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ORIGINAL ARTICLE
Year : 2018  |  Volume : 14  |  Issue : 12  |  Page : 1041-1047

Meta-analysis of the relationship between excision repair cross-complementing Group 5 rs17655 gene polymorphism and head and neck cancer susceptibility


1 Department of Chemotherapy, People's Hospital of Gaozhou, Gaozhou, China
2 Department of Traditional Chinese Medicine, Scientific Research Platform, The Second Clinical Medical College, Guangdong Medical University; Department of Dongguan Scientific Research Center, Sino-American Cancer Research Institute, Key Laboratory for Medical Molecular Diagnostics of Guangdong Province, Guangdong Medical University, Dongguan, Guangdong, China

Date of Web Publication11-Dec-2018

Correspondence Address:
Ying Zou
Department of Traditional Chinese Medicine, Scientific Research Platform, The Second Clinical Medical College, Guangdong Medical University, No.1, Xincheng Road of Songshan Lake Science and Technology Industry Park, Dongguan, Guangdong 523808
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1482.202888

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 > Abstract 


Background: Published studies have evaluated the association between excision repair cross-complementing Group 5 (ERCC5) rs17655 polymorphism and head and neck cancer (HNC) susceptibility. However, these studies showed inconsistent results.
Aims: The aim of this study was to get a more comprehensive estimation of this association.
Materials and Methods: Multiple databases were searched for the genetic association on the ERCC5 rs17655 polymorphism and HNC risk. Ten studies with a total of 3922 cases and 5871 controls were finally identified to be eligible studies in this meta-analysis. Odds ratio with 95% confidence intervals was used to assess the strength of association.
Results: Overall, this meta-analysis showed that there was no association between ERCC5 rs17655 polymorphism and HNC risk under all five genetic models. Further, no significant associations between the ERCC5 rs17655 polymorphism and HNC risk were found under the five genetic models in subgroup analyses based on the source of control. However, in stratified analyses by ethnicity, a significant association was found under the homozygous and recessive models in European.
Conclusions: Our investigations demonstrate that genotypes for the ERCC5 rs17655 polymorphism may be not associated with overall cancer risk. In a subgroup meta-analysis, the results suggest that the ERCC5 rs17655 polymorphism is probably associated with HNC risk in European, but the results should be interpreted with caution for the low number of studies.

Keywords: Excision repair cross-complementing Group 5 rs17655, head and neck cancer, meta-analysis, polymorphism, susceptibility


How to cite this article:
Li T, Ling H, Lu Y, Wu X, Cai M, Su B, Zou Y. Meta-analysis of the relationship between excision repair cross-complementing Group 5 rs17655 gene polymorphism and head and neck cancer susceptibility. J Can Res Ther 2018;14, Suppl S5:1041-7

How to cite this URL:
Li T, Ling H, Lu Y, Wu X, Cai M, Su B, Zou Y. Meta-analysis of the relationship between excision repair cross-complementing Group 5 rs17655 gene polymorphism and head and neck cancer susceptibility. J Can Res Ther [serial online] 2018 [cited 2019 Sep 17];14:1041-7. Available from: http://www.cancerjournal.net/text.asp?2018/14/12/1041/202888




 > Introduction Top


Head and neck cancer (HNC) is a relatively common cancer including cancer of oral, oropharyngeal, laryngeal, pharyngeal, thyroid, and nasopharyngeal.[1],[2] The etiology of nasopharyngeal carcinoma is still not clear. Accumulated evidence of studies had shown that infection of human papillomavirus and exposure to smoking and alcohol consumption play an important role in the development of HNC.[3],[4],[5] However, not all of these infected individuals, drinkers, and smokers will ever develop HNC cancer. The genetic susceptibility, environmental, dietary preferences, and lifestyle factors also contribute to the progression of the disease.[6] Several studies have provided evidence that polymorphism in genes is also a risk factor for its etiology.[7]

DNA repair mechanisms are important for maintaining DNA integrity after exposure to carcinogenic and cytotoxic compounds.[8] There are at least five distinct DNA repair pathways in humans: nucleotide excision repair (NER), base excision repair, mismatch repair, homologous recombination, and nonhomologous end-joining.[8] Among them, NER is the major repair mechanism for removing DNA damage caused by the carcinogenic as well as other chemical mutagens present in the environmental agents and endogenous metabolites.[9] The polymorphisms in this pathway-related genes may weaken its DNA repair capacity (DRC) and eventually result in the genesis of tumors.

