单核细胞趋化因子-1受体CCR2基因190A/G、烟酰胺腺嘌呤二核苷酸磷酸氧化酶p22phox亚基基因C242T多态性与吸烟的交互作用增加非酒精性脂肪性肝病的发病风险

目的探讨单核细胞趋化因子-1(MCP-1)受体CCR2基因190A/G、烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶p22phox亚基基因C242T多态性与吸烟的交互作用与非酒精性脂肪性肝病(NAFLD)的关系。方法采用病例-对照研究的方法,以600例NAFLD患者及600例健康对照者的外周血白细胞为样本,利用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)技术分析了MCP-1受体CCR2基因190A/G和NADPH氧化酶p22phox亚基基因C242T多态性。结果 190A/G(GG)基因型和C242T(TT)基因型频率分布在病例组分别为50.17%、50.00%,在对照组分别为23.83%、24.17%,二者经χ2检验差异有统计学意义(χ2=88.8462,P=0.0031;χ2=85.8100,P=0.0039)。190A/G(GG)基因型者患NAFLD的风险显著增加(OR=3.2171,95%CI 1.9351~5.2184)。C242T(TT)基因型者患NAFLD的风险也显著增加(OR=3.1379,95%CI 1.7973~5.2362)。基因突变的协同分析发现190A/G(GG)/C242T(TT)基因型者在NAFLD组和对照组中的分布频率分别为39.67%和13.00%,二者经χ2检验差异有统计学意义(χ2=118.3021,P=0.0017)。190A/G(GG)/C242T(TT)基因型者患NAFLD的风险显著增加(OR=5.0211,95%CI 3.1853~7.7926)。病例组的吸烟率显著高于对照组(χ2=92.2234,P=0.0025),吸烟者患NAFLD的风险显著增加(OR=3.3032,95%CI 1.9147~5.7413),吸烟与190A/G(GG)/C242T(TT)基因型均有交互作用(r=3.9983;r=3.8553)。结论 190A/G(GG)、C242T(TT)基因型和吸烟是NAFLD的易患因素,基因多态性与吸烟的交互作用增加了NAFLD的发病风险。     

XPG基因多态性与贲门癌遗传易感性关系

目的探讨着色性干皮病基因组G(XPG)rs751402 C/T与rs873601 G/A单核苷酸多态性(SNP)与河北省磁县高发区人群贲门腺癌(GCA)遗传易感性之间的关系。方法采用聚合酶链反应-连接酶检测反应(PCR-LDR)方法对431例GCA患者和432名健康对照XPG基因rs751402 C/T和rs873601 G/A SNP进行基因分型。结果 XPG基因rs751402 C/T SNP T/T基因型增加了≤61岁年龄组个体GCA的发病风险(OR=1.77,95%CI=1.12~3.30)。XPG基因rs873601 G/A SNP与GCA的发病风险无关。结论携带XPG基因rs751402 C/T SNP T/T基因型个体GCA的发病风险明显增加,应定期接受上消化道内镜检查,以便实现GCA的早诊早治。     

Fas基因启动子区670A/G多态性与子痫前期发病风险关系的Meta分析

目的系统评价Fas基因启动子区670A/G基因多态性与子痫前期发病风险的关系。方法计算机检索Pub Med、EMBASE、Cochorane、CNKI、万方和维普数据库,搜集Fas基因多态性与子痫前期相关性的病例对照研究,检索时限从建库至2017年10月31日。由两名研究者分别独立按照纳入与排除标准筛选文献、提取资料并评价纳入研究的偏倚风险后,采用Stata11. 0软件进行数据分析。结果共纳入8个病例对照研究,9组数据,Meta分析结果显示Fas基因启动子区670A/G等位基因多态性与子痫前期相关(G/A:OR=1. 606,95%CI:1. 268~2. 033,P=0. 000; GA/AA:OR=1. 764,95%CI:1. 211~2. 570,P=0. 003; GG/AA:OR=2. 647,95%CI:1. 963~3. 569,P=0. 000; GG+AG/AA:OR=1. 978,95%CI:1. 344~2. 912,P=0. 001;GG/AA+GA:OR=1. 843,95%CI:1. 432~2. 373,P=0. 000)。因存在异质性,按文献来源所在大洲进行分组后,Meta分析发现欧洲国家的文章不存在异质性,基因多态性与子痫前期的发病风险存在相关性(隐形模型GG/AA+GA除外)。结论 Fas基因670A/G多态性与子痫前期发病风险有关,特别是欧洲人群的研究可信性更大,G等位基因是其潜在危险因素。     

