據(jù)國外媒體報道來自中國,、新加坡和美國的專家組成的研究小組,，對中國南方的10000名志愿者進行了基因方面的研究,。有一半的志愿者被診斷出患有鼻咽癌，另外一半比較健康,。在患有鼻咽癌的一組志愿者中,，三個基因發(fā)生了變異。
這三個基因分別名為TNFRSF19,、MDSIEVI1 和 CDKN2A/2B,，這些基因與白血病有聯(lián)系。研究報告稱,，該項發(fā)現(xiàn)極為重要,，他們可以詳細了解鼻咽癌的分子路徑，解釋該病為何在中國南方非常流行,，特別是在廣東省,。
在這部分區(qū)域，每10萬人中就會有25人得鼻咽癌,，比世界其它地區(qū)平均高出25倍,。只有在阿拉斯加州、非洲北部部分地區(qū)以及東南亞有相似的高發(fā)病率,。
該項研究由位于廣州的中山大學癌癥研究中心和新加坡基因組協(xié)會聯(lián)合開展,。
鼻和喉部癌癥有遺傳因素。而吸煙是主要的病因,。在鼻咽癌患者中,，食用鹽漬的食物，以及高巴爾二氏病毒的食物的人居多,。
（生物谷Bioon.com）
關于GWAS
Nucleic Acids Res.：基于通路的GWAS數(shù)據(jù)網(wǎng)絡分析平臺開發(fā)成功
高燒的GWAS——生物谷盤點2009
AJHG：中國人基因差異研究
JGV：發(fā)現(xiàn)鼻咽癌血清診斷新標記
生物谷推薦原文出處：
Nature Genetics doi:10.1038/ng.601
A genome-wide association study of nasopharyngeal carcinoma identifies three new susceptibility loci
Jin-Xin Bei1,2,9, Yi Li3,9, Wei-Hua Jia1,2, Bing-Jian Feng1,2,4, Gangqiao Zhou5, Li-Zhen Chen1,2, Qi-Sheng Feng1,2, Hui-Qi Low3, Hongxing Zhang5, Fuchu He5, E Shyong Tai6,7, Tiebang Kang1,2, Edison T Liu8, Jianjun Liu1,3,10 & Yi-Xin Zeng1,2,10
To identify genetic susceptibility loci for nasopharyngeal carcinoma (NPC), a genome-wide association study was performed using 464,328 autosomal SNPs in 1,583 NPC affected individuals (cases) and 1,894 controls of southern Chinese descent. The top 49 SNPs from the genome-wide association study were genotyped in 3,507 cases and 3,063 controls of southern Chinese descent from Guangdong and Guangxi. The seven supportive SNPs were further confirmed by transmission disequilibrium test analysis in 279 trios from Guangdong. We identified three new susceptibility loci, TNFRSF19 on 13q12 (rs9510787, Pcombined = 1.53 × 10?9, odds ratio (OR) = 1.20), MDS1-EVI1 on 3q26 (rs6774494, Pcombined = 1.34 × 10?8, OR = 0.84) and the CDKN2A-CDKN2B gene cluster on 9p21 (rs1412829, Pcombined = 4.84 × 10?7, OR = 0.78). Furthermore, we confirmed the role of HLA by revealing independent associations at rs2860580 (Pcombined = 4.88 × 10?67, OR = 0.58), rs2894207 (Pcombined = 3.42 × 10?33, OR = 0.61) and rs28421666 (Pcombined = 2.49 × 10?18, OR = 0.67). Our findings provide new insights into the pathogenesis of NPC by highlighting the involvement of pathways related to TNFRSF19 and MDS1-EVI1 in addition to HLA molecules.