The excision repair cross-complementing Group 5 (ERCC5) gene, also known as the xeroderma pigmentosum Group G (XPG) gene which located on chromosome 13q22-q33, is an important component of the NER pathway.[10],[11] One common nonsynonymous single-nucleotide polymorphism (SNP) in its coding region is ERCC5 rs17655 (His1104Asp) which can result in an amino acid alteration within the protein sequence.[12] It has been largely investigated in a variety of cancers, including breast,[13] lung,[14] stomach,[15] bladder,[16] and colorectal cancers.[17]

A relatively large number of studies have also evaluated the association between ERCC5 rs17655 polymorphism and HNC risk. Due to the relatively small sample size and different population, these studies showed inconsistent results. To get a more comprehensive estimation of this association, we performed this meta-analysis on all eligible case–control studies to clarify the effect of rs17655 polymorphism on the risk of HNC.


 > Materials and Methods Top


Searching strategy

All studies reported the associations between the ERCC5 rs17655 polymorphism and HNC risk and published from their inception to April 2014 were identified by comprehensive searches of electronic databases, including MEDLINE, EMBASE, Cochrane Library, China National Knowledge Infrastructure (CNKI), China Biological Medicine (CBM), and Wanfang Database. The following keywords were used in searching: “head and neck,” “oral,” “oropharyngeal,” “laryngeal,” “pharyngeal,” “thyroid,” “ERCC5,” “XPG,” “polymorphism,” and “variant.” The title and abstract of studies identified in the computerized search were scanned to exclude any study that was clearly irrelevant. In addition, the reference lists of all retrieved articles were reviewed for further identification of potentially relevant studies.

Inclusion criteria and exclusion criteria

We included full-text publications when the following inclusion criteria were met: (a) the study assessed the correlation between the HNC risk and the ERCC5 Asp1104His (rs17655) polymorphism, (b) the study design was case–controlled and (c) sufficient genotype data were provided for the calculation of odds ratio (OR) and 95% confidence interval (95% CI); exclusion criteria were the following: (a) lack of controls; (b) overlapping study populations; (c) lack of enough pertinent data; and (d) not concerned with cancer risk and (e) letters, reviews, and editorial articles.

Data extraction

Data of eligible studies were extracted by two authors independently in duplicate with a predesigned data collection form. The following data were extracted from all eligible publications: the first author's name, year of publication, cancer site, country and ethnicity of the study population, sample size, number of cases and controls, genotype frequency, and evidence of Hardy–Weinberg equilibrium (HWE) in controls. Different ethnicities of participants were categorized as Asian, American, or European population. Discrepancies in the evaluation of some of the studies were resolved through discussion between the authors. If necessary, the primary authors were contacted to retrieve additional information.

Statistical analysis

ORs with 95% CI were used to measure the strength of the association between the ERCC5 Asp1104His (rs17655) polymorphism and cancer risk based on genotype frequencies in cases and controls. The pooled ORs with 95% CIs for all studies were first calculated in the allelic model (C vs. G), homozygous model (CC vs. GG), heterozygote model (CG vs. GG), dominant model (CC + CG vs. GG), and recessive model (CC vs. CG + GG), and subgroup analyses were then carried out according to ethnicity (categorized as Asians, Americans, or Europeans) and source of controls (population-based and hospital-based). Statistical heterogeneity among studies was evaluated with Q and I2 statistics. Studies with an I2 statistic of <25% are considered to have no heterogeneity, those with an I2 statistic of 25%–50% are considered to have low heterogeneity, those with an I2 statistic of 50%–75% are considered to have moderate heterogeneity, and those with an I2 statistic of >75% are considered to have high heterogeneity.[18] A fixed-effects model or random-effects model was used, depending on the absence or presence of heterogeneity. We performed a random-effects model meta-analysis for heterogeneous outcomes (PQ<0.10 and I2 > 50%) and a fixed-effect model meta-analysis for homogeneous outcomes.[19],[20] To test the distribution of HWE in controls, Chi-square test for goodness of fit was conducted and P < 0.05 indicated disequilibrium of HWE. The Z-test was performed to assess the significance of the pooled ORs, and P ≤ 0.05 was considered statistically significant. To evaluate the stability of the results, sensitivity analyses were performed by omitting one study in each turn. In addition, we also evaluate the association by excluding studies in which the genotype frequencies in the controls significantly deviated from the HWE. We evaluated publication bias of the studies included in the Begg's test and Egger's regression model (P < 0.05 was considered representative of statistically significant publication bias).[21],[22] All tests were two-tailed, and P < 0.05 was deemed statistically significant. All statistical tests were performed with the STATA software (Version 12.0; STATA Corporation, College Station, Texas, USA).


