Although the etiology of gastric cancer has been completely obscure for many decades, several considerable advances in the knowledge of the carcinogenesis and development of gastric cancer have been made in the present era. First, it is well known that Helicobacter pylori infection is associated with the carcinogenesis and development of gastric cancer, suggesting that chronic infl ammation may be implicated in the development of intestinal metaplasia and mutations in oncogenes that precede the development of gastric cancer; indeed, the International Agency for Research on Cancer classifi ed H. pylori as a class I human carcinogen in 1994 [2]. Second, the long-suspected infl uence of genetic susceptibility has been elucidated and several polymorphisms of infl ammatory cytokine genes have been implicated as risk factors for gastric cancer [3][4][5][6][7].Although immune cells constitute an additional and prominent component of the host response to cancer, their participation in tumor pathogenesis remains unclear. Increasing evidence is being reported regarding the hypothesis that several proinfl ammatory and antiinfl ammatory cytokines may promote tumor progression and affect the host antitumor response. Efforts to understand cytokine function during tumor development are complicated by the pleiotropy and redundancy of cytokine action and the manner in which the overall cytokine environment shapes the effects of individual cytokines [8]. At present, most current data support the notion that acute infl ammation triggered by tumorinfi ltrating lymphocytes (TILs) does not induce the normal immunoprotective mechanisms that lead to the eradication of an evolving cancer. Instead, excessively and chronically produced proinfl ammatory mediators are thought to promote tumor progression [9][10][11][12]. In the tumor microenvironment, there is a delicate balance between antitumor immunity and tumor-originated proinfl ammatory activity, which weakens antitumor immunity [12][13][14]. Many researchers have reported that perioperative blood transfusion [15,16], postoperative Abstract Increasing evidence is being reported regarding the hypothesis that several proinfl ammatory and anti-infl ammatory cytokines may promote tumor progression and affect the host antitumor response. However, the manner in which a local cytokine network operates in tumor development remains unclear. We reviewed the literature to examine the consequences of novel insights into infl ammatory cytokines associated with gastric cancer progression. The Medline and EMBASE databases were searched for publications regarding the role of infl ammatory cytokines in the development of gastric cancer. A number of studies have suggested that several proinfl ammatory and anti-infl ammatory cytokines promote tumor progression through the direct activation of nuclear factor-ÎșB (NF-ÎșB) and the upregulation of angiogenesis and adhesion molecules. Furthermore, these processes suppress host antitumor immunity, leading to tumor progression and metastasis. In patients with ad...