炎症因子基因与缺血性脑卒中患者预后的相关性分析

目的探讨炎症因子MCP-1、CCR2、E-selectin基因多态性与缺血性脑卒中患者预后之间的相关性。方法采用病例对照研究方法,选取2014年10月-2016年10月于本院连续住院的缺血性脑卒中患者200例作为观察组,均经计算机断层扫描(CT)、磁共振成像(MRI)明确诊断,同期选择本院健康体检者200例作为对照组,接受问卷调查、体格检查、采集血标本。抽取患者外周静脉血并提取DNA,采用Sequenom Massyarray技术检测单核细胞趋化蛋白-1(MCP-1)(rs1024611、rs3760396)、C-C趋化因子受体2 (CCR2)(rs1799864、rs1799865)、E-selectin (rs2076059、rs10800469、rs3917412、rs5368)的基因型。由经过统一培训的医护人员在缺血性脑卒中发病90 d后进行随访,记录改良Rankin评分(mRS)。采用Logistic回归分析评价各基因型与脑卒中预后之间的关系。结果在缺血性脑卒中患者中,E-selectin的rs2076059基因型和等位基因频率与对照组相比差异具有统计学意义(P 0. 05)。缺血性脑卒中患者E-selectin的rs2076059基因型多态性显著增加,MCP-1、CCR2基因的单核苷酸多态性(SNP)之间没有显著关联。经回归分析发现E-selectin基因rs2076059位点也是缺血性脑卒中发病的独立危险因素。根据mRS评分,E-selectin基因rs2076059位点G/A基因型携带者较G/G基因型患者发生预后不良的相对风险度为2.17(P=0.007,OR=2.17,95%CI:1.48～5.79)。结论E-selectin基因rs2076059位点是缺血性脑卒中发病的独立危险因素; rs2076059位点与缺血性脑卒中的预后有关;相较于G/G基因型,G/A基因型为风险基因型,更易导致缺血性脑卒中预后不良。     

河北省汉族人群肺癌患者IFNGR1和IFNG基因多态性分析

目的探讨IFNGR1和IFNG基因多态性与肺癌风险的相关性。方法选择2016年6月至2017年6月邯郸市中心医院肿瘤科收治的肺癌患者300例为病例组,另选择同期体检健康者300例为对照组,采集所有受试者血样,采用Mass ARRAY方法对rs9376268、rs1327475、rs1861494和rs2069705四个位点的基因型进行测定,分析其多态性与肺癌风险的相关性。结果 IFNGR1基因上rs9376268和rs1327475的最小等位基因A与降低肺癌风险具有相关性,而IFNG基因上rs2069705的最小等位基因A与增加肺癌风险具有相关性(P<0.05)。rs9376268位点在最佳模型-显性模型下,G/A和A/A基因型与降低肺癌风险显著相关(OR=0.76,95%CI:0.61~0.97,P=0.025)。rs1327475位点在最佳模型-隐性模型下,A/A基因型与降低肺癌风险显著相关(OR=0.27,95%CI:0.09~0.77,P=0.009)。此外,rs2069705位点在最佳模型-显性模型下,G/A和A/A基因型与增加肺癌风险显著相关(OR=1.59,95%CI:1.11~2.28,P=0.012)。结论 IFNGR1基因rs9376268、rs1327475和IFNG基因rs2069705位点可能与肺癌风险具有相关性。     