 > Results Top


Identification of eligible studies

Based on the search strategy, a total of sixty citations were obtained by the initial database search in PubMed, EMBASE, CNKI, CBM, and Wanfang Database, and 50 studies were excluded because of duplicate studies, reviews, letter, meeting proceedings, or not relevant to our analysis, not related to rs17655 polymorphism, and note case–control studies. Finally, ten case–control studies that met our inclusion criteria were included in the present meta-analysis, containing 3922 cancer patients and 5871 controls.[8],[10],[11],[23],[24],[25],[26],[27],[28],[29] A flow diagram that shows how we located relevant studies is presented in [Figure 1].
Figure 1: Flow diagram of study selection process

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Characteristics of published studies

The meta-analysis included five studies in Asian population, three studies in American population, and two studies in European population. The detailed characteristics of eligible studies are shown in [Table 1]. Of these included studies, four were conducted in the China,[23],[24],[25],[27] three in America,[8],[26],[29] one in Portugal,[10] one in Germany,[11] and one in Japan.[28] Among the included studies, control populations in three studies deviated from HWE.[23],[24],[27]Studies with controls not in HWE were also pooled, but further excluded to test the stability of the results in this meta-analysis.
Table 1: Association between individual study characteristics and excision repair cross-complementing Group 5 rs17655 polymorphism

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Meta-analysis results

The association between ERCC5 rs17655 polymorphism and HNC risk was investigated in ten studies. Based on the Q-test and I2 test, there was obvious heterogeneity among the included studies under all four genetic models of the meta-analysis; thus, the random-effects model was used in the meta-analysis of the ten studies. The aggregated results suggest that ERCC5 rs17655 polymorphism was not significantly associated with cancer risk in any of the genetic models [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]. Furthermore, subgroup analysis by ethnicity suggested that there were no significant associations observed among Asian and American population under all genetic models [Table 2]. However, there was a significant association found in following models (for the homozygous modelCC vs. GG: OR =0.52, 95% CI 0.27–0.99; for recessive model CC vs. CG + GG: OR =0.47, 95% CI 0.25–0.89) among European population. Subgroup analysis by source of controls suggested that no significant associations were observed both in the hospital-based and population-based between ERCC5 rs17655 polymorphism and the risk of risk of HNC [Table 2].
Figure 2: Forest plot of the meta-analysis on the association between excision repair cross-complementing rs17655 polymorphism and head and neck cancer risk in allele model (C vs. G). Error bars indicate 95% confidence interval. Solid squares represent each study in the meta-analysis. Solid diamonds represent pooled odds ratio

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Figure 3: Forest plot of the meta-analysis on the association between excision repair cross-complementing rs17655 polymorphism and head and neck cancer risk in the homozygous model (CC vs. GG). Error bars indicate 95% confidence interval. Solid squares represent each study in the meta-analysis. Solid diamonds represent pooled odds ratio

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Figure 4: Forest plot of the meta-analysis on the association between excision repair cross-complementing rs17655 polymorphism and head and neck cancer risk in heterozygote model (CG vs. GG). Error bars indicate 95% confidence interval. Solid squares represent each study in the meta-analysis. Solid diamonds represent pooled odds ratio

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Figure 5: Forest plot of the meta-analysis on the association between excision repair cross-complementing rs17655 polymorphism and head and neck cancer risk in dominant model (CC + CG vs. GG). Error bars indicate 95% confidence interval. Solid squares represent each study in the meta-analysis. Solid diamonds represent pooled odds ratio

