Macrophage migration inhibitory factor gene -173G&gt;C polymorphism and risk of bladder cancer in southeast China: a case–control analysis

Yuan, Qinbo; Wang, Meilin; Wang, Miaomiao; Zhang, Zhengdong; Zhang, Wei

doi:10.1007/s11033-011-1075-9

Cited by 12 publications

(11 citation statements)

References 19 publications

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“…Studies in patients from the Chinese mainland showed a RR of 5.85 for developing TCC after kidney transplantation when exposed to Chinese herbs. Furthermore, infection with high-risk HPV (especially HPV16; Li et al , 2011) and various gene polymorphisms (Yuan et al , 2012; Xie et al , 2013) have been postulated to have a role in bladder carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Risk of bladder cancer in renal transplant recipients: a meta-analysis

Lü

Chen

et al. 2014

Br J Cancer

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Background:Renal transplantation has been associated with a significantly increased risk of developing cancers during long-term follow-up, but for bladder cancer, this risk is less clear. We therefore performed a meta-analysis to determine whether bladder cancer risk in renal transplant recipients was increased.Methods:Eligible studies were identified through searches of PubMed and other public resources. Random-effects meta-analyses were used to pool overall estimates for standardised incidence ratios (SIRs). Heterogeneity test, sensitivity analysis, and assessment of publishing bias were also performed.Results:We identified a 3.18-fold higher SIR (95% confidence intervals (CI): 1.34–7.53, P=0.008) of bladder cancer in patients following renal transplantation compared with the general population, based on data from 79 988 patients with a total follow-up of 308 458 patient-years. When stratified by ethnicity, the SIRs for bladder cancer were 2.00 (95% CI: 1.51–2.65, P=0.001) and 14.74 (95% CI: 3.66–59.35, P<0.001) between European and Asian renal transplant recipients, respectively.Conclusions:Our study demonstrated that the risk of developing bladder cancer in transplant populations was increased. Such association suggests that physicians should be more vigilant in checking for bladder cancer in transplantation recipient population.

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Section: Discussionmentioning

confidence: 99%

Risk of bladder cancer in renal transplant recipients: a meta-analysis

Lü

Chen

et al. 2014

Br J Cancer

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“…Three studies assessed prostate cancer; 20 , 22 , 26 three studies assessed leukemia 17 , 19 , 25 and one each for gastric cancer, 24 cervical cancer, 18 colorectal cancer, 21 and bladder cancer. 23 The genotype distribution in one study deviated from HWE. 26 The main characteristics of all the included studies are listed in Table 1 .…”

Section: Resultsmentioning

confidence: 94%

“…Only one study reported that MIF −173G/C polymorphism is associated with a decreased risk of cancer. 23 All the other studies reported the opposite conclusion. We also found a meta-analysis that investigated the association between the MIF −173G/C polymorphism and cancer risk.…”

Section: Discussionmentioning

confidence: 92%

“…Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used in seven studies. 17 , 18 , 20 , 21 , 23 , 25 , 26 One study used polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP). 24 The other two studies employed denaturing high-performance liquid chromatography (DHLPC) wave analysis 19 and a Genetic Analyzer, 22 respectively.…”

Section: Resultsmentioning

confidence: 99%

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The association between the migration inhibitory factor -173G/C polymorphism and cancer risk: a meta-analysis

Zhou¹,

Weng²,

Wen³

et al. 2015

OTT

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Previous studies have suggested that macrophage migration inhibitory factor (MIF) −173G/C polymorphism may be associated with cancer risk. However, previous research has demonstrated conflicting results. Therefore, we followed the preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines and the meta-analysis on genetic association studies checklist, and performed a meta-analysis to investigate the association between MIF −173G/C polymorphisms and the risk of cancer. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were combined to measure the association between MIF promoter polymorphisms and cancer risk. The pooled ORs were performed for the dominant model, recessive model, allelic model, homozygote comparison, and heterozygote comparison. The publication bias was examined by Begg’s funnel plots and Egger’s test. A total of ten studies enrolling 2,203 cases and 2,805 controls met the inclusion criteria. MIF (−173G/C) polymorphism was significantly associated with increased cancer risk under the dominant model (OR=1.32, 95%, CI=1.00–1.74, P=0.01) and the heterozygote comparison (OR=1.38, CI=1.01–1.87, P=0.04). In subgroup analysis, MIF polymorphism and prostate were related to increased risk of prostate and non-solid cancer. In conclusion, MIF polymorphism was significantly associated with cancer risk in heterozygote comparison. The MIF −173G/C polymorphism may be associated with increased cancer risk.

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“…MIF is a constitutively expressed protein produced in many cell types, including parenchymal and NPCs within the liver. MIF is associated with pathology of multiple liver diseases, including viral hepatitis, nonalcoholic and alcoholic liver disease, cirrhosis, and hepatocellular carcinoma [20][21][22][23][24]. To date, there has only been one study that examined the role of MIF in hepatic fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Macrophage migration inhibitory factor is required for recruitment of scar-associated macrophages during liver fibrosis

Barnes

McMullen

Roychowdhury

et al. 2014

Journal of Leukocyte Biology

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Recruitment of peripheral monocytes to the liver is a key contributor to the response to injury. MIF can act as a chemokine and cytokine, regulating innate immune responses in many tissues and cell types. We hypothesized that MIF contributes to the progression of CCl4-induced hepatic fibrosis by regulating recruitment of SAM. SAMs dynamically regulate HSC activation and ECM degradation. To gain insight into the role of MIF in progression of liver fibrosis, we investigated markers of fibrosis and immune responses after chronic CCl4 administration to female C57BL/6 and MIF(-/-) mice. Chronic CCl4 exposure increased activation of HSC in WT mice, indicated by increased expression of αSMA mRNA and protein, as well as mRNA for collagen 1α1; these responses were blunted in female MIF(-/-) mice. Despite lower activation of HSC in MIF(-/-) mice, accumulation of ECM was similar in WT and MIF(-/-)mice, suggesting a decreased rate of ECM degradation. Recruitment of SAMs was lower in MIF(-/-) mice compared with WT mice, both in their initial inflammatory phenotype, as well as in the later phase as proresolution macrophages. The decreased presence of resolution macrophages was associated with lower expression of MMP13 in MIF(-/-) mice. Taken together, these data indicate that MIF-dependent recruitment of SAMs contributes to degradation of ECM via MMP13, highlighting the importance of appropriate recruitment and phenotypic profile of macrophages in the resolution of fibrosis.

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Macrophage migration inhibitory factor gene -173G>C polymorphism and risk of bladder cancer in southeast China: a case–control analysis

Cited by 12 publications

References 19 publications

Risk of bladder cancer in renal transplant recipients: a meta-analysis

Risk of bladder cancer in renal transplant recipients: a meta-analysis

The association between the migration inhibitory factor -173G/C polymorphism and cancer risk: a meta-analysis

Macrophage migration inhibitory factor is required for recruitment of scar-associated macrophages during liver fibrosis

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