亚洲人群MDM2基因SNP309多态性与乳腺癌易感性的Meta分析

目的综合评价MDM2基因SNP309多态性与亚洲人群乳腺癌易感性的关系。方法电子检索PubMed、Embase、VIP、CNKI和万方数据库中关于MDM2基因多态性与乳腺癌关系的病例对照研究,按照纳入与排除标准筛选文献,提取数据、评价纳入研究质量后进行Meta分析,计算合并OR值及95%CI,并进行敏感性分析和发表偏倚评估。结果共纳入11篇文献,涉及3 439例乳腺癌患者和3 499例对照。Meta分析结果显示,与携带TT基因型个体相比,携带GG基因型个体与乳腺癌风险增高相关(OR=1.37,95%CI:1.00~1.88),而携带GT基因型个体乳腺癌发病风险并未明显增高(OR=1.21,95%CI:0.99~1.49);与携带TT基因型个体相比,携带GT、GG基因型个体的乳腺癌发病风险增加(OR=1.26,95%CI:1.01~1.59);与携带GT、TT基因型个体相比,携带GG基因型个体的乳腺癌发病风险未明显增高(OR=1.18,95%CI:0.95~1.47)。结论在亚洲人群中,MDM2基因SNP309G可能是乳腺癌易感性增加的危险因素。     

p53基因第4外显子第72密码子多态性与中国女性宫颈癌相关性的Meta分析

目的评价p53基因第4外显子第72密码子G/C多态性与中国女性宫颈癌的相关性。方法检索中国知网、万方数据库、维普数据库、中国生物医学文献数据库、Pub Med、EMBase、the Cochrane Library和Wan Fang Data数据库,收集国内外关于p53基因第4外显子第72密码子G/C多态性与中国女性宫颈癌相关性的病例对照研究文献,筛选符合纳入标准的研究,根据研究对象是否感染人乳头瘤病毒(HPV)分为2个亚组,并对相关数据进行Meta分析。结果共纳入13篇文献,调查宫颈癌患者1 780例及对照1 517例。Meta分析显示对于非HPV感染亚组,具有基因型G/G、基因型G/C和等位基因G的中国女性,与具有基因型C/C(OR=0.980,95%CI:0.558~1.723)、基因型G/C(OR=0.843,95%CI:0.556~1.277)和等位基因C(OR=1.070,95%CI:0.789~1.449)的中国女性发生宫颈癌的风险相当;同样对于HPV感染亚组,具有基因型G/G、基因型G/C和等位基因G的中国女性,也与具有基因型C/C(OR=0.891,95%CI:0.213~3.722)、基因型G/C(OR=1.351,95%CI:0.942~1.937)和等位基因C(OR=0.981,95%CI:0.493~1.951)的中国女性发生宫颈癌的风险相当。所纳入文献不存在发表偏倚,本研究Meta分析结果稳定。结论目前尚未发现p53基因第4外显子第72密码子G/C单核苷酸多态性与中国女性宫颈癌的发病有关。     

