Skip to main content
Download PDF

The pertinence of gastric cancer and interleukin 10–819 single nucleotide polymorphisms: a meta-analysis and systematic review

BMC Gastroenterology volume 24, Article number: 76 (2024) Cite this article

Abstract

Purpose

Cytokines regulate the interaction between the immune system and malignant tumors. Among them, interleukin-10 (IL-10) is a multifunctional anti-inflammatory cytokine mainly produced by immune cells. The correlation between gastric cancer and T/C single nucleotide polymorphism (SNP) of interleukin-10 (IL-10) promoter−819(rs1800871)was opaque and remained to be determined. We aim to explore the pertinence of gastric cancer and SNP of interleukin 10–819 by meta-analysis via five statistical models.

Methods

Databases including PubMed, Cochrane Library, Embase, the Scopus, and Google Scholars were comprehensively retrieved for the eligible studies on the related topic from inception to March 2022. Odds ratios (ORs) were generated for dichotomous variants by meta-analysis in each model via STATA 17.0 MP. The statistical models comprised recessive model, over-dominant model, allele model, co-dominant model and dominant model. Subgroup analysis was performed to investigate the difference across races as well as the source of heterogeneity if necessary.

Results

Eventually a total of 15 articles reporting 7779 patients were enrolled in our study. There were 2383 patients and 5396 controls, collectively. There was no correlation between gastric cancer and IL-10 819 in recessive model, co-dominant model or dominant model, and subgroup analysis showed that Asian, Latin American and Caucasian had no correlation with the risk of gastric cancer. In the allelic model, there was significant correlation between gastric cancer and IL-10 819 (OR = 3.96%, 95%CI: 3.28 to 3.78). In the over-dominant model, there is no correlation between gastric cancer and IL-10 819, but subgroup analysis uncovered significant vulnerability of Asian people with regard to gastric cancer.

Conclusions

In our study, both Asians, Latin Americans, and Europeans showed an increased risk of gastric cancer in the allelic model, whereas only Asians showed significant susceptibility in the super dominant model. Of course, more large cohort studies are needed to confirm our results.

Peer Review reports

Introduction

Gastric cancer is the fifth most common cancer and the fourth leading cause of cancer death worldwide [1]. It is most common in Asia, Latin America and some European countries. In China, gastric cancer is the second most common cancer and the second leading cause of cancer-related death. Compared with most developed countries, China has higher mortality/morbidity and 5-year prevalence [1]. As an aggressive malignant tumor, GC has high incidence and poor prognosis. For a long time, identifying reliable biomarkers related to GC risk changes has been the research goal to improve the early detection of diseases [2].

Gastric cancer develops from multi-step gastropathy cascade, involving multiple causes, such as multiple gene sequence changes [3]. Activation of the proto-oncogene or the proliferating gene, inactivation, and mutation of the tumor suppressor gene can render cell growth uncontrolled. Single nucleotide polymorphism refers to the DNA sequence polymorphism caused by the mutation of a single nucleotide at the genome level due to the transformation, transversion and mutation of a single base [4]. With the deepening of human genomics research, many studies in recent ten years have shown that both genetic polymorphism and epigenetic changes are related to the risk of gastric cancer to some extent [5].

Cytokines are small molecular peptides or glycoproteins that are synthesized and secreted by a variety of tissue cells. Interleukins, interferons, tumor necrosis factors, hematopoietic factors, growth factors, and chemokines are collectively referred to as cytokines. Cytokines are involved in the regulation of almost all types of cellular responses, such as immune proliferation, differentiation and effector functions, and are essential for immune cells to fight against tumor cells and pathogens [6]. Cytokines may have pro-inflammatory or anti-inflammatory activities, and may be involved in immunomodulatory activities according to microenvironment [7]. Previous studies have shown that IL-10 can increase proliferation, accelerate cell growth and prolong cell survival of melanoma cells [8].

