Cyclooxygenase-2 (COX-2): a molecular target in prostate cancer
| Autor: | G. Aparicio Gallego, S. Díaz Prado, J. Cassinello Espinosa, L. M. Antón Aparicio, P. Jiménez Fonseca, R. García Campelo |
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| Rok vydání: | 2007 |
| Předmět: |
Oncology
PCA3 Male Cancer Research medicine.medical_specialty Colorectal cancer Gene Expression Regulation Enzymologic Familial adenomatous polyposis Prostate cancer Prostate Internal medicine Carcinoma medicine Humans Cyclooxygenase-2 Intraepithelial neoplasia Molecular target Cyclooxygenase 2 Inhibitors business.industry Inhibitors Cancer Prostatic Neoplasms General Medicine medicine.disease medicine.anatomical_structure Cyclooxygenase 2 business Pharmacological treatment Signal Transduction |
| Zdroj: | RUC. Repositorio da Universidade da Coruña instname |
| ISSN: | 1699-048X |
| Popis: | [Abstract] Epidemiological studies provided the first evidence that COX may be involved in the pathogenesis of cancer. In the process of carcinogenesis and in the route of intracellular signalling during carcinogenesis, COX-2 expression may be a universal phenomenon. In general, COX-2 is up-regulated throughout the tumorigenic process, from early hyperplasia to metastatic disease. COX-2 has been reported to be constitutively overexpressed in a variety of malignancies and is frequently constitutively elevated in prostate carcinoma. COX-2 was consistently overexpressed in premalignant lesions such as prostatic intraepithelial neoplasia, and carcinoma. Cases are described with evolution of proliferative inflammatory atrophy of the prostate and prostate carcinoma. The increase of evidence implicating COX-2 in cancer has stimulated clinical trials to investigate the efficacy of selective COX-2 inhibitors in individuals at risk for human cancer. Regarding prostate carcinoma there is much direct or indirect evidence to support the use of COX-2 inhibitors in this disease. Trials using these drugs in familial adenomatous polyposis (FAP) and other patients with a high risk of colorectal carcinoma are ongoing. |
| Databáze: | OpenAIRE |
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