Increased risk of intestinal type of gastric adenocarcinoma in Japanese women associated with long forms of CCTTT pentanucleotide repeat in the inducible nitric oxide synthase promoter

Tatemichi, Masayuki; Sawa, Tomohiro; Gilibert, Isabelle; Tazawa, Hiroshi; Katoh, Takahiko; Ohshima, Hiroshi

doi:10.1016/j.canlet.2004.09.002

Cited by 54 publications

(38 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Of the remaining 38 publications, three were eliminated, due to reporting duplicate data 17, 18, 19. Ultimately, 37 studies from 35 publications 6, 10, 14, 15, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50 including 6108 cases and 8980 controls were included in the meta‐analysis (Fig. 1).…”

Section: Resultsmentioning

confidence: 99%

Interleukin‐1B 31 C>T polymorphism combined with Helicobacter pylori‐modified gastric cancer susceptibility: evidence from 37 studies

Hua-yong

Zong³

et al. 2016

J Cellular Molecular Medi

View full text Add to dashboard Cite

Gastric cancer is one of the most common malignancies worldwide. Interleukin‐1‐beta (IL‐1β) is a pro‐inflammatory cytokine and potent inhibitor of gastric acid secretion. Some studies provided evidence of the association between IL‐1B 31 polymorphism and gastric cancer risk while other studies did not. Therefore, we conducted a comprehensive meta‐analysis to reassess the association. A systematic literature search of the PubMed and EMBASE databases identified 37 studies with 6108 cases and 8980 controls for this meta‐analysis. The crude odd ratios (ORs) and the 95% confidence intervals (CIs) were calculated to evaluate the strength of the association. Meta‐regression was used to determine the major source of heterogeneity across the studies. The pooled analysis did not suggest the significant association of IL‐1B 31 C>T polymorphism with gastric cancer risk. Stratified analysis was performed by ethnicity, source of control, genotype method, and indicated a significantly increased gastric cancer risk associated with IL‐1B 31T variant in the population‐based subgroup (heterozygous model: OR = 1.22, 95% CI = 1.03–1.45). Moreover, stratified analysis by Helicobacter pylori infection status indicated that IL‐1B 31 polymorphism increased gastric cancer risk in infection‐positive subgroup (homozygous model: OR = 1.35, 95% CI = 1.02–1.78; heterozygous model: OR = 1.31, 95% CI = 1.04–1.66; recessive model: OR = 1.29, 95% CI = 1.04–1.61). The study suggested that IL‐1B 31 polymorphism might confer susceptibility to gastric cancer in the presence of H. pylori infection, indicating a gene–environment interaction in gastric carcinogenesis.

show abstract

Section: Resultsmentioning

confidence: 99%

Interleukin‐1B 31 C>T polymorphism combined with Helicobacter pylori‐modified gastric cancer susceptibility: evidence from 37 studies

Hua-yong

Zong³

et al. 2016

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…NO may also regulate angiogenesis, leukocyte adhesion and infiltration, and metastasis (167). A recent population-based study found that specific polymorphisms in the promoter region of iNOS gene led to higher promoter activities correlated with a higher incidence of gastric cancer in nonsmoking Japanese women (169). It was also suggested that, due to the higher promoter activities of iNOS, excess NO may be produced and cause chronic inflammation, which contributes to the H. pylori -induced gastric cancer (169).…”

Section: Key Molecular Players In Linking Inflammation To Cancermentioning

confidence: 99%

“…A recent population-based study found that specific polymorphisms in the promoter region of iNOS gene led to higher promoter activities correlated with a higher incidence of gastric cancer in nonsmoking Japanese women (169). It was also suggested that, due to the higher promoter activities of iNOS, excess NO may be produced and cause chronic inflammation, which contributes to the H. pylori -induced gastric cancer (169). Noticeably, studies using a wide range of in vitro and in vivo models show that iNOS/NO signaling can also induce COX-2, which itself is a promising link between inflammation and cancer (167).…”

Section: Key Molecular Players In Linking Inflammation To Cancermentioning

confidence: 99%

Inflammation, a Key Event in Cancer Development

Ouyang

Huang

2006

Molecular Cancer Research

946

753

View full text Add to dashboard Cite

Several recent studies have identified nuclear factor-KB as a key modulator in driving inflammation to cancers. Besides this transcription factor, essential in regulating inflammation and cancer development, an inflammatory microenvironment inhabiting various inflammatory cells and a network of signaling molecules are also indispensable for the malignant progression of transformed cells, which is attributed to the mutagenic predisposition of persistent infection-fighting agents at sites of chronic inflammation. As a subverted host response to inflammation-induced tumors, the inflammatory cells and regulators may facilitate angiogenesis and promote the growth, invasion, and metastasis of tumor cells. Thus far, research regarding inflammation-associated cancer development has focused on cytokines and chemokines as well as their downstream targets in linking inflammation and cancer. Moreover, other proteins with extensive roles in inflammation and cancer, such as signal transducers and activators of transcription, Nrf2, and nuclear factor of activated T cells, are also proposed to be promising targets for future studies. The elucidation of their specific effects and interactions will accelerate the development of novel therapeutic interventions against cancer development triggered by inflammation.

show abstract

“…p53 allele is inactivated by an increase of inflammation-mediated RNS. 71 Association between RNS and p53 mutations is evidenced in inflamed lesions of the colon with ulcerative colitis, 72 stomach, 73 brain 74 and breast. 75 The susceptibility to foreign-body-related carcinogenesis does exist across species, and in strain-and gender-dependent manner.…”

Section: Foreign-body-induced Experimental Carcinogenesismentioning

confidence: 99%

Beyond foreign‐body‐induced carcinogenesis: Impact of reactive oxygen species derived from inflammatory cells in tumorigenic conversion and tumor progression

Okada

2007

Intl Journal of Cancer

View full text Add to dashboard Cite

Foreign-body-induced carcinogenesis is a traditional, maybe old, way of understanding cancer development. A number of novel approaches are available today to elucidate cancer development. However, there are things we learn from the old, and thus I bring out some examples of various clinical cases and experimental models of foreign-body-induced tumorigenesis. What is notable is that the foreign bodies themselves are unrelated to each other, whereas commonly underlying in them is to induce inflammatory reaction, especially stromal proliferation, where those exogenous materials are incorporated and undigested. Such foreign-body-induced carcinogenesis is also recognized in the step of tumor progression, the final step of carcinogenesis that tumor cells acquire malignant phenotypes including metastatic properties. And the phenomenon is universally observed in several cell lines of different origins. In this review I would like to show the evidence that tumor development and progression are accelerated inevitably by inflammation caused from foreign bodies, and that reactive oxygen species derived from inflammatory cells are one of the most important genotoxic mediators to accelerate the process. ' 2007 Wiley-Liss, Inc.

show abstract

Increased risk of intestinal type of gastric adenocarcinoma in Japanese women associated with long forms of CCTTT pentanucleotide repeat in the inducible nitric oxide synthase promoter

Cited by 54 publications

References 22 publications

Interleukin‐1B 31 C>T polymorphism combined with Helicobacter pylori‐modified gastric cancer susceptibility: evidence from 37 studies

Interleukin‐1B 31 C>T polymorphism combined with Helicobacter pylori‐modified gastric cancer susceptibility: evidence from 37 studies

Inflammation, a Key Event in Cancer Development

Beyond foreign‐body‐induced carcinogenesis: Impact of reactive oxygen species derived from inflammatory cells in tumorigenic conversion and tumor progression

Contact Info

Product

Resources

About