The Role of Inflammation in Gastric Cancer

Şenol, Kazım; Özkan, Murat; Vural, Selahattin; Tez, Mesut

doi:10.1007/978-3-0348-0837-8_10

Cited by 18 publications

(19 citation statements)

References 139 publications

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“…In stomach, the pro-inflammatory mediators are secreted by cells of the gastric mucosa or carcinoma (autocrine route) or/and by infiltrating macrophages, neutrophils, lymphocytes (paracrine route) in response to pathogens (see above), some chemicals and physical insults [69,70,71]. High levels of IL-6, IL-10, IL-11, IL-32, and chemokine C-C motif ligands (CCL)7 and CCL21 in circulation, high expression of CXC chemokine receptor 4, chemokine C-C motif receptor 3 (CCR3), CCR4, CCR5, CCR7 and orphan nuclear receptor 4A2 in tumors were found to be associated with disease progression and an unfavorable prognosis in gastric cancer [72,73].…”

Section: Pro-inflammatory Mediators and Growth Factors In The Gastmentioning

confidence: 99%

NF‐κB Signaling in Gastric Cancer

Sokolova

Naumann

2017

Toxins

182

122

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Gastric cancer is a leading cause of cancer death worldwide. Diet, obesity, smoking and chronic infections, especially with Helicobacter pylori, contribute to stomach cancer development. H. pylori possesses a variety of virulence factors including encoded factors from the cytotoxin-associated gene pathogenicity island (cagPAI) or vacuolating cytotoxin A (VacA). Most of the cagPAI-encoded products form a type 4 secretion system (T4SS), a pilus-like macromolecular transporter, which translocates CagA into the cytoplasm of the host cell. Only H. pylori strains carrying the cagPAI induce the transcription factor NF-κB, but CagA and VacA are dispensable for direct NF-κB activation. NF-κB-driven gene products include cytokines/chemokines, growth factors, anti-apoptotic factors, angiogenesis regulators and metalloproteinases. Many of the genes transcribed by NF-κB promote gastric carcinogenesis. Since it has been shown that chemotherapy-caused cellular stress could elicit activation of the survival factor NF-κB, which leads to acquisition of chemoresistance, the NF-κB system is recommended for therapeutic targeting. Research is motivated for further search of predisposing conditions, diagnostic markers and efficient drugs to improve significantly the overall survival of patients. In this review, we provide an overview about mechanisms and consequences of NF-κB activation in gastric mucosa in order to understand the role of NF-κB in gastric carcinogenesis.

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Section: Pro-inflammatory Mediators and Growth Factors In The Gastmentioning

confidence: 99%

NF‐κB Signaling in Gastric Cancer

Sokolova

Naumann

2017

Toxins

182

122

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“…The inflammatory process increases the risk of the development of carcinogenesis [ 4 , 5 ]. Chronic inflammation due to chronic atrophic gastritis and H. pylori infection plays an important role in developing gastric carcinogenesis [ 6 ]. Furthermore, a recent study indicated that the use of non-steroidal anti-inflammatory drugs (NSAIDs) such as low-dose aspirin as a preventive and treatment measure to inhibit inflammation reduced gastric cancer risk [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Dietary inflammatory index and the risk of gastric cancer in a Korean population

Lee

Choi

et al. 2017

Oncotarget

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We aimed to investigate the association with the Dietary Inflammatory Index (DII™) on the risk of gastric cancer and whether histological type modifies this association. From March 2011 to December 2014, 388 cases and 776 controls were enrolled at the National Cancer Center. Utilizing a food frequency questionnaire, thirty-five food components were used to score the DII. The tertile distribution of DII for controls was as follows: T1: <0.96, T2: 0.96-2.97, and T3: ≥2.97. To investigate the association between DII and the gastric cancer risk, multivariable logistic models were constructed. In subgroup analyses, histological types including intestinal and diffuse types were examined. As the DII increased, gastric cancer risk increased (p-value for trend =0.007). Participants in the highest DII tertile had a greater gastric cancer risk compared to those in the lowest tertile [Odds Ratio (OR) =1.63, 95% Confidence Interval (CI) 1.15-2.29]. Stratification by sex revealed that men who were in the highest DII tertile showed a greater risk of intestinal type (OR=2.03, 95% CI 1.09-3.77). Participants positive for H. pylori infection had higher risk of intestinal type (OR=2.16, 95% CI 1.21-3.87). In this case-control study, we found a significantly positive association with a pro-inflammatory diet on gastric cancer risk, after adjusting for covariates. Future studies are suggested to prospectively examine the effect of a pro-inflammatory diet on gastric cancer risk.

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“…Inflammation has long been considered to contribute to tumour progression [ 80 ]. Previous reviews have also suggested the involvement of inflammation in a variety of gastrointestinal cancers [ 81 , 82 , 83 , 84 ], therefore indicating the potential of anti-inflammatory strategies in the prevention of gastrointestinal cancers. In fact, previous studies have generated ample evidence for the inter-relationship between oxidative stress and inflammation.…”

Section: Other Potential Oxidative-stress-related Mechanisms For Tmentioning

confidence: 99%

Hypotheses on the Potential of Rice Bran Intake to Prevent Gastrointestinal Cancer through the Modulation of Oxidative Stress

Law

Waye

2017

IJMS

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Previous studies have suggested the potential involvement of oxidative stress in gastrointestinal cancers. In light of this, research efforts have been focused on the potential of dietary antioxidant intake to prevent gastrointestinal cancer through the modulation of oxidative stress. Rice bran, a by-product of rice milling, has been shown to contain an abundance of phytochemicals, which are dietary antioxidants. To date, a number of studies have shown the antioxidative effect of rice bran intake, and some demonstrated that such an effect may contribute to gastrointestinal cancer prevention, largely through the antioxidative properties of rice bran phytochemicals. In addition, these phytochemicals were shown to provide protection against cancer through mechanisms linked to oxidative stress, including β-catenin-mediated cell proliferation and inflammation. The present article provides an overview of current evidence for the antioxidative properties of rice bran and its phytochemicals, and for the potential of such properties in cancer prevention through the oxidative-stress-linked mechanisms mentioned above. The article also highlights the need for an evaluation of the effectiveness of rice bran dietary interventions among cancer survivors in ameliorating oxidative stress and reducing the level of gastrointestinal cancer biomarkers, thereby establishing the potential of such interventions among these individuals in the prevention of cancer recurrence.

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The Role of Inflammation in Gastric Cancer

Cited by 18 publications

References 139 publications

NF‐κB Signaling in Gastric Cancer

NF‐κB Signaling in Gastric Cancer

Dietary inflammatory index and the risk of gastric cancer in a Korean population

Hypotheses on the Potential of Rice Bran Intake to Prevent Gastrointestinal Cancer through the Modulation of Oxidative Stress

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