oliver W. Hakenberg, Stefan Koch, Sven Gunia, Andreas Erbersdobler |
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| Rok vydání: | 2013 |
| Předmět: |
Male
Pathology medicine.medical_specialty Time Factors C-Met Biopsy Cell Kaplan-Meier Estimate In situ hybridization Biology Pathology and Forensic Medicine Polysomy 7 chemistry.chemical_compound Breast cancer Predictive Value of Tests Risk Factors medicine Humans Genetic Predisposition to Disease MET oncogene Penile Neoplasms In Situ Hybridization Aged Proportional Hazards Models Retrospective Studies Chi-Square Distribution Tissue microarray Gene Amplification Cell Biology Middle Aged Proto-Oncogene Proteins c-met Aneuploidy Prognosis medicine.disease Immunohistochemistry Phenotype medicine.anatomical_structure chemistry Tissue Array Analysis Multivariate Analysis Carcinoma Squamous Cell Cancer research |
| Zdroj: | Pathology - Research and Practice. 209:215-220 |
| ISSN: | 0344-0338 |
| DOI: | 10.1016/j.prp.2013.02.002 |
| Popis: | We assessed c-MET expression and oncogene amplification in a cohort enrolling 92 surgically treated penile squamous cell carcinomas (PSCCs). A tissue microarray was constructed for c-MET immunohistochemistry (IHC) and chromogenic silver in situ hybridization (SISH). Two independent pathologists evaluated IHC by employing the breast cancer scoring rules, and scored the presence of MET oncogene amplification and/or polysomy-7. Eighty study cases (87%) showed c-MET expression. No study case had MET oncogene amplification, but 42 patients (45.7%) had polysomy-7. Polysomy-7 showed a significant positive correlation with c-MET expression (ρ = 0.323, p = 0.002). Neither c-MET expression nor polysomy-7 was associated with histopathologic parameters or with cancer-specific survival (median post-surgical follow-up 32 months). Our data suggest that the majority of PSCCs exhibit c-MET expression which is not associated with oncogene amplification, but might be attributable to polysomy-7. Further studies should investigate the expression and activation of downstream molecules functionally involved in c-MET pathway signaling, and clarify the so far unresolved role of c-MET inhibitors as potential targeted therapies in PSCCs with metastatic dissemination. |
| Databáze: | OpenAIRE |
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