The potential contributions of chronic inflammation to lung carcinogenesis.
The potential contributions of chronic inflammation to lung carcinogenesis.
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DOI：
10.3816/clc.2003.n.021
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发表时间：
2003-07-01
影响因子：
3.6
通讯作者：
Mulshine, James L
中科院分区：
文献类型：
--
作者：
Ballaz, Santiago;Mulshine, James L
许多证据表明，慢性炎症有助于致癌过程。在这篇文章中，这一主题是探讨特别强调炎症的参与肺癌的发展。在慢性炎症中激活的许多分子通路可能有助于肺癌的发生。挑战是概念化这个复杂的生物学，允许有效的药物干预的凝聚力的图片。最初的治疗努力涉及阻断单一途径的策略，例如用环氧合酶（考克斯）活性。然而，对考克斯活性的结果了解得越多，这种酶与其他类型的调节分子如有效的核因子-kB的关系就越明显。鉴于这一新出现的情况，更多的全球干预战略，如药物组合，可能是成功的关键。进一步的基础研究是必要的，以整理出可能的分子关系，并允许阐明最关键的调节电路。考虑到这些分子相互作用的复杂性，精心设计的临床试验，专门评估特定抗癌药物对肺癌发生的确切影响，对于解决复杂性和验证成功阻止肺癌发生的方法也至关重要。
A number of lines of evidence suggests that chronic inflammation contributes to the process of carcinogenesis. In this article, this theme is explored with particular emphasis on the involvement of inflammation in the development of lung cancer. A number of molecular pathways activated in chronic inflammation may contribute to lung carcinogenesis. The challenge is to conceptualize a cohesive picture of this complex biology that allows for effective pharmaceutical intervention. Initial therapeutic efforts involve strategies to block single pathways, such as with cyclooxygenase (COX) activity. However, the more that is learned about the consequences of COX activity, the more evident are the relationships of this enzyme to other classes of regulatory molecules such as the potent nuclear factor-kB. In light of this emerging picture, more global intervention strategies, such as with drug combinations, may be essential for success. Further basic study is essential to sort out possible molecular relationships and to permit elucidation of the most critical regulatory circuits. Given the complexity of these molecular interactions, well-designed clinical trials that specifically evaluate the precise effects of particular antiinflammatory drugs on lung carcinogenesis will also be critical to sort out the complexity and to validate successful approaches to arresting lung carcinogenesis.