RTEL1基因多态性与冠心病患病风险的相关性研究

目的研究RTEL1基因多态性与冠心病(CHD)患病风险的相关性。方法选择2015年1月至2016年12月于西安医学院第二附属医院就诊的符合入选条件的CHD患者共300例,以及健康对照人群300例,分别采集血样。采用Mass ARRAY方法对RTEL1基因上rs6089953、rs6010620、rs6010621、rs4809324和rs2297441共五个位点的基因型进行测定,用SPSS 19.0软件统计基因多态性与CHD患病风险的相关性。结果采用χ2检验比较病例对照两组间各位点的等位基因频率差异,结果显示RTEL1基因上的rs6010620位点的等位基因"G"与降低冠心病患病风险具有相关性(OR=0.776,95%CI:0.649~0.928,P=0.005)。引入遗传模型后,结果显示rs6010620位点在隐性模型下,携带G/G基因型的个体患冠心病风险显著降低,是携带A/A和G/A基因型的0.49倍(OR=0.49,95%CI:0.30~0.80,P=0.0039);rs4809324在隐性模型下,携带C/C基因型的个体患冠心病风险显著降低,是携带T/T和T/C基因型的0.3倍(OR=0.30,95%CI:0.11~0.83,P=0.015);rs2297441在显性模型下,携带A/G和A/A基因型的个体患冠心病风险显著降低,是携带G/G基因型的0.62倍(OR=0.62,95%CI:0.43~0.91,P=0.014)。连锁不平衡分析发现,由rs6010620,rs6010621和rs4809324三个位点组成的GTT单体型与降低冠心病风险显著相关(OR=0.03,95%CI:0.01-0.12,P0.0001),结论 RTEL1基因上rs6010620、rs4809324和rs2297441三个位点与降低冠心病患病风险显著相关。     

CTLA-4基因多态性与张家口地区汉族人桥本甲状腺炎的相关性

目的探讨细胞毒性T淋巴细胞相关抗原-4(CTLA-4)基因多态性与张家口地区汉族人群桥本甲状腺炎(HT)的相关性。方法选取2014-2015年张家口地区HT患者和健康体检者各170例为研究对象,提取外周血DNA后进行聚合酶链式反应(PCR)测序,检测rs231775基因型。用SPSS 13.0统计软件进行数据处理,通过Hardy Weinberg平衡检验确定研究样本的代表性,用基因计数法计算各组的基因频率和等位基因频率。结果 rs231775基因型频率分布均符合Hardy-Weinberg遗传平衡定律,病例组和健康对照组之间各基因型与等位基因分布频率差异均有统计学意义(P0.05)。HT的危险度因携带G/G基因型而增加,即G等位基因能增加HT的发病风险(OR=1.43,95%CI:1.23~1.87)。而A等位基因减少了HT的发病风险(OR=0.70,95%CI:0.12~0.83)。结论张家口地区汉族人群桥本甲状腺炎易感性与CTLA-4基因多态性具有关联,与基因型及等位基因相关性还有待进一步研究确认。     

中国南方汉族人群哮喘与GSDMB/ORMDL3基因多态性

目的研究GSDMB/ORMDL3基因相关单核苷酸多态性位点(SNP)与中国广东人群哮喘发病、吸烟行为的相关性。方法于2014年3月—2015年3月对广东医学院附属医院就诊的394例哮喘患者、395名健康成人进行血样采集和问卷调查,用SNa Pshot技术检测GSDMB/ORMDL 3基因单核苷酸多态性(SNP)rs7216389、rs4794820、rs11650680基因型,并分析SNP变异与哮喘风险及吸烟因素的相关性。结果 SNP位点rs7216389C-T和rs4794820 A-G变异增加哮喘发病风险(OR分别为1.8和1.7,均为P0.000 1),而rs11650680 C-T位点变异与哮喘风险无明显相关性(OR=0.8,P=0.170 0);吸烟哮喘患者rs7216389 T/T和rs11650680 C/C高于戒烟与非吸烟组,而rs4794820 A/A低于非吸烟组(均为P0.000 1)。结论 rs7216389 C-T、rs4794820 A-G位点变异与哮喘发病风险明显相关,吸烟增加rs7216389 C-T、rs4794820 A-G、rs11650680 T-C位点的变异风险。     

趋化因子受体CCR5和CCR5δ32在肝脏疾病中的作用

趋化因子受体CCR5是一种G-蛋白耦联受体,分布在T细胞和单核细胞表面,CCR5δ32是CCR5的一种变异型。研究发现,CCR5介导的信号通路参与了炎症反应、自身免疫性疾病和移植物抗宿主病等多种疾病的发病机制和转归过程。在肝脏疾病中,CCR5至少与病毒性肝炎、肝硬化、移植物抗宿主病等的发病过程有关。此文就CCR5与肝脏疾病的关系进行综述。     

