Survivin基因多态性与中国人群肿瘤易感性的Meta分析

目的：探讨survivin基因启动子－31G／C多态性与中国人群肿瘤易感性的关系。方法：在Pubmed、Medline和中国期刊网全文数据库等数据库中检索相关中外文文献,制定文献纳入及排除标准,运用statal1．0软件进行Meta分析,计算合并的比值比（0R）及95％可信区间（CI）。结果：在中国人群中,survivin基因启动子－31G／C位点携带C碱基的肿瘤易感性是携带G碱基的1．30倍（OR=1．30,95％CI：1．08～1．56）,且携带C／C基因型比携带其他基因型更容易导致肿瘤的发生。结论：survivin基因启动子－31G／C位点可能是中国人群肿瘤的一个重要分子标记物。     

TNFA-308等位基因多态与中重度成人牙周炎的相关性分析

目的：探讨肿瘤坏死因子-α（TNF-α）基因TNFA^-308等位基因2多态性与中重成人牙周炎遗传易感性的关系。方法：采用病例-对照研究方法和聚合酶链反应，限制性片段长度多态性分析（RFLP）的方法检测124例中重度成人牙周炎（AP）患者和172例正常对照的TNFA^-308基因型。结果：中重度成人牙周炎组TNFA^-308等位基因2阳性基因型出现的频率为29.03%(36/124)，对照组为11.05%(19/172)。两组差异有显著性意义（X^2=13.42,P=0.0002,OR=3.167,95%CI=1.71-5.87)。结论：TNFA^-308等位基因2阳性基因型可能与中重度成人牙周炎易感性有关。     

TNFA-308基因多态性与中国人群慢性牙周炎的相关性研究

目的：探讨TNFA～308基因多态性与慢性牙周炎易感性的关系。方法：收集63例重度慢性牙周炎（CP）患者、103例轻、中度慢性牙周炎患者及80例健康对照者的颊黏膜拭子,提取DNA,采用多聚酶链反应-限制性内切酶片段长度多态性（PCR—RFLP）法测定TNFA-308位点的基因多态性,实验结果输入SPSS10．0统计软件包处理,进行各组间基因型分布和等位基因频率的X^2检验,比较各组间基因型分布的差异。计算等位基因2的OR和95％可信区间,以确定等位基因2与牙周炎易感性的关系。结果：重度CP组、轻、中度CP组及健康对照组均以TNF1／1纯合子占优势,TNF1／2杂合子基因型次之,仅在轻、中度CP组检出1例TNF2／2纯合子基因型。TNFA-308／NcoI基因型分布及等位基因频率在3组间无显著性差异。结论：对此位点基因型是否对慢性牙周炎的易感性及进程预后产生影响。尚不能肯定,需要进一步的研究。     

let-7基因多态与中国汉族人群头颈癌易感性的关联研究

目的：探讨 let-7基因多态与中国汉族人群头颈癌易感性的关联。方法：采用病例-对照研究设计,以经确诊的503例头颈部癌患者作为病例组,选取900例健康人群作为对照组。对病例-对照进行流行病学调查,内容包括：一般人口学特征、疾病史、肿瘤家族史、吸烟、饮酒情况,并进行体格检查。收集研究对象血液标本5 mL,提取基因组 DNA。以 let-7 rs10877887和rs13293512为研究位点,应用TaqMan探针方法进行多态性检测,并用logistic 回归计算比值比（odds ratio,OR）及其95％可信区间（confidence interval,CI）,比较不同基因型与头颈癌患病风险的关系。结果：rs10877887位点3种基因型 TT、CT及 CC 在病例组分布频率分别为45．7％（227/503）、42．9％（213/503）及11．4％（57/503）;在对照组中分别为40．8％（361/900）、47．7％（422/900）及11．5％（101/900）。rsl3293512位点3种基因型 TT、CT 及 CC 在病例组分布频率分别为31．9％（157/503）、52．3％（257/503）及15．8％（78/503）,在对照组中分别为30．2％（270/900）、49．2％（439/900）及20．6％（194/900）。多因素 logistic 回归分析显示,携带 rs10877887位点至少1个突变等位基因 C 的个体与携带 TT基因型的个体相比,头颈部肿瘤患病风险差异无统计学意义（CC ＋CT/TT调整 OR＝0．82,95％ CI：0．90～1．23,P＝0．087）;与携带 TT＋CT基因型个体相比较,携带 rs13293512位点2个突变等位基因 C 的个体头颈部肿瘤患病风险显著降低（CC/TT＋CT 调整 OR＝0．73,95％ CI：0．55～0．98,P＝0．039）。结论：let-7 rs13293512位点多态可影响中国汉族人群的罹患头颈癌的风险。     