Compared with the previous articles, we have included more articles, which means that we have included a wider range of people, better extrapolating and better distinguishing regions and races. At the same time, we have enlarged the sample size. From the statistical point of view, this led to the reduction of random error and confidence interval, so the data became more stable and convincing. From the model point of view, the previous research did not involve so many genetic models, which may lead to the lack of related genetic models, and our advantage lies in the profound interpretation from the perspective of genetics and clinic [9,10,11,12].

Therefore, we conducted this meta-analysis to further update the evidence of evidence-based medicine, deeply clarify the role of IL-10 819 gene polymorphism in gastric cancer, provide reference for clinical work, and better evaluate the potential correlation between IL-10 819 gene polymorphism and gastric cancer risk.

Method

Search strategy

Databases including PubMed, Cochrane Library, Embase, the Scopus, and Google Scholars were comprehensively retrieved for the eligible studies on the related topic from inception to March 2022 with the following Mesh terms:(“Interleukin10“ OR ”IL-10“ OR ”Interleukin“ OR ”Cytokine“) AND (”Gene“ OR ”Polymorphism“ OR ”Variant“ OR ”SNP“) AND (“Neoplasm, Stomach” OR “Stomach Neoplasm” OR “Neoplasms, Stomach” OR “Gastric Neoplasms” OR “Gastric Neoplasm” OR “Neoplasm, Gastric” OR “Neoplasms, Gastric” OR “Cancer of Stomach” OR “Stomach Cancers” OR “Gastric Cancer” OR “Cancer, Gastric” OR “Cancers, Gastric” OR “Gastric Cancers” OR “Stomach Cancer” OR “Cancer, Stomach” OR “Cancers, Stomach” OR “Cancer of the Stomach” OR “Gastric Cancer, Familial Diffuse”).

Criteria for inclusion and exclusion

Inclusion criteria:

  1. 1.

    Any study describing the association of the IL-10-819 C/T SNP with gastric cancer;

  2. 2.

    The number of controls and gastric cancer cases reported in any study;

  3. 3.

    Any study reporting the number of individuals of each genotype (TT, TC, CC) in cases and controls;

  4. 4.

    Results are expressed as odds ratios (ORs) with 95% confidence intervals (CIs);

  5. 5.

    The study is a case-control or nested case-control study.

Exclusion criteria:

  1. 1.

    There is no control group in the literature;

  2. 2.

    In the literature trial, the design is not rigorous (such as the diagnostic and efficacy judgment standard are not standardized, the sample data are unclear or incomplete, etcetera);

  3. 3.

    The statistical approach is inadequate;

  4. 4.

    Repeated publications, review and conference papers and so on.

Literature screening and data extraction

Two investigators independently searched, assessed, and extracted data from literature. Any discrepancy was arbitrated by a senior investigator. Data were collected including first author, year of publication, country, ethnic origin (classified as Asian, Caucasian or mestizo), genotyping method, number of cases and controls.

Quality evaluation literature screening

The NOS scale was adopted as the evaluation method. The evaluation content includes three aspects: (1) selection of case and control groups; (2) comparability between the case and controls; (3) exposure of the case group and control group. The score is 1–9 points, 1–5 points are low-quality, 6–9 points are high-quality, and low-quality literature is directly discarded. If there are differences between researchers, a third-party ruling may be used.

Statistical analysis

The software utilized was STATA version 17.0 MP. Mean difference (MD) was generated as effect-size for continuous variants. Odds ratios (ORs) were generated for dichotomous variants. If I2 ≤ 50% and P > 0.01, a fixed effect model would be implemented, otherwise a random effect model would be performed. If I2 > 75%, then subgroup analysis would be performed to explore the source of heterogeneity. Publication bias was assessed by Egger’s test. Probability value P < 0.05 was considered statistically significant.

