Inflammation as a target for prostate cancer chemoprevention: Pathological and laboratory rationale.
Inflammation as a target for prostate cancer chemoprevention: Pathological and laboratory rationale.
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DOI：
10.1097/01.ju.0000108142.53241.47
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发表时间：
2004-02-01
影响因子：
6.6
通讯作者：
Torkko, Kathleen C.
中科院分区：
文献类型：
--
作者：
Lucia, M. Scott;Torkko, Kathleen C.
目的：我们回顾了有关慢性或复发性炎症或感染在前列腺癌发展中的潜在因果作用的文献。材料与方法：使用MEDLINE进行文献检索，以识别关于慢性炎症作为癌症风险因素的文章，特别是前列腺癌。结果：慢性或复发性炎症或感染在前列腺癌发展中的因果作用尚未得到证实。炎症可能通过一种或多种可能相互关联的机制促进致癌，包括1）促进肿瘤细胞生长的细胞因子和生长因子的产生，2）诱导巨噬细胞和上皮细胞中的环氧合酶-2，3）产生致突变活性氧和氮物质。以淋巴细胞和组织细胞的基质和上皮浸润形式的慢性炎症在前列腺的外周区极为常见，大多数癌症都发生在前列腺的外周区。虽然这些炎性和萎缩性病变在组织学和术语上存在差异，但作为一个组，它们通常显示上皮增殖的证据。GST 1基因在这些病变中的异质性表达被认为是氧化损伤易感性的证据，从而为致癌提供了肥沃的土壤。结论：尽管累积的证据表明慢性炎症可能是化学预防努力的合理目标，但需要更多的研究来证明其在前列腺癌中的病因学作用。
Purpose: We review the literature addressing a potential causal role for chronic or recurrent inflammation or infection in the development of prostate cancer. Materials and Methods: A literature search was conducted using MEDLINE to identify articles on chronic inflammation as a risk factor for cancer, particularly prostate cancer. Results: A causal role for chronic or recurrent inflammation or infection in the development of prostate cancer has yet to be proven. Inflammation may contribute to carcinogenesis by 1 or more of several potentially interrelated mechanisms, including 1) the elaboration of cytokines and growth factors that favor tumor cell growth, 2) induction of cyclooxygenase-2 in macrophages and epithelial cells, and 3) generation of mutagenic reactive oxygen and nitrogen species. Chronic inflammation in the form of stromal and epithelial infiltrates of lymphocytes and histiocytes is extremely common in the peripheral zone of the prostate where most cancers arise. Although differences in histology and terminology exist for these inflammatory and atrophic lesions, as a group they often display evidence of epithelial proliferation. Heterogeneous expression of the GSTP1 gene in such lesions has been proposed as evidence for susceptibility to oxidative damage, thereby providing fertile ground for carcinogenesis. Conclusions: Although the cumulative evidence demonstrates that chronic inflammation may be a legitimate target for chemopreventive efforts, more study is needed to prove its etiological role in prostate cancer.