白介素12A基因多态性与OLP的相关性研究

目的：研究华东地区汉族人群IL-12A基因多态性与口腔扁平苔藓（orallichenplanus,OLP）的相关性。方法：采用TaqMan荧光定量PCR法检测华东地区292例OLP患者及686例正常对照者的IL-12A基因的5个SNP位点（rs3024415,rs2243123,rs583911,rs568408和rs2243143）,分析IL-12A基因多态性与OLP的相关性。结果：①华东地区健康人群IL-12A基因3′-UTRrs568408位点AA、GA和GG基因型频率分别是0．7％、12．4％和86．8％,而OLP患者分别是1．1％、18．4％和80．5％,其中GA和AA基因型分布频率显著高于正常对照组@=O．0427）。②正常对照组IL-12A基因rs583911位点AA、GA和GG基因型频率分别是4．2％、38．6％和57．1％,而OLP患者分别是9．5％、36．5％和54％,其中AA基因型分布频率显著高于对照组（p=O．00805）。③糜烂型OLP组IL-12A—rs568408／A等位基因频率显著高于正常对照组,分别为11．6％和6．94％（OR=I．76,95％CI：1．133—2,732,P=0．011）。结论：华东地区汉族OLP人群IL-12A基因rs568408位点存在多态性变异,可能与OLP的疾病易感性和严重程度有关。     

白细胞介素基因多态性与汉族广泛型侵袭性牙周炎易感性的相关性研究

目的探讨白细胞介素10（interleukin-10,IL-10）启动子区域基因多态性与广泛型侵袭性牙周炎易感性的关系。方法收集30例广泛型侵袭性牙周炎患者和30名健康对照者的颊黏膜拭子,提取基因组DNA,采用PCR-RFLP方法检测IL-10基因启动子-1082G/A、-819C/T、-592A/C位点基因多态性,比较广泛型侵袭性牙周炎患者和健康对照组中等位基因频率和基因型分布。结果IL-10-1082G/A、-819C/T、-592A/C位点等位基因频率和基因型分布在患者和对照组之间差异无统计学意义（P〉0.05）。结论IL-10启动子区基因多态性与汉族人群广泛型侵袭性牙周炎易感性无明显相关关系。     

肿瘤坏死因子A-308位点基因多态性与侵袭性牙周炎的关系

目的探讨肿瘤坏死因子（tumor necrosis factor，TNF）A-308位点基因多态性与侵袭性牙周炎的关系。方法选择64例侵袭性牙周炎（aggressive periodontitis，AgP）患者及78名健康对照者，提取其外周静脉血基因组DNA，采用多聚酶链反应-限制性内切酶片段长度多态性的方法检测TNF A-308位点的基因多态性。结果TNFA-308位点的GA基因型频率在两组间差异无统计学意义；但是在按性别和吸烟分层的条件下，携带基因型GA和等位基因A使男性不吸烟者患病的风险明显增加（OR值分别为22．2和16．1）。结论提示TNFA-308基因型GA和等位基因A可能与中国人群中男性个体的AgP易感性有关。     

IL-10-1082 G／A基因位点单核苷酸多态性与汉族人群重度慢性牙周炎发病风险的病例对照研究

目的探讨白细胞介素10（interleukin-10,IL-10）基因1082 C／A位点单核苷酸多态性与汉族人群重度慢性牙周炎（chronic periodontitis,CP）发病风险的关系。方法收集汉族重度慢性牙周炎患者146例及牙周健康对照者138人的颊黏膜拭子,以Chelex-100法提取基因组DNA,采用聚合酶链反应-限制性片段长度多态性（polymerase chain reaction restriction fragment length polymorphism,PCR-RFLP）分析法测定IL-10—1082 G／A基因型,并分析组间基因型和等位基因频率的差异。结果CP组和对照组AA基因型分布分别率为91．8％和89．1％,P=0．45;A等位基因频率分别为95．9％和94．6％,P=0．46,差异无统计学意义。结论IL-10—1082 G／A位点单核苷酸多态性与汉族人群重度慢性牙周炎发病风险无相关关系。     