Result

Literature search and study selection

A total of 986 potentially relevant articles were retrieved. After screening, a total of 15 articles meeting the inclusion criteria of Meta-analysis were included (Fig. 1) [13,14,15,16,17,18,19,20,21,22,23,24,25,26,27]. All eligible studies were published between 2003 and 2018. Thirteen of them were published in English and two in Chinese. These 15 articles had high NOS quality scores, with ratings fluctuating between 6 and 8. A total of 7,778 people were involved in 15 studies, including 2,383 cases and 5,395 controls. The basic characteristics of the included studies are shown in Table 1. Genes are divided into wild-type and mutant. Gene mutation is the transformation of wild-type genes into mutant genes. In this paper, the wild-type gene of IL-10 819 is denoted by A, and the mutant gene is denoted by B.

Fig. 1
figure 1

Flow chart of article inclusion and exclusion

Full size image
Table 1 The features of the included study
Full size table

Statistical analysis results

Significant associations with the risk of gastric cancer were detected for the IL-10 819.

Recessive model: Heterogeneity test analysis: The study showed statistically significant heterogeneity, the Meta-analysis results showed that the two groups were significantly different. The difference between the two groups was not statistically significant [OR = 1.11, 95%CI (0.91, 1.35), p = 0.315]. Subgroup analysis by ethnicity found no difference in the risk of gastric cancer among Asians, Latinos, and Caucasians in this model (Fig. 2).

Fig. 2
figure 2

Recessive model

Full size image

Super-dominant model: Heterogeneity test analysis: This research shows statistically insignificant heterogeneity. The difference was not statistically significant [OR = 1.06, 95%CI (0.94, 1.18), p = 0.341]. A Subgroup analysis based on ethnicity found significant statistical heterogeneity in Asian related studies (I2 = 0%, P = 0.467). The meta-analysis showed significant differences between the two groups [OR = 1.17, 95%CI (1.03, 1.34), p = 0.017] (Fig. 3). The risk of leukemia in the AA + BB genotype population is higher than that in the AB genotype population [OR = 1.43, 95%CI (1.06, 1.91), P = 0.02], this difference only exists in the Asian population [OR = 2.00, 95%CI (1.37, 2.92), P = 0.0003], no significant difference among Caucasians [OR = 1.13, 95%CI (0.86, 1.49), P = 0.37].

Fig. 3
figure 3

Super-dominant model

Full size image

Allelic model: Heterogeneity test analysis: There was significant statistical heterogeneity in the study, and the meta-analysis results showed that the difference between the two groups Statistically significant [OR = 3.96, 95%CI (3.28, 3.78), p = 0], indicating that the IL-10–819 C > T variant genotype significantly increased the risk in the allelic model. Subgroup analysis by ethnicity found that the IL-10–819 C > T variant genotype significantly increased risk in Asians, Latinos, and Caucasians (Fig. 4).

Fig. 4
figure 4

Allelic model

Full size image

Codominant models

Homozygous: Heterogeneity test analysis: There was no significant statistical heterogeneity in the study, the Meta-analysis results showed that the difference between the two groups was not statistically significant [OR = 1, 95% CI (0.83, 1.21), p = 0.999]. Subgroup analysis by ethnicity found no difference in the risk of gastric cancer among Asians, Latinos, and Caucasians in this model (Fig. 5).

Fig. 5
figure 5

Homozygous ofCodominant models

Full size image

Heterozygote: Heterogeneity test analysis: There was no significant statistical heterogeneity in the study, and the Meta-analysis results showed that the difference between the two groups was not statistically significant [OR = 1.05, 95% CI (0.9, 1.22), p = 0.055]. Subgroup analysis by ethnicity found no difference in the risk of gastric cancer among Asians, Latinos, and Caucasians in this model (Fig. 6).

Fig. 6
figure 6

Heterozygote of Codominant models

Full size image

Dominant model: Heterogeneity test analysis: There was no significant statistical heterogeneity in the study. The difference was not statistically significant [OR = 1.06, 95%CI (0.93, 1.21), p = 0.999]. Subgroup analyses by ethnicity revealed that there was no difference in gastric cancer risk among Asians, Latinos and Caucasians in this model (Fig. 7).

