期刊
CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
卷 66, 期 3, 页码 208-217出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.critrevonc.2008.01.004
关键词
inflammation; lung cancer; cyclooxygenase 2; COX-2; NSCLC; chemoprevention; targeted therapy; bronchogenic carcinoma
资金
- NCI NIH HHS [K12 CA076905-10, P50 CA090388, P50 CA090388-05S3, K23 CA131577, K12 CA076905] Funding Source: Medline
Lung carcinogenesis is a complex process involving the acquisition of genetic mutations that confer cancer development and the malignant phenotype, and is critically linked to apoptosis resistance, unregulated proliferation, invasion, metastasis, and angiogenesis. Epithelial mesenchymal transition (EMT) in cancer is an unregulated process in a host environment with deregulated inflammatory response that impairs cell-mediated immunity and permits cancer progression. Given the immunosuppressive tumor environment, strategies to reverse these events by stimulating host immune responses are an important area of investigation. Cyclooxygenase 2 (COX-2) and its downstream signaling pathways are potential targets for lung cancer chemoprevention and therapy. Clinical trials are underway to evaluate COX-2 inhibitors as adjuvants to chemotherapy in patients with lung cancer and to determine efficacy in prevention of bronchogenic carcinoma. The understanding of molecular mechanisms involved in inflammation and lung carcinogenesis provide insight for new drug development that target reversible, non-mutational events in the chemoprevention and treatment of lung cancer. Published by Elsevier Ireland Ltd.
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