Cyclooxygenase-2: a target for the prevention and treatment of cancers of the upper digestive tract.

Cyclooxygenase-2: a target for the prevention and treatment of cancers of the upper digestive tract.
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Cyclooxygenase-2:预防和治疗上消化道癌症的靶点。

DOI:
10.1159/000071369
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发表时间:
2003
期刊:
Progress in experimental tumor research
影响因子:
--
通讯作者:
Dannenberg,AndrewJ
Dannenberg,AndrewJ
中科院分区:
--
文献类型:
--
作者:
Altorki,NasserK;Subbaramaiah,Kotha;Dannenberg,AndrewJ

文献摘要

相似文献

Cancers of the upper digestive tract including the head and neck, esophagus and stomach are among the most lethal malignancies worldwide. Approximately 40,000 new cases of head and neck cancer were reported in the USA in 2001 [1]. Despite advances in radiotherapy and chemotherapy, the survival of patients with head and neck squamous cell cancer (HNSCC) has not improved significantly over the past three decades. Esophageal cancer is the third most common gastrointestinal malignancy and ranks among the ten most common cancers worldwide [2]. Approximately 12,000 new cases are diagnosed annually in the USA and the overall survival rate is in the range of 5–10%[1]. The majority of patients are incurable by current treatment modalities including surgical resection, chemotherapy, radiotherapy or any combination thereof. Gastric cancer is the second leading cause of cancer deaths in the world. Nearly 750,000 cases are detected annually worldwide and overall 5-year survival is less than 25%[3].Given the poor prognosis associated with cancers of the upper digestive tract, new preventive and/or treatment strategies are needed. In this chapter, evidence is presented that COX-2, an inducible enzyme that catalyzes the synthesis of prostaglandins (PGs), represents a potential therapeutic target [4]. PGs appear to be important in the pathogenesis of cancer because they modulate cell proliferation, apoptosis, angiogenesis and immune surveillance [5–10]. Moreover, a variety of cancers including those of the upper digestive tract form more PGs than the normal tissues from which they arise [11–14]. The notion that PGs contribute to carcinogenesis is supported by epidemiological and