Fig. 7
figure 7

Dominant model

Full size image

Publication bias analysis

Egger’s test showed no significant Publication bias in all models(P > 0.05).

Discussion

In recent years, many studies have attempted to link IL-10 gene polymorphisms with gastric cancer risk, but these studies have yielded conflicting results. For example, Sarah, Jie Liu, Su SPbelieve that IL-10 819 gene polymorphism is not related to the risk of gastric cancer [22, 23, 26].

L. Li et al. showed that IL-10 C819T polymorphism was associated with increased risk of gastric cancer in co-dominant, dominant and recessive models [25]. Xiangting Zeng et al. think that the existence of IL-10-819 C allele is related to the increased risk of gastric cancer development [24]. The above different results may be related to the lack of proper models and the heterogeneity of the studied population. Therefore, we performed this meta-analysis to better analyze the correlation between IL-10 gene polymorphisms and gastric cancer.

Previous studies have shown that excessive and sustained production of pro-inflammatory mediators is a major factor in tumor promotion and progression [28]. Interleukins are a group of strong immunomodulatory cytokines secreted by lymphocytes, antigen-presenting cells and endothelial cells and are essential for the maintenance of normal immune function [20]. Any alteration in the level of interleukin expression or disruption of its action may result in severe immune dysfunction and lead to the development of malignancy [21]. Therefore, it is biologically plausible that functional interleukin gene polymorphisms may be associated with the risk of developing gastric cancer.IL-10 is a multifunctional cytokine with immunosuppressive and antiangiogenic functions, and it reduces the expression of MHC class in antigen presenting cells (APCs)17 and tumor cells by downregulating the expression of MHC class or inhibit antigen presentation, thereby contributing to an immunosuppressive environment [29,30,31]. IL-10 is located on chromosome 1 of 1q31-32 with a span of approximately 4.7 kb, including 4 introns and 5 exons. SNPs in the promoter region of the IL10 gene have been shown to alter IL-10 mRNA and protein levels [8]. Individual genetic susceptibility diversity is established based on genetic polymorphisms, and sequence variation in the gene promoter of cytokines may alter the associated transcription factor recognition sites, while the binding of specific recognition sequences in the promoter to regulatory factors affects the transcriptional level of gene expression, thus influencing transcriptional activation and cytokine production. For example, polymorphisms on the IL-10 promoter site-1082 are distributed at recognition sites similar to ETS and thus may have an effect on the binding of this transcription factor, which has been shown to act as a negative regulator in IL-2 production.

Our meta-analysis involved 15 studies, including 2383 cases and 5395 controls. The results revealed that there was no significant relationship between promoter polymorphism of IL10 819 and GC risk of recessive, super dominant, co-dominant and dominant genes models. However, compared with IL-10 819 wild type allele, IL-10 819 mutant allele can increase the risk of GC, which indicates that the mutant allele of IL-10,819 C/T polymorphism is dangerous. In other words, in the allele model, there is a significant correlation between gastric cancer and IL-10 819. In recent years, a number of studies have shown that the presence of the IL-10 819 C allele is associated with an increased risk of gastric cancer [13, 18], and further studies have found that the IL-10 819 C allele is associated with an increased risk of gastric cancer in patients with HP infection [24]. Zambon pointed out that the IL-10-819 TT genotype is related to intestinal metaplasia and NCGC [16]. The genotyping detection of anti-inflammatory cytokines will help to detect individuals at higher risk of gastric cancer.

Heterogeneity is a potential problem in meta-analysis. The data will be affected by subgroup differences, so subgroup analysis is needed. Most of the published related studies have chosen Helicobacter pylori for subgroup analysis, and our research has chosen race for analysis. Subgroup analysis showed that in the allele genetic model of IL-10 819 C/T polymorphism, the mutant allele was significantly associated with the increased risk of gastric cancer among Asians, Latinos and Caucasians. In addition, in the super dominant model, there is no correlation between gastric cancer and IL-10 819, but subgroup analysis shows that Homozygous genotype is related to the significantly increased risk of Asians. We found that overall, heterogeneity between studies was greatly reduced after data stratification by subject race, indicating that heterogeneity between included studies could be partially explained by race-induced differences. According to the above conclusions, we can consider whether the difference of race will affect the immunotherapy of gastric cancer from the perspective of genes, and then we can screen out the corresponding dominant population to achieve accurate treatment.

