全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

中国人群肝癌的易感基因研究

DOI: 10.1360/052011-581, PP. 785-789

Keywords: 肝癌,易感基因,全基因组关联研究,单核苷酸多态性

Full-Text   Cite this paper   Add to My Lib

Abstract:

以单核苷酸多态性(singlenucleotidepolymorphism,SNP)为遗传标记的遗传关联研究是近年来鉴定复杂疾病易感基因的主要策略之一.尤其是新近发展成熟的全基因组关联研究(genome-wideassociationstudy,GWAS),已被公认是行之有效的系统搜寻重大疾病易感基因的研究方法.军事医学科学院与国内同行合作开展的HBV相关肝癌GWAS结果表明,1p36.22的UBE4B-KIF1B-PGD区域是一个全新的肝癌易感基因区域,证明了遗传易感性在肝癌发生发展中的病因学意义.肝癌易感基因的发现,不仅为深入阐明肝癌的发生机制开辟了新的研究方向,而且为肝癌的风险预测和早期预警研究提供了理论依据;同时,也为后续开发新型的治疗药物奠定了基础.

References

[1]  31 Kryukov G V, Pennacchio L A, Sunyaev S R. Most rare missense alleles are deleterious in humans: implications for complex disease andassociation studies. Am J Hum Genet, 2007, 80: 727-739??
[2]  32 Biesecker L G. Exome sequencing makes medical genomics a reality. Nat Genet, 2010, 42: 13-14??
[3]  1 Gomaa A I, Khan S A, Toledano M B, et al. Hepatocellular carcinoma: Epidemiology, risk factors and pathogenesis. World J Gastroenterol,2008, 14: 4300-4308??
[4]  2 Nguyen V T, Law M G, Dore G J. Hepatitis B-related hepatocellular carcinoma: Epidemiological characteristics and disease burden. J Viral Hepat, 2009, 16: 453-463??
[5]  3 Farazi P A, DePinho R A. Hepatocellular carcinoma pathogenesis: From genes to environment. Nat Rev Cancer, 2006, 6: 674-687??
[6]  4 Yu M W, Chang H C, Liaw Y F, et al. Familial risk of hepatocellular carcinoma among chronic hepatitis B carriers and their relatives. J NatlCancer Inst, 2000, 92: 1159-1164
[7]  5 Krawczyk M, Müllenbach R, Weber S N, et al. Genome-wide association studies and genetic risk assessment of liver diseases. Nat RevGastroenterol Hepatol, 2010, 7: 669-681??
[8]  6 Altshuler D, Pollara V J, Cowles C R, et al. An SNP map of the human genome generated by reduced representation shotgun sequencing.Nature, 2000, 407: 513-516??
[9]  7 Kao J H, Chen P J, Chen D S. Recent advances in the research of hepatitis B virus-related hepatocellular carcinoma: Epidemiologic andmolecular biological aspects. Adv Cancer Res, 2010, 108: 21-72??
[10]  8 Kim Y J, Lee H S. Single nucleotide polymorphisms associated with hepatocellular carcinoma in patients with chronic hepatitis B virusinfection. Intervirology, 2005, 48: 10-15??
[11]  9 de Bakker P I, Yelensky R, Pe’er I, et al. Efficiency and power in genetic association studies. Nat Genet, 2005, 37: 1217-1223??
[12]  10 International HapMap Consortium. A haplotype map of the human genome. Nature, 2005, 437: 1299-1320??
[13]  11 International HapMap Consortium, Frazer K A, Ballinger D G, et al. A second generation human haplotype map of over 3.1 million SNPs.Nature, 2007, 449: 851-861
[14]  12 1000 Genomes Project Consortium, Durbin R M, Abecasis G R, et al. A map of human genome variation from population-scale sequencing.Nature, 2010, 467: 1061-1073??
[15]  13 Wellcome Trust Case Control Consortium. Genome-wide association study of 14,000 cases of seven common diseases and 3,000 sharedcontrols. Nature, 2007, 447: 661-678
[16]  14 Easton D F, Pooley K A, Dunning A M, et al. Genome-wide association study identifies novel breast cancer susceptibility loci. Nature, 2007,447: 1087-1093??
[17]  15 http: //www.genome.gov/26525384
[18]  16 Van Noorden R, Ledford H, Mann A. New year, new science. Nature, 2011, 469: 12??
[19]  17 Krawczyk M, Müllenbach R, Weber S N, et al. Genome-wide association studies and genetic risk assessment of liver diseases. Nat RevGastroenterol Hepatol, 2010, 7: 669-681??
[20]  18 Bagchi A, Mills A A. The quest for the 1p36 tumor suppressor. Cancer Res, 2008, 68: 2551-2556??
[21]  19 Li S P, Wang H Y, Li J Q, et al. Genome-wide analyses on loss of heterozygosity in hepatocellular carcinoma in Southern China. J Hepatol,2001, 34: 840-849
[22]  20 Bagchi A, Papazoglu C, Wu Y, et al. CHD5 is a tumor suppressor at human 1p36. Cell, 2007, 128: 459-475??
[23]  21 Munirajan A K, Ando K, Mukai A, et al. KIF1Bbeta functions as a haploinsufficient tumor suppressor gene mapped to chromosome 1p36.2by inducing apoptotic cell death. J Biol Chem, 2008, 283: 24426-24434
[24]  22 Schlisio S, Kenchappa R S, Vredeveld L C, et al. The kinesin KIF1Bbeta acts downstream from EglN3 to induce apoptosis and is a potential1p36 tumor suppressor. Genes Dev, 2008, 22: 884-893??
[25]  23 Hirokawa N, Takemura R. Biochemical and molecular characterization of diseases linked to motor proteins. Trends Biochem Sci, 2003, 28:558-565??
[26]  24 Yang H W, Chen Y Z, Takita J, et al. Genomic structure and mutational analysis of the human KIF1B gene which is homozygously deletedin neuroblastoma at chromosome 1p36.2. Oncogene, 2001, 20: 5075-5083
[27]  25 Yeh I T, Lenci R E, Qin Y, et al. A germline mutation of the KIF1B beta gene on 1p36 in a family with neural and nonneural tumors. HumGenet, 2008, 124: 279-285
[28]  26 Manolio T A. Genomewide association studies and assessment of the risk of disease. N Engl J Med, 2010, 363: 166-176??
[29]  27 Kraft P, Wacholder S, Cornelis M C, et al. Beyond odds ratios—communicating disease risk based on genetic profiles. Nat Rev Genet, 2009, 10:264-269??
[30]  28 Yuen M F, Tanaka Y, Fong D Y, et al. Independent risk factors and predictive score for the development of hepatocellular carcinoma inchronic hepatitis B. J Hepatol, 2009, 50: 80-88??
[31]  29 Wong V W, Chan S L, Mo F, et al. Clinical scoring system to predict hepatocellular carcinoma in chronic hepatitis B carriers. J Clin Oncol,2010, 28: 1660-1665??
[32]  30 Yang H I, Sherman M, Su J, et al. Nomograms for risk of hepatocellular carcinoma in patients with chronic hepatitis B virus infection. JClin Oncol, 2010, 28: 2437-2444??

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133