亚甲基四氢叶酸还原酶C677T多态性与非综合征性唇腭裂的关系

目的研究亚甲基四氢叶酸还原酶基因C677T多态性与非综合征性唇腭裂的关系。方法利用聚合酶链反应-限制性片段长度多态性方法（PCR-RFLP）,在168例非综合征性唇腭裂患者和192名正常对照中,对MTHFR基因C677T单核苷酸多态性（SNP,rs1801133）进行检测。利用拟合优度卡方检验,分析基因型分布频率是否符合Hardy-Weinberg平衡定律;应用UNPHASED软件包分析多态性位点与非综合征性唇腭裂的相关性。结果MTHFRC677T多态性基因型频率分布符合Hardy-Weinberg平衡;MTHFR C677T等位基因分布在NSCL／P组与对照组之间有显著性差异（P〈0.05）,正常组中T等位基因的频率明显高于NSCL／P组。结论MTHFR C677T多态性位点在中国人群中与非综合征性唇腭裂形成的发生相关联。     

白细胞介素-4基因-590C／T多态性与慢性牙周炎的相关性研究

目的研究白细胞介素-4（interleukin-4,IL-4）基因-590C／T多态性与慢性牙周炎易感性的关系。方法采用病例对照试验设计,聚合酶链反应一限制性内切酶片段长度多态性基因分析方法,比较104例慢性牙周炎患者（慢性牙周炎组）和106例牙周健康者（健康对照组）IL-4基因-590位点基因型和等位基因分布特点。结果IL-4基因-590位点C、T等位基因频率（X2=0．771,P=0．380）及基因型频率（X2=1．904,P=0．386）在两组间分布差异无统计学意义。结论IL-4基因-590位点的多态性与汉族人群慢性牙周炎的易感性无明显相关性。     

黑龙江地区PECAM-1多态性与慢性牙周炎的相关研究

目的:探讨黑龙江地区血小板内皮细胞粘附分子1(platelet-endothelial cell adhesion molecule-1, PECAM-1)基因Val125Leu rs281865545位点多态性与慢性牙周炎的相关性。方法:选取2012年9月~2014年3月在哈尔滨医科大学附属口腔医院牙周科就诊的146例牙周炎患者,分为3个牙周炎病例组(轻度57例、中度53例、重度36例)和91例健康者(健康对照组)作为研究对象,基因组DNA提取自口腔颊粘膜拭子,采用多重单碱基延伸SNP分型技术(multiplex SNaPshot technique)对所有受试者PECAM-1基因rs281865545位点进行检测,比较两组间此位点基因型分布和等位基因频率的差异。结果:PECAM-1基因rs281865545位点各基因型(GG、GC、CC)分布均符合Hardy-Weinberg遗传平衡定律;PECAM-1基因rs281865545位点GG、GC、CC在牙周炎各组和健康对照组的分布频率分别为24.7%、52.7%、22.6%和13.2%、57.1%、29.7%,两组人群基因型分布频率差异无统计学意义;等位基因G、C在牙周炎组和健康对照组分布频率分别为51.0%、49.0%和41.8%、58.2%,两组人群的等位基因分布频率差异具有统计学意义(P<0.05)。结论:PECAM-1基因rs281865545位点基因多态性与黑龙江地区慢性牙周炎的易感性不具有相关性,仍需对其进行深度研究来判断是否该位点可以作为牙周炎的基因诊断指标。     

Association analysis between interleukin-1 family polymorphisms and generalized aggressive periodontitis in a Chinese population