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Figure 6: Forest plot of the meta-analysis on the association between excision repair cross-complementing rs17655 polymorphism and head and neck cancer risk in a recessive model (CC vs. CG + GG). Error bars indicate 95% confidence interval. Solid squares represent each study in the meta-analysis. Solid diamonds represent pooled odds ratio

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Table 2: Main results of pooled odds ratios in the meta-analysis

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Sensitivity analysis

Sensitivity analysis was also performed to explore individual study's influence on the pooled results by omitting one single study each time from pooled analysis. The pooled OR and 95% CI were not significantly altered when any part of the study was omitted (data not shown), which indicated that any single study had little impact on the overall OR.

Publication bias

Begg's funnel plot and Egger's test were performed to assess the publication bias. No evidence of publication bias was detected by both Begg's and Egger's tests [Table 3].
Table 3: Egger's test and Begger's test for publication bias in population

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 > Discussion Top


Although tobacco and alcohol consumption are the major risk factors of HNC, a number of studies have demonstrated that genetic variations of DNA repair genes involved in several biological pathways may affect the susceptibility to HNC.[30] NER is one of the most important pathways in removing bulky adducts induced by environmental carcinogens.[31] XPG/ERCC5, as one of the key factors of the NER pathway, has been widely explored for its role in carcinogenesis with various tumor cell lines or tissues.[32] In addition, rs17655 of XPG/ERCC5 and other NER genes jointly contributed to the variability of DRC, thereby modifying the susceptibility to cancer.[33] Several studies have investigated the associations of SNPs in XPG/ERCC5 with risk of various cancers. The His1104Asp polymorphism (rs17655), located in the XPG C-terminus, has been largely investigated in studies of susceptibility to some cancers types, such as breast,[13] lung,[14] stomach,[15] bladder,[16] and colorectal cancers.[17] To date, a number of case–control studies were conducted to investigate the association between ERCC5 rs17655 polymorphism and HNC risk in humans. Yuan et al. showed that ERCC5 rs17655 polymorphisms may not play a major role in HNC susceptibility in Chinese population. Santos et al. suggest that ERCC5 rs17655polymorphisms may not influence thyroid cancer susceptibility. Abbasi et al. reported that the ERCC5 rs17655 polymorphism may not be associated with laryngeal cancer risk. Ma et al. showed that genetic variation in ERCC5 rs17655 may not affect the squamous cell carcinoma of the head and neck risk. Sugimura et al. found that the ERCC5 rs17655 polymorphism was not associated with oral squamous cell carcinoma susceptibility. However, Wen et al. provided evidence that genotypes for the ERCC5 rs17655 polymorphism may play an important role in the development of laryngeal and hypopharyngeal carcinomas. Lu et al. observed that ERCC5 rs17655 polymorphisms are associated with increased risk of laryngeal cancer, and that they confer more risk among smokers and drinkers. Cui et al. reported that the XPG Asp1104Asp genotype may be associated with decreased susceptibility to lung cancer and squamous cell carcinomas of the oropharynx, larynx, and esophagus. Li et al. suggested that genetic variations in ERCC5 rs17655 are associated with laryngeal cancer risk in a Chinese population, especially in ever smokers and drinkers. An et al. showed that ERCC5 rs17655 polymorphism may contribute to susceptibility to squamous cell carcinoma of the head and neck. However, the results of these studies remain conflicting rather than conclusive.

To provide the comprehensive and reliable conclusion, we performed the present meta-analysis of ten independent case–control studies to investigate the associations between the ERCC5 rs17655 polymorphism and HNC risk. The pooled results indicated that ERCC5 rs17655 polymorphism was not significantly associated with overall HNC risk in any of the genetic models in overall analysis. These associations were very robust, which did not vary materially when the sensitivity analyses were performed. Similar results were also found on subgroup analysis by and source of controls. Furthermore, the stratification subgroup analysis by ethnicity implied that there were no significant associations observed among Asian and American population under all genetic models. However, evidence of association was observed in the homozygous model (CC vs. GG: OR =0.52, 95% CI 0.27–0.990) and recessive model (CC vs. CG + GG: OR =0.47, 95% CI 0.25–0.89) in European population. The funnel plot did not reflect obvious asymmetry, and Egger's test further indicated no considerable publication bias in this meta-analysis. This made the results of this meta-study more reliable to some extent.