CCR2, CCR5, and CXCL12 variation and HIV/AIDS in Papua New Guinea

Polymorphisms in chemokine receptors, serving as HIV co-receptors, and their ligands are among the well-known host genetic factors associated with susceptibility to HIV infection and/or disease progression. Papua New Guinea (PNG) has one of the highest adult HIV prevalences in the Asia-Pacific region. However, information regarding the distribution of polymorphisms in chemokine receptor (CCR5, CCR2) and chemokine (CXCL12) genes in PNG is very limited. In this study, we genotyped a total of nine CCR2-CCR5 polymorphisms, including CCR2 190G > A, CCR5 − 2459G > A and Δ32, and CXCL12 801G > A in PNG (n = 258), North America (n = 184), and five countries in West Africa (n = 178). Using this data, we determined previously characterized CCR5 haplotypes. In addition, based on the previously reported associations of CCR2 190, CCR5 − 2459, CCR5 open reading frame, and CXCL12 801 genotypes with HIV acquisition and/or disease progression, we calculated composite full risk scores, considering both protective as well as susceptibility effects of the CXCL12 801 AA genotype. We observed a very high frequency of the CCR5 − 2459A allele (0.98) in the PNG population, which together with the absence of Δ32 resulted in a very high frequency of the HHE haplotype (0.92). These frequencies were significantly higher than in any other population (all P-values < 0.001). Regardless of whether we considered the CXCL12 801 AA genotype protective or susceptible, the risk scores were significantly higher in the PNG population compared with any other population (all P-values < 0.001). The results of this study provide new insights regarding CCR5 variation in the PNG population, and suggest that the collective variation in CCR2, CCR5, and CXCL12 may increase the risk of HIV/AIDS in a large majority of Papua New Guineans.     

CCR5 and beta-chemokines in HIV-1 infected children

The duration from initial infection with HIV-1 to CD4 lymphocyte depletion and progression to AIDS varies among infected individuals. Despite treatment with highly active antiretroviral therapy (HAART), patients still show different stages of disease progression. We examined the role of beta-chemokines and its receptor, CCR5 in HIV-1 infected children in order to define determinants of HIV progression among treated individuals. Population was divided in two groups: Group 1--Long Term Non Progressors (LTNP) includes 10 patients with B1-B2 CDC disease classification and with a less aggressive therapy (only 2 in HAART); Group 2--Rapid Progressors (RP) includes 9 patients with C3 disease classification. All the patients had a CCR5 wild type (wt) genotype indicating that they do not have the 32 base-pair deletion associated with slower progression. There was an increased production of MIP 1-beta in 8/10 LTNP but only in 4/9 Progressors (Paired t-test/Wilcoxon Sign test, p-value < 0.05). The change in the levels of MIP-1 beta after PHA stimulation was statistically significant in both groups. The levels of RANTES increased in LTNP and RP and the change of the levels after mitogen stimulation was statistically significant for both groups included. The production of RANTES and MIP-1 beta in response to stimulation between both groups was not statistically significant. The production of MIP-1 alpha was variable in both groups and the difference in the levels after mitogen stimulation between the groups was not statistically significant. These results suggest that beta-chemokines do not play an important role in HIV-1 progression in children undergoing HAART.     

