Interleukins 17 and 23 in patients with gastric neoplasms

Błogowski, Wojciech; Madej-Michniewicz, Anna; Marczuk, Natalia; Dołęgowska, Barbara; Starzyńska, Teresa

doi:10.1038/srep37451

Cited by 21 publications

(18 citation statements)

References 46 publications

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“…In the progression of gastric carcinogenesis, initially, H. pylori strongly induces specific cytokines, but the immune response generally is not sufficient to clear the H. pylori infection completely from the human epithelial cells. As a result, chronic inflammation may occur[ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Association between human leukocyte antigen gene polymorphisms and multiple EPIYA-C repeats in gastrointestinal disorders

Sarıbaş

Demiryas

Yılmaz

et al. 2020

WJG

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BACKGROUND Polymorphisms of human leukocyte antigen (HLA) genes are suggested to increase the risk of gastric cancer (GC). AIM To investigate the HLA allele frequencies of patients with GC relative to a control group in terms of CagA+ multiple (≥ 2) EPIYA-C repeats. METHODS The patient group comprised 94 patients [44 GC and 50 duodenal ulcer (DU) patients], and the control group comprised 86 individuals [(50 non-ulcer dyspepsia patients and 36 people with asymptomatic Helicobacter pylori ( H. pylori )]. Polymerase chain reaction was performed for the amplification of the H. pylori cagA gene and typing of EPIYA motifs. HLA sequence-specific oligonucleotide (SSO) typing was performed using Lifecodes SSO typing kits (HLA-A, HLA-B HLA-C, HLA-DRB1, and HLA-DQA1-B1 kits). RESULTS The comparison of GC cases in terms of CagA+ multiple (≥ 2) EPIYA-C repeats showed that only the HLA-DQB1*06 allele [odds ratio (OR): 0.37, P = 0.036] was significantly lower, but significance was lost after correction (Pc = 0.1845). The HLA-DQA1*01 allele had a high ratio in GC cases with multiple EPIYA-C repeats, but this was not significant in the univariate analysis. We compared allele frequencies in the DU cases alone and in GC and DU cases together using the same criterion, and none of the HLA alleles were significantly associated with GC or DU. Also, none of the alleles were detected as independent risk factors after the multivariate analysis. On the other hand, in a multivariate logistic regression with no discriminative criterion, HLA-DQA1*01 (OR = 1.848), HLA-DQB1*06 (OR = 1.821) and HLA-A*02 (OR = 1.579) alleles were detected as independent risk factors for GC and DU. CONCLUSION None of the HLA alleles were detected as independent risk factors in terms of CagA+ multiple EPIYA-C repeats. However, HLA-DQA1*01, HLA-DQB1*0601, and HLA-A*2 were independent risk factors with no criterion in the multivariate analysis. We suggest that the association of these alleles with gastric malignancies is not specifically related to cagA and multiple EPIYA C repeats.

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Section: Discussionmentioning

confidence: 99%

Association between human leukocyte antigen gene polymorphisms and multiple EPIYA-C repeats in gastrointestinal disorders

Sarıbaş

Demiryas

Yılmaz

et al. 2020

WJG

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“…Recent studies have found that the interaction of cytokines showed an important role in the development and progression of malignant tumors. Previous studies have revealed that IL-17 was involved in tumor occurrence, metastasis, angiogenesis, immune-resistance and other processes [26][27][28], and confirmed that IL-17 signaling pathway also played an important role in the occurrence and progression of GC [29], breast cancer [30] and pancreatic cancer [31]. Meanwhile, Liu et al [32] obtained the data of Helicobacter pylori GC samples from TCGA and revealed that cytokine-cytokine receptor interaction was enriched in H. pylori (+) GC through GO and KEGG analysis.…”

Section: Discussionmentioning

confidence: 99%

Genomic analysis and clinical implications of immune cell infiltration in gastric cancer