Changes in human DNA sequences can influence the occurrence and progression of human diseases. Single nucleotide polymorphism (SNP) is also key to individualized medical treatment. This study suggests that IL-10 819 gene polymorphism may be a genetic biomarker of gastric cancer, and clinical detection of gene mutation typing can provide scientific theoretical basis to further reveal the biological mechanism of the prognosis of gastric cancer.

In addition, in the future, we can investigate the role of IL-10 819 single nucleotide polymorphisms on in the prognosis of gastric cancer at different stages more accurately by further elaborate studies with cancer gene mutation screening kits.

The limitations of our meta-analysis should be considered when interpreting the results. First of all, the number of articles included in this paper is limited, and the sample size of our research is small. Secondly, the races involved are limited (only Asian, Hispanic and white). Thirdly, this paper only uses recessive model, super dominant model, allele model, co-dominant model and dominant model for analysis. More models are expected to explore the relationship between IL-10 819 promoter polymorphism and gastric cancer.

Conclusion

Generally speaking, our meta-analysis study in different populations confirmed that interleukin-10-819 promoter polymorphism could be used as a genetic biomarker of gastric cancer. If they have the financial ability, it is suggested that people with family history of gastric cancer should be tested for susceptibility genes for early detection and treatment. In addition, our findings still need further well-designed research to confirm, and the possible role of other interleukin gene polymorphisms in gastric cancer also needs further exploration.

Data availability

The datasets used and/or analysed during the current study available from the corresponding author on reasonable request.

References

  1. Wang FH, Zhang XT, Li YF et al. The Chinese Society of Clinical Oncology (CSCO): Clinical guidelines for the diagnosis and treatment of gastric cancer, 2021. Cancer Commun (Lond). 2021 Aug;41(8):747-795.

    Article  PubMed  Google Scholar 

  2. Suh YS, Yang HK. Screening and Early Detection of Gastric Cancer: East Versus West. Surg Clin North Am. 2015 Oct;95(5):1053-66. doi: 10.1016/j.suc.2015.05.012. Epub 2015 Jul 29. Suh YS, Yang HK. Screening and Early Detection of Gastric Cancer: East Versus West. Surg Clin North Am. 2015 Oct;95(5):1053-66. doi: 10.1016/j.suc.2015.05.012. Epub 2015 Jul 29.

    Article  PubMed  Google Scholar 

  3. Tannapfel A. Gegenwärtiger Stand Der Molekularpathologie Des Magenkarzinoms. Pathologe. 2001;22:37–43.

    Article  CAS  PubMed  Google Scholar 

  4. Azizzadeh-Roodpish S, Garzon M, Mainali S. Classifying single nucleotide polymorphisms in humans. Mol Genet Genomics. 2021;296(5):1161–73.

    Article  CAS  PubMed  Google Scholar 

  5. Yasui W, Sentani K, Motoshita J, et al. Molecular pathobiology of gastric cancer. Scand J Surg. 2006;95(4):225–31.

    Article  CAS  PubMed  Google Scholar 

  6. Zheng X, Wu Y, Bi J, et al. The use of supercytokines, immunocytokines, engager cytokines, and other synthetic cytokines in immunotherapy. Cell Mol Immunol. 2022;19(2):192–209.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  7. Seruga B, Zhang H, Bernstein LJ, et al. Cytokines and their relationship to the symptoms and outcome of cancer. Nat Rev Cancer. 2008;8(11):887–99.

    Article  CAS  PubMed  Google Scholar 

  8. Trifunović J, Miller L, Debeljak Ž, et al. Pathologic patterns of interleukin 10 expression–a review. Biochem Med (Zagreb). 2015;25(1):36–48.