Gene polymorphisms in CCR5, CCR2, SDF1 and RANTES among Chinese Han population with HIV-1 infection

Chemokines and chemokine receptors are crucial for immune response in HIV-1 infection. Although many studies have been done to investigate the relationship between chemokines and chemokine receptor gene polymorphisms and host’s susceptibility to HIV-1 infection, the conclusions are under debate. In the present study, a cohort of 287 HIV-1 seropositive patients, 388 ethnically age-matched healthy controls and 49 intravenous drug users (IDUs) HIV-1 exposed seronegative individuals (HESN) from Chinese Han population were enrolled in order to determine the influence of host genetic factors on HIV-1 infection. Seven polymorphisms on four known chemokines/chemokine receptor genes (CCR5Δ32, CCR5 m303, CCR5 59029A/G, CCR2 64I, RANTES −403A/G, RANTES −28C/G and SDF1 3′-A) were screened. CCR5Δ32 and CCR5 m303 were absent or infrequent in Chinese Han population, which may not be hosts’ genetic protective factors for HIV-1 infection. Our results showed the CCR5 59029A/G, CCR2 64I and SDF1 3′-A were not associated with host’s resistance to HIV-1 infection. The frequency of RANTES −403A allele was significantly lower in HIV-1 patients than in healthy blood donors (p = 0.0005) and HESN group (p = 0.035), which implied the association between A allele and reduced HIV-1 infection risk. Different genetic models were assessed to investigate this association (AA vs. GG + AG, OR = 0.38 95% CI, 0.22–0.65 p = 0.0004; A vs. G, OR = 0.66 95% CI, 0.52–0.84 p = 0.0006), which supported this association, either. The genotype and allele distribution of RANTES −28 between HIV-1 patients and healthy controls (genotype profile: p = 0.072; allele profile: p = 0.027) or HIV-1 seronegative group (genotype profile: p = 0.036; allele profile: p = 0.383) were both at the marginal level of significance, which were not observed after Bonferroni correction. All these results suggest the RANTES −403A may be associated with reduced susceptibility to HIV-1 infection, while the RANTES −28 locus not. By lack of the patients’ clinical information, whether these polymorphisms affect AIDS disease progression and their role in different HIV-1 infection routes could not performed in present study and needs to be assessed in ongoing studies.     

淋巴细胞表面CCR5在HCV与HIV感染中表达

目的探讨T淋巴细胞表面C—C趋化因子受体5（CCR5）在丙型肝炎病毒（HCV）感染、人类免疫缺陷病毒（HIV）感染和HCV／HIV合并感染过程中的表达及意义。方法采用流式细胞术检测HCV感染组（n=21例），HIV感染组（n=14例），HCV／HIV感染组（n=28例）及正常对照组（n=30例）人外周血CD4＋和CD8＋T淋巴细胞表面CCR5的表达。结果与正常对照组相比，外周血CD4^＋和CD8^＋T淋巴细胞表面CCR5，HIV感染组高表达（P〈0．01），HCV感染组和HCV／HIV合并感染组中低表达（P〈0．01）。结论淋巴细胞表面CCR5的表达，HIV感染时升高、HCV感染时降低，HCV／HIV合并感染时HCV感染的作用更强。     

四川彝族人群HIV-1辅助受体CCR5△32和CCR2-64I基因多态性分析

目的了解中国四川彝族人群艾滋病病毒-1(HIV-1)辅助受体CCR5△32和CCR2．64I基因多态性特点。方法提取119份彝族正常人和88份HIV-1感染人群外周血基因组DNA。用聚合酶链反应(PCR)方法检测CCR5△32突变,阳性产物经克隆、测序进一步证实;用PCR-限制性片段长度多态性技术检测CCR2．64I突变,并测序验证。结果119份正常人样本中,CCR5 wt／△32等位基因突变杂合子2例(1．68％),未检测到CCR5△32／△32突变纯合子,CCR5△32等位基因频率为0．0084;CCR2-64I突变杂合子26例(21．85％),突变纯合子2例(1．68％),等位基因频率为01261。88份HIV-1感染者样本中,未检测到CCR5△32突变;CCR2．64I突变杂合子12例(13．64％),突变纯合子7例(7．95％),等位基因频率为0．1327。统计分析表明,上述等位基因多态性在该群体中均呈Hardy-Weinberg平衡分布;两种等位基因的突变频率在正常人和感染人群中的差异均无统计学意义。结论研究获得了中国四川彝族人群CCR5△32、CCR2-64I等位基因多态性资料,结果有助于综合评估中国人群对HIV-1感染的遗传易感性,同时为深入研究HIV-1抗性基因在中国不同民族的HIV感染及发病机制中的作用奠定基础。     