BACKGROUND: It has been suggested that aggressive periodontitis (AgP) has a genetic basis, but this theory has not been confirmed. The intent of this investigation was to study whether specific interleukin (IL)-1 genotypes and/or alleles could be used to predict susceptibility to generalized AgP (GAgP) in Chinese. METHODS: The GAgP group consisted of 122 patients, and the control group included 95 healthy subjects. Single nucleotide polymorphisms at IL-1A (+4845) and IL-1B (-511, +3954) were analyzed by standard polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. The polymorphism of a variable number tandem repeat (VNTR) in intron 2 of IL-1RN was detected by PCR amplification and fragment size analysis. RESULTS: There was no significant association of IL-1 polymorphisms with GAgP in the unstratified subjects. However, when cases were stratified by gender, the frequencies of A2+ genotype and allele 2 at IL-1A +4845 were significantly increased in male patients compared to male controls (genotype: odds ratio [OR] 5.58, 95% confidence interval [CI]: 1.09 to 28.68, P = 0.039; allele: OR 4.97, 95% CI: 1.01 to 24.50, P = 0.049; adjusted for age and smoking status). The frequency of IL-1B -511 A1/A2 heterozygote was significantly increased in male GAgP group compared to male controls (adjusted OR 3.16, 95% CI: 1.01 to 9.89, P = 0.048). In females, no significant differences were found between patients and controls in corresponding analyses at all polymorphic loci. A possible combined effect of IL-1B -511 polymorphism and smoking on the elevated risk to GAgP was observed. The OR of GAgP for combined A2+ genotype and smoking was 12.45 (95% CI: 1.43 to 108.06, P = 0.022), and for combined allele 2 and smoking was 18.25 (95% CI: 2.32 to 143.86, P = 0.006). CONCLUSIONS: The polymorphisms of IL-1A +4845 and IL-1B -511 may play an important role in determining GAgP susceptibility in Chinese males. Furthermore, a possible combined effect of the polymorphism of IL-1B -511 and smoking on GAgP susceptibility was suggested.     

转化生长因子β1基因-509位点多态性与重度慢性牙周炎易感性的关系

目的 探讨转化生长因子β1(transforming growth factor beta-1,TGF-β1)基因-509位点多态性与重度慢性牙周炎易感性的关系,以期从基因水平探讨牙周炎发病的遗传学机制.方法 用聚合酶链反应-限制性片段长度多态性方法检测102例重度慢性牙周炎患者(牙周炎组)和102名健康对照者(健康对照组)的TGF-β1基因-509位点,比较两组间此位点基因型分布和等位基因频率的差异.结果 TGF-β1基因-509位点CC、CT、TT基因型在牙周炎组和健康对照组的分布频率分别为44.1%(45/102)、47.1%(48/102)、8.8%(9/102)和29.4%(30/102)、51.0%(52/102)、19.6%(20/102),两组人群基因型分布频率差异有统计学意义(P＜0.05);等位基因C、T在牙周炎组和健康对照组分布频率分别为67.6%(138/204)、32.4%(66/204)和54.9%(112/204)、45.1%(92/204),两组人群的等位基因分布频率差异亦有统计学意义(P＜0.05),C等位基因携带者患重度慢性牙周炎的风险是T等位基因的1.718倍(OR=1.718,95%CI:1.148～2.569).结论 TGF-β1基因-509位点多态性与重度慢性牙周炎的发病具有相关性,C等位基因可能是重度慢性牙周炎的遗传易感基因.     

The short vitamin D receptor is associated with increased risk for generalized aggressive periodontitis

BACKGROUND: Generalized aggressive periodontitis (GAP) exhibits severe inflammation and alveolar bone loss. Vitamin D receptor (VDR) regulates both bone metabolism and inflammation-related genes, and its polymorphisms and haplotypes may affect the functional activity of the VDR protein in GAP. OBJECTIVE: We analysed the genetic effect of VDR start codon, intron, and exon polymorphisms, and their haplotypes on the development of GAP. MATERIALS AND METHODS: The VDR start codon 27823C > T (rs2228570, FokI), intron 8 60890G > A (rs154410, BsmI), and exon 9 61968T > C (rs731236, TaqI) polymorphisms were determined by using the polymerase chain reaction-restriction fragment length polymorphism analysis among 93 GAP patients and 143 healthy controls. RESULTS: The VDR start codon 27823*C/*C genotype was associated with an increased risk for GAP [odds ratio (OR) = 1.83, p = 0.028], but the intron 8 60880G > A and exon 9 61968T > C polymorphisms were not associated with GAP. The VDR haplotype homozygote ht1(C-G-T) carrying 27823*C allele was associated with a 1.8-fold increased risk of GAP (OR = 1.84, p = 0.030). CONCLUSION: These results demonstrate that the short VDR (27823*C/*C) protein may influence GAP susceptibility.     

