中华预防医学杂志
中華預防醫學雜誌
중화예방의학잡지
CHINESE JOURNAL OF
2015年
5期
419-423
,共5页
潘欢欢%苏成豪%林勇%牛建军
潘歡歡%囌成豪%林勇%牛建軍
반환환%소성호%림용%우건군
多态性,单核苷酸%肝肿瘤%分子流行病学%驱动蛋白家族成员1B%病例对照研究
多態性,單覈苷痠%肝腫瘤%分子流行病學%驅動蛋白傢族成員1B%病例對照研究
다태성,단핵감산%간종류%분자류행병학%구동단백가족성원1B%병례대조연구
Polymorphism,single nucleotide%Liver neoplasms%Molecular epidemiology%KIF1B%Case-control study
目的：分析厦门市驱动蛋白家族成员1B（KIF1B）基因rs17401966位点多态性与原发性肝细胞癌（HCC）遗传易感性的关系。方法2011年1月至2014年10月在厦门市两家三甲医院，采用个体匹配病例-对照研究设计。病例组纳入标准：调查期间根据HCC诊断依据被首次确诊为HCC、≥18岁、现住址与调查地属同一区（县）级范围、无任何其他肿瘤史的患者；排除标准：患有其他肝脏疾病，患有HCC以外的肿瘤，患有自身免疫性肝炎或中毒性肝炎，拒绝调查或由于病危状态而无法接受调查者。对照组纳入标准：与病例组患者年龄相差不超过3岁，同性别，同期在同院接受健康普查，来自同一区（县），体检合格者；排除标准：患有肝脏疾病及既往肿瘤病史者。病例组376例，对照组403例，各采集晨起空腹静脉血5 ml，进行血细胞分离及基因分型。采用χ2检验和t检验比较病例组、对照组的基本情况，采用多因素logistic回归模型分析KIF1B基因rs17401966位点多态性与HCC遗传易感性的关系。结果病例组的年龄为（61.7±12.8）岁，对照组为（60.6±12.7）岁（t=1.15，P=0.251）。病例组有肿瘤家族史比例、HBV感染阳性率分别为28.7%（108/376）、26.9%（101/376），均高于对照组[15.9%（64/403）、2.7%（11/403）]（χ2分别为18.65、92.02，P值均<0.001）。rs17401966 GA、GG基因型HCC遗传易感性分别是AA基因型的0.64（0.46~0.89）、0.54（0.32~0.92）倍，G等位基因HCC遗传易感性是A等位基因的0.76（0.60~0.96）倍。HBsAg阳性者中，rs17401966 GG基因型HCC遗传易感性是AA基因型的0.12（0.02~0.75）倍，rs17401966 G等位基因HCC遗传易感性是A等位基因的0.38（0.15~0.98）倍；HBsAg阴性者中，rs17401966位点多态性与HCC遗传易感性相关性无统计学意义，与A等位基因相比，G等位基因HCC遗传易感性的OR（95%CI）值为0.79（0.62~1.01）。结论 KIF1B基因rs17401966 GG和GA基因型、G等位基因的HCC遗传易感性较低。
目的：分析廈門市驅動蛋白傢族成員1B（KIF1B）基因rs17401966位點多態性與原髮性肝細胞癌（HCC）遺傳易感性的關繫。方法2011年1月至2014年10月在廈門市兩傢三甲醫院，採用箇體匹配病例-對照研究設計。病例組納入標準：調查期間根據HCC診斷依據被首次確診為HCC、≥18歲、現住阯與調查地屬同一區（縣）級範圍、無任何其他腫瘤史的患者；排除標準：患有其他肝髒疾病，患有HCC以外的腫瘤，患有自身免疫性肝炎或中毒性肝炎，拒絕調查或由于病危狀態而無法接受調查者。對照組納入標準：與病例組患者年齡相差不超過3歲，同性彆，同期在同院接受健康普查，來自同一區（縣），體檢閤格者；排除標準：患有肝髒疾病及既往腫瘤病史者。病例組376例，對照組403例，各採集晨起空腹靜脈血5 ml，進行血細胞分離及基因分型。採用χ2檢驗和t檢驗比較病例組、對照組的基本情況，採用多因素logistic迴歸模型分析KIF1B基因rs17401966位點多態性與HCC遺傳易感性的關繫。結果病例組的年齡為（61.7±12.8）歲，對照組為（60.6±12.7）歲（t=1.15，P=0.251）。病例組有腫瘤傢族史比例、HBV感染暘性率分彆為28.7%（108/376）、26.9%（101/376），均高于對照組[15.9%（64/403）、2.7%（11/403）]（χ2分彆為18.65、92.02，P值均<0.001）。rs17401966 GA、GG基因型HCC遺傳易感性分彆是AA基因型的0.64（0.46~0.89）、0.54（0.32~0.92）倍，G等位基因HCC遺傳易感性是A等位基因的0.76（0.60~0.96）倍。HBsAg暘性者中，rs17401966 GG基因型HCC遺傳易感性是AA基因型的0.12（0.02~0.75）倍，rs17401966 G等位基因HCC遺傳易感性是A等位基因的0.38（0.15~0.98）倍；HBsAg陰性者中，rs17401966位點多態性與HCC遺傳易感性相關性無統計學意義，與A等位基因相比，G等位基因HCC遺傳易感性的OR（95%CI）值為0.79（0.62~1.01）。結論 KIF1B基因rs17401966 GG和GA基因型、G等位基因的HCC遺傳易感性較低。
목적：분석하문시구동단백가족성원1B（KIF1B）기인rs17401966위점다태성여원발성간세포암（HCC）유전역감성적관계。방법2011년1월지2014년10월재하문시량가삼갑의원，채용개체필배병례-대조연구설계。병례조납입표준：조사기간근거HCC진단의거피수차학진위HCC、≥18세、현주지여조사지속동일구（현）급범위、무임하기타종류사적환자；배제표준：환유기타간장질병，환유HCC이외적종류，환유자신면역성간염혹중독성간염，거절조사혹유우병위상태이무법접수조사자。대조조납입표준：여병례조환자년령상차불초과3세，동성별，동기재동원접수건강보사，래자동일구（현），체검합격자；배제표준：환유간장질병급기왕종류병사자。병례조376례，대조조403례，각채집신기공복정맥혈5 ml，진행혈세포분리급기인분형。채용χ2검험화t검험비교병례조、대조조적기본정황，채용다인소logistic회귀모형분석KIF1B기인rs17401966위점다태성여HCC유전역감성적관계。결과병례조적년령위（61.7±12.8）세，대조조위（60.6±12.7）세（t=1.15，P=0.251）。병례조유종류가족사비례、HBV감염양성솔분별위28.7%（108/376）、26.9%（101/376），균고우대조조[15.9%（64/403）、2.7%（11/403）]（χ2분별위18.65、92.02，P치균<0.001）。rs17401966 GA、GG기인형HCC유전역감성분별시AA기인형적0.64（0.46~0.89）、0.54（0.32~0.92）배，G등위기인HCC유전역감성시A등위기인적0.76（0.60~0.96）배。HBsAg양성자중，rs17401966 GG기인형HCC유전역감성시AA기인형적0.12（0.02~0.75）배，rs17401966 G등위기인HCC유전역감성시A등위기인적0.38（0.15~0.98）배；HBsAg음성자중，rs17401966위점다태성여HCC유전역감성상관성무통계학의의，여A등위기인상비，G등위기인HCC유전역감성적OR（95%CI）치위0.79（0.62~1.01）。결론 KIF1B기인rs17401966 GG화GA기인형、G등위기인적HCC유전역감성교저。
