Enflamatuvar Meme Kanserinde Moleküler Alt Tip Dağılımı ve Siklooksijenaz-2 Ekspresyon Durumu

Year 2016, Volume: 17 Issue: 2, 54 - 58, 01.08.2016

Püsem Patır Burçak Karaca Alper Şener Osman Zekioğlu Güray Saydam Canfeza Sezgin

Abstract

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Keywords

Enflamatuvar meme kanseri, moleküler alt tip, siklooksijenaz-2

Molecular Subtype Distribution and Cyclooxygenase-2 Expression Situation in Inflammatory Breast Cancer

Abstract

Objective: Inflammatory breast cancer (IBC) is a rare and aggressive form of locally advanced breast cancer. Currently, almost all women with IBC have lymph node involvement and approximately one-third have distant metastases. Therefore, there is still need for understanding of the molecular biology and new therapy alternatives in IBC. The purpose of this study was to determine the potential role of the cyclooxygenase-2 (COX-2) expression pattern in the aggressive and fatal course of IBC and to investigate the possibility of using COX-2 inhibitors as therapy options in the treatment of IBC. Materials and Methods: IBC samples obtained from breast cancer patients treated Between 2000-2009 in Ege University Faculty of Medicine Department of Medical Oncology were retrospectively evaluated. Immunohistochemical analysis was performed by a special breast cancer pathologist and manually assessed using an immunohistochemical scoring for both staining intensity and percentage. Results: In this study, the molecular subtypes identified in IBC patients were: basal (31%), luminal B/human epidermal growth factor receptor 2 (HER2)- (22%), luminal B/HER2+ (22%), HER2 (17%) and luminal A (8%). COX-2 expression was found to be positive in 92.6% of patients. Conclusion: In this context, it was concluded that the relatively high expression rate of COX-2 could be a reason for poor prognosis and also might lead to the use of COX-2 inhibitors not only as a single agent but also in combination with current chemotherapeutic agents in patients with IBC.

Keywords

Inflammatory breast cancer, molecular subtype, cyclooxygenase-2

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