Influence of methylenetetrahydrofolate reductase polymorphisms in oral cancer patients

J Oral Pathol Med (2011) 40 : 61–66 Background: Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme in folate metabolism. Two common polymorphisms associated with MTHFR gene – C677T and A1298C – influence the thermolabile nature and activity of the enzyme. This study aimed to investigate the role of MTHFR polymorphisms on oral cancer susceptibility and its potential impact on the prognostic outcome. Methods: Oral cancer cases and controls were genotyped using PCR‐RFLP technique for MTHFR C677T and A1298C polymorphisms. Disease susceptibility analysed using regression analysis. The association between clinical outcomes and the polymorphisms were analysed using univariate and multivariate model. Results: The 677CT+TT genotype showed a significant three‐fold reduction in oral cancer risk (RR‐0.35, p‐0.009). 1298CC genotype showed decreased cancer risk when compared to AA+AC genotype (RR‐0.55, p‐0.062). When prognostic significance of MTHFR polymorphism was evaluated, 677CT+TT patients showed improved survival than the CC individuals (RR = 0.56, P = 0.378). The 1298 CC and AC+CC showed an increased risk for treatment failure and poor survival when compared with the wild AA genotype (HR = 4.27, P = 0.001). Conclusion: Here we observed MTHFR C677T to influence oral cancer susceptibility, while A1298C polymorphism associated with patient prognosis. Our data support MTHFR polymorphism to be an independent prognostic marker in oral carcinoma.     

Association between lactoferrin gene polymorphisms and aggressive periodontitis among Taiwanese patients

Background and Objective: A dramatic difference in the frequencies of the Lys/Arg single nucleotide polymorphism in the lactoferrin genotype between a small population of patients with localized juvenile periodontitis and healthy subjects has been reported. As the single nucleotide polymorphism could be associated with ethnicity, the present study aimed to investigate the association between polymorphisms of the lactoferrin gene and periodontitis. Material and Methods: Sixty‐five patients with aggressive periodontitis, 278 with chronic periodontitis and 88 healthy controls were genotyped for the Lys/Arg polymorphism of the lactoferrin gene at position 29 [reference sequence (rs) 1126478] in the N‐terminal alpha‐helical region. Results: The frequencies of the GG genotype and the G allele were highest in the aggressive periodontitis group, followed by the chronic periodontitis group and then the healthy controls. The frequency of the G allele was significantly higher in aggressive periodontitis and chronic periodontitis groups than in healthy controls (p = 0.0037 and 0.0212). Although the difference of the GG genotype distribution between subjects with chronic periodontitis and healthy controls did not reach significance, the distribution of genotypes between aggressive periodontitis and healthy controls was significantly different. The association of the gene polymorphism and aggressive periodontitis still existed, even after adjusting for age, gender and smoking status by logistic regression analysis (GG/AG+AA: odds ratio = 2.16, 95% confidence interval = 1.09–4.35, p = 0.0287). After the study, subjects were further stratified by their smoking status; the GG genotype was still significantly associated with the risk of aggressive periodontitis in the nonsmoking group (odds ratio = 2.69, p = 0.018). However, there were no statistical differences between chronic periodontitis vs. healthy controls and aggressive periodontitis vs. healthy controls in the smoking group. Conclusion: The present study revealed that the A/G polymorphism in the lactoferrin gene might be associated with aggressive periodontitis. The A allele might reduce the risk of development of aggressive periodontitis in a Taiwanese population. Our results also support the hypothesis that lactoferrin genetic polymorphisms could play a role in the risk for periodontitis separate from the smoking factor. The functionality of this gene’s polymorphisms has to be further elucidated.     

Gene polymorphisms of tissue plasminogen activator and plasminogen activator inhibitor-1 in Turkish patients with generalized aggressive periodontitis

AIM: Tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) have important roles in proteolytic events in periodontitis. The aim of this study was to investigate TPA and PAI-1 gene polymorphisms in relation to susceptibility to generalized aggressive periodontitis (G-AgP). METHODS: Genomic DNA was obtained from peripheral blood of 90 G-AgP patients and 154 periodontally healthy subjects. 4G/5G polymorphism in the promoter region of the PAI-1 gene and Alu-repeat insertion/deletion (I/D) polymorphism in intron 8 of the TPA gene were genotyped by polymerase chain reaction and endonuclease digestion. RESULTS: The genotype distributions of TPA and PAI-1 genes were similar between G-AgP and healthy subjects (p>0.05). The distribution of TPA genotypes in G-AgP patients was 33.4% D/D, 44.4% I/D, and 22.2% I/I and was 26.3% D/D, 40.4% I/D, and 33.3% I/I in healthy subjects. The D allele was 55.6% in G-AgP and 46.6% in healthy subjects. There was a significant difference among study groups in D allele frequencies (p=0.044). The PAI-1 genotype distribution in G-AgP was 29.1% 4G/4G, 43.0% 4G/5G, and 27.9% 5G/5G, while it was 35.7% 4G/4G, 43.8% 4G/5G, and 20.5% 5G/5G in healthy subjects. CONCLUSION: These data suggest that the D polymorphic allele of TPA gene polymorphism could be associated with susceptibility to G-AgP in Turkish subjects.     