CCR5 antagonists: a new class of antiretrovirals

Inhibition of CCR5 co-receptor which is also a chemokine receptor, is a new way for inhibition of HIV-1 replication. Small antagonist molecules exert non competitive inhibition of the HIV co-receptor CCR5, which is essential for HIV entry. The CCR5 antagonists aplaviroc (GlaxoSmithKine), vicriviroc (Schering-Plough), and maraviroc (Pfizer) have reached phases III of clinical development. The development of aplaviroc was stopped because of its hepatotoxicity in some of the HIV-infected patients. In ACTG 5211 and MOTIVATE trials, treatment-experienced subjects who added respectively vicriviroc and maraviroc demonstrated substantially greater reductions in plasma HIV-1 RNA levels than those who received the placebo ; maraviroc currently having obtained European authorization. The place of this new class in the strategies of initial, switch or rescue treatment remains to be clarified. The limitations of the use of these small molecules depend on their mechanism of action : obligation for monitoring the evolution of coreceptor usage, risk of failure by emergence of pre-existing strains with CXCR4 (X4) tropism or by resistant strains with CCR5 tropism, potential risks related to blocking of the physiological functions of this chemokine receptor.     

CXCR4和CCR7趋化因子受体在宫颈癌中的表达

目的:探讨CXC族趋化因子受体4(CXCR4)和CC族趋化因子受体7(CCR7)在宫颈癌中的表达及意义。方法:选择2006年1月～2007年1月淮北市矿工总医院69例宫颈癌组织标本作为病例组,以20例正常宫颈组织作为观察组,应用免疫组织化学技术检测两组CXCR4和CCR7的表达,并分析不同临床病理特征中表达的差异。结果:观察组中CXCR4和CCR7的表达阳性率均明显高于对照组,差异均有统计学意义(P<0.01),CXCR4表达与宫颈癌患者的淋巴结转移密切相关,CXCR4表达与宫颈癌患者的FIGO分期、肿瘤大小、肌层浸润深度、组织病理类型、阴道浸润、子宫旁浸润无关。CCR7的表达与宫颈癌患者的FIGO分期、肿瘤大小、肌层浸润深度、淋巴结转移密切相关(P<0.01)。结论:宫颈癌中CXCR4和CCR7异常表达,二者在宫颈癌淋巴转移中发挥重要作用。     

人类免疫缺陷病毒1感染相关的基因多态性在中国汉族人群中的分布

目的　调查中国汉族人群中人类免疫缺陷病毒 1(HIV 1)感染相关的CCR5△ 32、CCR2 6 4I和SDF1 3’A等位基因突变频率和多态性的特点。方法　以 12 5 1例汉族人群为研究对象 ,应用PCR、PCR/RFLP(聚合酶链反应 /限制性片段长度多态性分析 )和DNA直接测序等方法进行检测 ,并用统计学方法进行分析。结果　发现中国汉族人群中存在CCR5△ 32等位基因突变 (均为杂合子基因型 ) ,突变频率为 0 .0 0 119,和西欧及美国白人相比 ,中国人群中CCR5△ 32基因突变频率极低 ,而CCR2 6 4I和SDF1 3’A基因突变频率相对较高 ,分别为 0 .2 0 0 2 3和 0 .2 872 3。结论　中国汉族人群的CCR5△ 32、CCR2 6 4I和SDF1 3’A等位基因的突变和多态性特点 ,具有一定的代表性。由于CCR5△ 32突变率低 ,中国汉族人群对性接触传播的HIV 1病毒 (R5 )株可能有较大的遗传易感性