Variation in <i>IL10</i> and Other Genes Involved in the Immune Response and in Oxidation and Prostate Cancer Recurrence

Dluzniewski, Paul; Wang, Ming‐Hsi; Zheng, S. Lilly; Marzo, Angelo M. De; Drake, Charles G.; Fedor, Helen; Partin, Alan W.; Han, Misop; Fallin, M. Daniele; Xu, Jianfeng; Isaacs, William B.; Platz, Elizabeth A.

doi:10.1158/1055-9965.epi-12-0458

Cited by 50 publications

(57 citation statements)

References 37 publications

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“…This suggests that unrepaired DNA damage could induce systemic induction of the immunosuppressive cytokine. Additional evidence suggests that IL10 single nucleotide polymorphism (SNP) variants are associated with basal cell carcinoma alongside with DNA repair gene variants and also with genes such as iNOS that is associated with prostate cancer recurrence (Dluzniewski et al , 2012; Festa et al , 2005). Since the relationship between IL10 and the DNA damage response is unclear, future studies will require molecular and biochemical characterization of this pathway.…”

Section: Tumor Microenvironment Inflammation and Dna Repairmentioning

confidence: 99%

Interplay between DNA repair and inflammation, and the link to cancer

Kidane¹,

Chae

Czochor³

et al. 2014

Critical Reviews in Biochemistry and Molecular Biology

137

114

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DNA damage and repair are linked to cancer. DNA damage that is induced endogenously or from exogenous sources has the potential to result in mutations and genomic instability if not properly repaired, eventually leading to cancer. Inflammation is also linked to cancer. Reactive oxygen and nitrogen species (RONs) produced by inflammatory cells at sites of infection can induce DNA damage. RONs can also amplify inflammatory responses, leading to increased DNA damage. Here, we focus on the links between DNA damage, repair, and inflammation, as they relate to cancer. We examine the interplay between chronic inflammation, DNA damage and repair and review recent findings in this rapidly emerging field, including the links between DNA damage and the innate immune system, and the roles of inflammation in altering the microbiome, which subsequently leads to the induction of DNA damage in the colon. Mouse models of defective DNA repair and inflammatory control are extensively reviewed, including treatment of mouse models with pathogens, which leads to DNA damage. The roles of microRNAs in regulating inflammation and DNA repair are discussed. Importantly, DNA repair and inflammation are linked in many important ways, and in some cases balance each other to maintain homeostasis. The failure to repair DNA damage or to control inflammatory responses has the potential to lead to cancer.

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Section: Tumor Microenvironment Inflammation and Dna Repairmentioning

confidence: 99%

Interplay between DNA repair and inflammation, and the link to cancer

Kidane¹,

Chae

Czochor³

et al. 2014

Critical Reviews in Biochemistry and Molecular Biology

137

114

View full text Add to dashboard Cite

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“…1 article was exclude since it mainly discussed IL-1B and PCa aggressiveness (Zabaleta et al, 2009). 1 article was exclude since it mainly discussed IL-1B and PCa recurrence (Dluzniewski et al, 2012). The other article was exclude since it mainly discussed IL-1B and fatigue in PCa patients treated with androgen deprivation therapy (Jim et al, 2012).…”

Section: Study Characteristicsmentioning

confidence: 99%

Genetic Polymorphism of Interleukin-1A (IL-1A), IL-1B, and IL-1 Receptor Antagonist (IL-1RN) and Prostate Cancer Risk

Xu¹,

Ding²,

Jiang³

2014

Asian Pacific Journal of Cancer Prevention

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“…Study carried out by Agalliu I, et al [17] suggested a positive relationship between GSTM1 polymorphism and BCR while others did not comply with their findings [15], [16]. The influence of GSTP1 polymorphism on BCR has also been shown to have inconsistent findings [15]–[18] (Table 1). However, these inconsistent results may due to the limited cases included and/or the potential differences in ethnicity across these studies.…”

Section: Introductionmentioning

confidence: 99%

“…However, these inconsistent results may due to the limited cases included and/or the potential differences in ethnicity across these studies. For instance, study by Cotignola J, et al [15] included only 105 patients; even for the largest studies, there are only 968 patients included [18]. So a meta-analysis of these studies is needed to yield more comprehensive understanding of GSTs polymorphisms on PCa prognosis.…”

Section: Introductionmentioning

confidence: 99%

“…So we believe it is good practice to investigate these hypermethylated genes together with GSTP1. Currently available studies reported DNA methylation levels of the promoters of GSTP1, APC and RARb2 might be associated with higher risk of BCR with inconsistent results [18], [19], [21]–[24]. Since the inconsistent results may be due to relatively small sample sizes of individual studies, we carried out a meta-analysis of the available published studies.…”

Section: Introductionmentioning

confidence: 99%

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Impact of Glutathione-S-Transferases (GST) Polymorphisms and Hypermethylation of Relevant Genes on Risk of Prostate Cancer Biochemical Recurrence: A Meta-Analysis

et al. 2013

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IntroductionAccurate prediction of the biochemical recurrence (BCR) is critical for patients after intended curative therapy like radical prostatectomy (RP) or definitive radiotherapy for prostate cancer. Glutathione-S-transferases polymorphisms as well as hypermethylation of GSTP1 and functional genes in carcinogenesis, including tumor suppression gene (APC), hormone receptor that regulates cell growth and differentiation gene (RARbeta) were reported to be associated with BCR. Nevertheless, the reported results are inconsistent. To evaluate the relationship between glutathione-S-transferases polymorphisms and hypermethylation of these genes and the risk of prostate cancer BCR, we carried out a meta-analysis of the published studies.Methods and MaterialsWe performed a search in Medline, Embase and CNKI database with GST, APC, RARbeta in combination with single nucleotide polymorphism, hypermethylation, prostate cancer and recurrence. Languages were restricted to English and Chinese.ResultsOur study included 4 case-control studies and 7 cohort studies including 12 data sets and 3,037 prostate cancer patients. We confirmed that APC hypermethylation is associated with a modest hazard for biochemical recurrence after RP (HR = 1.85, 95%CI = 1.12–3.06). We also suggest GSTP1 polymorphism and CpG hypermethylation tested in serum are associated with BCR (HR = 1.94, 95%CI = 1.13–3.34). We also identified a possible association between GSTM1 null polymorphism and prostate cancer biochemical recurrence risk with borderline significance (HR = 1.29, 95%CI = 0.97–1.71).ConclusionTo our knowledge, this is the first meta-analysis evaluating the relationship of polymorphisms and hypermethylation in GSTs and biochemical recurrence. GSTM1, GSTP1 polymorphisms and hypermethylation of GSTP1, APC may be potential biomarkers for the evaluation of the probability of BCR. Further studies are warranted to validate these findings in larger cohorts with longer follow-up.

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Variation in IL10 and Other Genes Involved in the Immune Response and in Oxidation and Prostate Cancer Recurrence

Cited by 50 publications

References 37 publications

Interplay between DNA repair and inflammation, and the link to cancer

Interplay between DNA repair and inflammation, and the link to cancer

Genetic Polymorphism of Interleukin-1A (IL-1A), IL-1B, and IL-1 Receptor Antagonist (IL-1RN) and Prostate Cancer Risk

Impact of Glutathione-S-Transferases (GST) Polymorphisms and Hypermethylation of Relevant Genes on Risk of Prostate Cancer Biochemical Recurrence: A Meta-Analysis

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