p53 polymorphism, human papillomavirus infection in the oral cavity, and oral cancer

OBJECTIVES: Human papillomavirus (HPV) infection has emerged as a risk factor in oral carcinogenesis. An arginine-coding polymorphism of the tumor suppressor protein p53 at codon 72 is more readily degraded by the HPV oncoprotein E6. Our objective was to evaluate the association between p53 polymorphism at codon 72 and HPV infection in the oral cavity, as well as its association with oral cancer.Study Design: Oral squamous cells from 202 patients with oral cancer and 333 age-sex frequency matched controls were evaluated by polymerase chain reaction for the presence and type of HPV and for alleles of codon 72 in p53. Fisher exact test and chi(2) tests were used to evaluate the data. RESULTS: The p53 codon 72 polymorphism is not associated with HPV infection, whether comparing HPV-negative controls with HPV-positive controls or comparing HPV-negative cases with HPV-positive cases. Additionally, we found no association with the codon 72 polymorphism and oral cancer, whether comparing HPV-negative controls with HPV-negative cases or comparing HPV-positive controls with HPV-positive cases. CONCLUSIONS: There is no association between p53 codon 72 polymorphism and HPV infection or between the p53 polymorphism and the risk of oral cancer.     

GSTM1 polymorphism and oral leukoplakia

BACKGROUND: Molecular epidemiological studies have now provided evidence that an individual susceptibility to cancer is mediated by genetic and environmental factors. Genetic polymorphisms have been described for enzymes involved in the metabolism of tobacco carcinogens and cancer risk is determined by the degree of expression and/or activity of enzymes involved in carcinogen activation or deactivation. The objective of this study was to investigate the GSTM1 null polymorphism and the risk for oral leukoplakia in individuals with tobacco-smoking habit in a Brazilian population. METHODS: A total of 52 tobacco-smoking patients with oral leukoplakia and 52 tobacco-smoking controls were recruited in a Brazilian population. The GSTM1 genotypes were studied by polymerase chain reaction-based methods. RESULTS: The frequency of the GSTM1 null genotype in the group with oral leukoplakia (57.7%) was statistically different from the controls (34.6%; OR: 2.57, 95% CI: 1.16-5.69, P < 0.05). The stratification of the samples according to the level of dysplasia showed increased prevalence of GSTM1 null genotype on lesions with moderate/severe histological dysplasia (68.2%) compared with the control group (31.9%). This difference was statistically significant (OR: 4.59, 95% CI: 1.29-16.33, P < 0.05). CONCLUSION: In conclusion, the GSTM1 null genotype may increase the risk for oral leukoplakia development.     

MCP-1 and CCR2 gene variants in oral squamous cell carcinoma

Oral Diseases (2011) 18 , 55–59 Aim: We aimed to investigate a possible association of the MCP‐1 and CCR2 polymorphisms with the risk of developing oral squamous cell carcinoma (OSCC). Methods: MCP‐1 A2518G and CCR2 V64I gene polymorphisms were performed by polymerase chain reaction and restriction fragment length polymorphism, in 129 patients with OSCC and 140 healthy control subjects. Results: Individuals who had G allele and GG genotype of MCP‐1, and 64I allele and wt/64I genotype of CCR2 had increased risk for OSCC (P < 0.05.) In contrast, individuals with CCR2 wt/wt genotype seem to be protected from OSCC (P < 0.01). Haplotype analysis revealed that MCP‐1G: CCR2 64I haplotype frequencies were significantly higher in patients than those of controls (P = 0.001). Conclusions: We can suggest that the G allele of MCP‐1 and 64I allele of CCR2 may be risk factors for OSCC.