    Article  PubMed  Google Scholar 

  9. Yu Z, Liu Q, Huang C, et al. The interleukin 10 -819 C/T polymorphism and cancer risk: a HuGE review and meta-analysis of 73 studies including 15,942 cases and 22,336 controls. OMICS. 2013;17(4):200–14.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Wang X, Yang F, Xu G, Zhong S. The roles of IL-6, IL-8 and IL-10 gene polymorphisms in gastric cancer: a meta-analysis. Cytokine. 2018;111:230–6.

    Article  CAS  PubMed  Google Scholar 

  11. Chen KF, Li B, Wei YG, Peng CJ. Interleukin-10 -819 promoter polymorphism associated with gastric cancer among Asians. J Int Med Res. 2010 Jan-Feb;38(1):1–8.

  12. Xue H, Lin B, An J, Zhu Y, Huang G. Interleukin-10-819 promoter polymorphism in association with gastric cancer risk. BMC Cancer. 2012;12:102.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Wu MS, Wu CY, Chen CJ, et al. Interleukin-10 genotypes associate with the risk of gastric carcinoma in Taiwanese Chinese. Int J Cancer. 2003;104(5):617–23.

    Article  CAS  PubMed  Google Scholar 

  14. Savage SA, Abnet CC, Haque K, et al. Polymorphisms in interleukin– 2, -6, and– 10 are not associated with gastric cardia or esophageal cancer in a high-risk Chinese population. Cancer Epidemiol Biomarkers Prev. 2004;13(9):1547–9.

    Article  CAS  PubMed  Google Scholar 

  15. Alpízar-Alpízar W, Pérez-Pérez GI, Une C, et al. Association of interleukin-1B and interleukin-1RN polymorphisms with gastric cancer in a high-risk population of Costa Rica. Clin Exp Med. 2005;5(4):169–76.

    Article  PubMed  Google Scholar 

  16. Zambon CF, Basso D, Navaglia F, et al. Pro- and anti-inflammatory cytokines gene polymorphisms and Helicobacter pylori infection: interactions influence outcome. Cytokine. 2005;29(4):141–52.

    Article  CAS  PubMed  Google Scholar 

  17. Kamangar F, Abnet CC, Hutchinson AA, et al. Polymorphisms in inflammation-related genes and risk of gastric cancer (Finland). Cancer Causes Control. 2006;17(1):117–25.

    Article  PubMed  Google Scholar 

  18. Sugimoto M, Furuta T, Shirai N, et al. Effects of interleukin-10 gene polymorphism on the development of gastric cancer and peptic ulcer in Japanese subjects. J Gastroenterol Hepatol. 2007;22(9):1443–9.

    Article  CAS  PubMed  Google Scholar 

  19. Crusius JB, Canzian F, Capellá G, et al. Cytokine gene polymorphisms and the risk of adenocarcinoma of the stomach in the European prospective investigation into cancer and nutrition (EPIC-EURGAST). Ann Oncol. 2008;19(11):1894–902.

    Article  CAS  PubMed  Google Scholar 

  20. Xiao H, Jiang Y, Li R, et al. [Association of IL-10 gene polymorphisms with gastroduodenal diseases in Hubei Han population]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2009;26(4):423–6.

    CAS  PubMed  Google Scholar 

  21. Ko KP, Park SK, Cho LY, et al. Soybean product intake modifies the association between interleukin-10 genetic polymorphisms and gastric cancer risk. J Nutr. 2009;139(5):1008–12.

    Article  CAS  PubMed  Google Scholar 

  22. SU SP, Yang ZB, Tian YL, et al. Association between IL-10-819 C/C and TNF-α-1031 C/C genes and susceptibility of gastrodnodenai diseases. Chin J Microecology. 2010;22:811–5.