Two meta-analyses quantifying the association between ERCC5 rs17655 polymorphism and risk of cancer have been published.[34],[35] Zhu et al.[34] had only three case–control studies of HNC with a total of 1429 cases and 1954 controls and used two genetic model (homozygous and recessive model) to assay the association. Their meta-analysis suggested that ERCC5 rs17655 polymorphism may not contribute to HNC risk. He et al.[35] had five case–control studies of HNC with a total of 1709 cases and 2691 controls and used four genetic model (additive model, codominant model, dominant model, and recessive model) to assay the association. Their meta-analysis also suggested that ERCC5 rs17655 polymorphism was not associated with HNC risk. In contrast with the previous studies,[34],[35] our study included other five recent studies. In total, our study included ten case–control studies with a total of 3922 cases and 5871 controls. The sample size of our meta-analysis is almost twice larger than the previous studies, giving a greater power to evaluate the association. We used five genetic models to evaluate the association between ERCC5 rs17655 polymorphism and HNC risk. Our meta-analysis results suggest that the ERCC5 rs17655 polymorphism is probably not associated with HNC risk. In the sensitivity analysis by omitting the study one by one did not change the pooled results, which adds robustness to our finding.

One of the most important objectives of the meta-analysis is to identify the source of heterogeneity. In our study, significant heterogeneity was found existed in overall comparisons, which may affect the reliability of results in a meta-analysis. To explore the possible explanations for heterogeneity, we therefore conducted the subgroup analyses to identify the source of heterogeneity but failed to find any statistical significance. When we excluded the studies which the genotype frequencies in the controls significantly deviated from the HWE, the pooled result did not change [Table 2]. However, the heterogeneity was effectively reduced or removed among the overall analysis (for the allele model C vs. G, I2 = 0%; for the homozygous model CC vs. GG, I2 = 16.7%; for heterozygote model CG vs. GG, I2 = 0%; for dominant model CC + CG vs. GG, I2 = 0%; for the recessive model CC vs. CG + GG, I2 = 16.3%; respectively). Our sensitivity analysis suggests that the heterogeneity may be attributed to differences in quality of research. During subgroup analyses, we found that ethnicity greatly affected the association between ERCC5 rs17655 polymorphism and HNC risk. The pooled result from the current study shown that ERCC5 rs17655 polymorphism was associated with HNC risk in European population; whereas, no association was found in the Asian or American population. The differences may be explained by genetic diversities, different risk factors in lifestyles, and exposure to different environmental factors. Other factors such as selection bias and different matching criteria may also play a role. However, it should be noted that these results are not conclusive due to the limited number of studies with available data, which had insufficient statistical power to detect a slight effect or may have generated a fluctuated risk estimate.

The current meta-analysis has several limitations which should be noted. First, we pooled the data using unadjusted information, and other factors, such as age, family history, interactions among gene-gene, and even gene-environment, may potentially impact on our results and result in the heterogeneity. Lack of information relevant to the data analysis may also cause serious confounding bias. Second, the lack of original data of the reviewed studies, we did not carry out subgroup analysis to other potential factors, which may participate in the progression of the disease, such as drinking, smoking, and other lifestyle. Third, lacking sufficient eligible studies limited our comprehensive analysis, particularly for the single type of cancer, so the subgroup base on cancer type was not conducted in the present study. Finally, for European population, the number of the included studies was limited, and their sample sizes were small. It may be underpowered to explore the real association. Thus, the results should be interpreted with caution.


 > Conclusions Top


This meta-analysis suggests that ERCC5 rs17655 polymorphism may be not associated with genetic susceptibility of overall HNC under the current published studies. In a subgroup meta-analysis, however, ERCC5 rs17655 polymorphism might contribute to HNC susceptibility in the European population. Due to limitations showed above in this analysis, it is critical that larger and well-designed studies are needed to confirm our results.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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