Richardson C M, Sharma R A, Cox G, O'Byrne Kenneth J
Department of Oncology, University of Leicester, Osborne Building, Leicester Royal Infirmary, University Hospitals of Leicester NHS Trust, Leicester LEI 5WW, UK.
Lung Cancer. 2003 Jan;39(1):1-13. doi: 10.1016/s0169-5002(02)00382-3.
The epidermal growth factor receptor (EGFR) is part of a family of plasma membrane receptor tyrosine kinases that control many important cellular functions, from growth and proliferation to cell death. Cyclooxygenase (COX)-2 is an enzyme which catalyses the conversion of arachidonic acid to prostagladins and thromboxane. It is induced by various inflammatory stimuli, including the pro-inflammatory cytokines, Interleukin (IL)-1beta, Tumour Necrosis Factor (TNF)-alpha and IL-2. Both EGFR and COX-2 are over-expressed in non-small cell lung cancer (NSCLC) and have been implicated in the early stages of tumourigenesis. This paper considers their roles in the development and progression of lung cancer, their potential interactions, and reviews the recent progress in cancer therapies that are directed toward these targets. An increasing body of evidence suggests that selective inhibitors of both EGFR and COX-2 are potential therapeutic agents for the treatment of NSCLC, in the adjuvant, metastatic and chemopreventative settings.
表皮生长因子受体（EGFR）是质膜受体酪氨酸激酶家族的一部分，该家族控制着许多重要的细胞功能，从生长、增殖到细胞死亡。环氧合酶（COX）-2是一种催化花生四烯酸转化为前列腺素和血栓素的酶。它由多种炎症刺激诱导，包括促炎细胞因子白细胞介素（IL）-1β、肿瘤坏死因子（TNF）-α和IL-2。EGFR和COX-2在非小细胞肺癌（NSCLC）中均过度表达，并与肿瘤发生的早期阶段有关。本文探讨了它们在肺癌发生发展中的作用、潜在相互作用，并综述了针对这些靶点的癌症治疗的最新进展。越来越多的证据表明，EGFR和COX-2的选择性抑制剂在辅助、转移和化学预防环境中是治疗NSCLC的潜在治疗药物。