Objective To study the relationship between SNP rs17401966 at the KIF1B gene and the genetic susceptibility to Hepatocellular carcinoma(HCC).Methods All study objects were recruited from two Grade A hospitals of Amoy from January 2011 to October 2014.They were surveyed in individual matching case-control study . Accepting criterias in the cases:HCC was first diagnosed based on diagnostic basis during the investigations, over 18 years old, present addresses were as same as surveyed areas in the district (county) level range, no past history of cancers;Exclusion criterias:patients with other liver diseases. The tumor patients without HCC, patients with autoimmune hepatitis or toxic hepatitis, patients who refused to be investigated or too ill to be investigated. Accepting criterias in the controls:the control who passed the physical examination matched the case in ages (no more than 3 years old) ,sex , health screening in the same hospital over the same period and district (county);Exclusion criterias: people with liver disease or any history of cancers. This study consisted of 376 HCC patients and 403 controls, 5 ml morning fasting venous blood of all subjects were obtained to isolate cells and distribute genotype. The differences in general information between cases and controls were tested by χ2 test and t-test. The association between SNP rs17401966 and the risk of developing HCC were assessed by using the multiple factors logistic regression. Results The mean age and standard deviation for case and control groups were (61.7 ± 12.8) years and (60.6 ± 12.7) years(t=1.15,P=0.251), respectively. The proportion of family history of cancer[28.7%(108/376)]and the HBsAg positive rate [26.9%(101/376)] in case group were higher than these in control group [15.9%(64/403),2.7%(11/403)](χ2=18.65,92.02,P<0.001). In HBsAg carriers, GG genotype genetic susceptibility to HCC is 0.12(0.02-0.75)times for AA genotype, and G allele susceptibility to HCC is 0.38 (0.15-0.98) times for A allelc. In HBsAg negative group,it showed no statistical significance in the relationship between SNP rs17401966 and susceptibility to HCC,and compared with the A allele,the risk for HCC of G allele is 0.79(0.62-1.01).Conclusion The results demonstrated that the presence of the GG genotype,the GA genotype and the G allele at rs17401966 of the KIF1B gene might decrease the risk for HCC.