    CAS  Google Scholar 

  23. Liu J, Song B, Wang J, et al. Polymorphisms of interleukin-10 promoter are not associated with prognosis of advanced gastric cancer. World J Gastroenterol. 2011;17(10):1362–7.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  24. Zeng X, Li Y, Liu T, et al. Pylori strains, IL-10 promoter polymorphisms with high morbidity of gastric cancer in Hexi area of Gansu Province, China. Mol Cell Biochem. 2012;362(1–2):241–8.

    Article  CAS  PubMed  Google Scholar 

  25. Li L, Tang XY, Ye LM et al. Investigation on the association between IL-10 C819T gene polymorphisms and susceptibility to gastric cancer. Genet Mol Res. 2016;15(4).

  26. Sarah Y, Park Y, Lee J, et al. Effects of Soy Product Intake and Interleukin Genetic Polymorphisms on early gastric Cancer risk in Korea: a case-control study. Cancer Res Treat. 2017;49(4):1044–56.

    Article  Google Scholar 

  27. Liu S, Liu JW, Sun LP, et al. Association of IL10 gene promoter polymorphisms with risks of gastric cancer and atrophic gastritis. J Int Med Res. 2018;46(12):5155–66.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Coussens LM, Werb Z. Inflammation and cancer. Nature. 2002;420:860–7.

    Article  CAS  PubMed  PubMed Central  ADS  Google Scholar 

  29. Steinbrink K, Jonuleit H, Müller G, et al. Interleukin-10-treated human dendritic cells induce a melanoma-antigen-specific anergy in CD8(+) T cells resulting in a failure to lyse tumor cells. Blood. 1999;93(5):1634–42.

    Article  CAS  PubMed  Google Scholar 

  30. Adris S, Klein S, Jasnis M, et al. IL-10 expression by CT26 colon carcinoma cells inhibits their malignant phenotype and induces a T cell-mediated tumor rejection in the context of a systemic Th2 response. Gene Ther. 1999;6(10):1705–12.

    Article  CAS  PubMed  Google Scholar 

  31. Sato T, Terai M, Tamura Y, et al. Interleukin 10 in the tumor microenvironment: a target for anticancer immunotherapy. Immunol Res. 2011;51(2–3):170–82.

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

Not applicable.

Funding

The authors declare that no funds, grants, or other support were received during the preparation of this manuscript.

Author information

Authors and Affiliations

  1. Medical School of Southeast University, 210000, Nanjing, China

    Qianqian Mao

  2. Department of Oncology, Zhongda Hospital, Medical School of Southeast University, 210000, Nanjing, China

    Yanwen Liu

  3. School of health, Brooks College (Sunnyvale) the United States of America, Department of epidemiology and statistics, School of public health, Medical College, Zhejiang University, 310000, Hangzhou, China

    Xi Chen

  4. Department of General Medicine, Affiliated Anqing First People’s Hospital of Anhui Medical University, 246000, Anqing, China

    Cheng Jiang Liu

Authors
  1. Qianqian Mao
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Yanwen Liu
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Xi Chen
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Cheng Jiang Liu
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

M.Q. wrote the main manuscript text and prepared pictures and tables. L.Y. is the overall planner and supervisor of this research and paper. All the authors have reviewed the manuscript.

Corresponding author

Correspondence to Yanwen Liu.

Ethics declarations

Ethics approval and consent to participate

This is a systematic review and meta-analysis, ethics approval and consent to participate are not applicable.

Consent for publication

Not applicable. This study does not involve human participants.

Competing Interests

The authors have no relevant financial or non-financial interests to disclose.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Electronic supplementary material

Below is the link to the electronic supplementary material.

Supplementary Material 1

Supplementary Material 2

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Mao, Q., Liu, Y., Chen, X. et al. The pertinence of gastric cancer and interleukin 10–819 single nucleotide polymorphisms: a meta-analysis and systematic review. BMC Gastroenterol 24, 76 (2024). https://doi.org/10.1186/s12876-024-03151-9

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12876-024-03151-9

Keywords

BMC Gastroenterology

ISSN: 1471-230X

Contact us