Wang

Liu

et al. 2020

Bioscience Reports

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The immune infiltration of patients with gastric cancer (GC) is closely associated with clinical prognosis. However, previous studies failed to explain the different subsets of immune cells involved in immune responses and diverse functions. The present study aimed to uncover the differences in immunophenotypes in a tumor microenvironment (TME) between adjacent and tumor tissues and to explore their therapeutic targets. In our study, the relative proportion of immune cells in 229 GC tumor samples and 22 paired matched tissues was evaluated with a Cell type Identification By Estimating Relative Subsets Of known RNA Transcripts (CIBERSORT) algorithm. The correlation between immune cell infiltration and clinical information was analyzed. The proportion of 22 immune cell subsets was assessed to determine the correlation between each immune cell type and clinical features. Three molecular subtypes were identified with ‘CancerSubtypes’ R-package. Functional enrichment was analyzed in each subtype. The profiles of immune infiltration in the GC cohort from The Cancer Genome Atlas (TCGA) varied significantly between the 22 paired tissues. TNM stage was associated with M1 macrophages and eosinophils. Follicular helper T cells were activated at the late stage. Monocytes were associated with radiation therapy. Three clustering processes were obtained via the ‘CancerSubtypes’ R-package. Each cancer subtype had a specific molecular classification and subtype-specific characterization. These findings showed that the CIBERSOFT algorithm could be used to detect differences in the composition of immune-infiltrating cells in GC samples, and these differences might be an important driver of GC progression and treatment response.

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“…Additionally, other types of cytokines, such as the interleukin (IL) family (e.g., IL-17 and IL-6), contribute to the inflammatory response 30 , 31 . Indeed, many studies have reported abnormal IL concentrations in GC patients and suggested promising indicators of GC development 32 , 33 . Therefore, further studies are needed to identify whether genetic polymorphisms associated with other cytokines can modify the diet effect that increases the risk of cancer.…”

Section: Discussionmentioning

confidence: 99%

TNF genetic polymorphism (rs1799964) may modify the effect of the dietary inflammatory index on gastric cancer in a case–control study

Kim

Lee

Choi

et al. 2020

Sci Rep

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The inflammatory process is known to increase the risk of gastric carcinogenesis, and both genetic and dietary factors are associated with inflammation. In the present study of 1,125 participants (373 cases and 752 controls), we determined whether the dietary inflammatory index (DII) is associated with the risk of gastric cancer (GC) and investigated whether a TNF polymorphism (rs1799964) modifies this association. Semi-quantitative food frequency questionnaire derived data were used to calculate the DII scores. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using multivariable logistic models adjusted for confounders. When we stratified the data by sex, the association between GC and the DII was significant only among the women (OR, 2.27; 95% CI 1.25-4.19), and the DII effect on the risk of GC differed depending on the TNF genotype (OR, 2.30; 95% CI 1.27-4.24 in TT genotype; OR, 0.78; 95% CI 0.37-1.65 in CC + CT, p for interaction = 0.035). Furthermore, the association between the DII and GC was significant in the Helicobacter pylori-positive group; similarly, the effect differed based on the TNF genotype (OR, 1.76; 95% CI 1.13-2.73 in TT genotype; OR,0.98; 95% CI 0.54-1.77 in CT + CC, p for interaction = 0.034). In conclusion, rs1799964 may modify the effect of the DII on GC. According to the GLOBOCAN results reported in 2018, gastric cancer (GC) is the fifth most common cancer worldwide, and the highest mortality rates are found in East Asia, including Korea 1. In 2016, the incidence of GC was first and second among all types of cancer in Korea 2. Such a high prevalence of GC may be attributed to Helicobacter pylori infection and chronic inflammation caused by chronic gastritis 3. The inflammatory process is caused by cytokine secretion and increases the risk of the development of gastric carcinogenesis 4,5. Among these cytokines, tumor necrosis factor (TNF) is among the most important factors inhibiting gastric acid secretion, causing the development of GC 6. TNF production is generally regulated at the transcriptional level 6. Polymorphisms located in the promoter region of the TNF gene affect the level of TNF. Indeed, genetic polymorphisms of the TNF gene have been proposed as candidate risk factors for GC 7. However, the results of studies investigating the association between TNF genetic polymorphism and GC risk have been inconsistent 8,9. These results indicate the need for further studies considering other factors, such as individual lifestyle factors. Environmental factors and host genetic factors also contribute to the chronic inflammatory response. Among these factors, dietary components contain both carcinogens and anticancer substances and are known to control the risk of cancer 10. For example, the consumption of fruits, vegetables, and beans containing antioxidants has been reported to help reduce inflammation, whereas the consumption of saturated fats, refined carbohydrates, and processed meat can cause inflammation 11,12. However, the analysis of a single food group or singl...

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Interleukins 17 and 23 in patients with gastric neoplasms

Cited by 21 publications

References 46 publications

Association between human leukocyte antigen gene polymorphisms and multiple EPIYA-C repeats in gastrointestinal disorders

Association between human leukocyte antigen gene polymorphisms and multiple EPIYA-C repeats in gastrointestinal disorders

Genomic analysis and clinical implications of immune cell infiltration in gastric cancer

TNF genetic polymorphism (rs1799964) may modify the effect of the dietary inflammatory index on gastric cancer in a case–control study

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