p53 Pro72Arg多态与中国南北食管/贲门癌遗传易感性的关联研究
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
背景与目的
     食管癌(Esophageal Cancer,EC)、贲门癌(Cardicac Cancer,CC)是世界上常见的恶性肿瘤,发病率呈地区分布不均衡现象。虽然潮汕和太行山地区环境和人们的生活方式截然不同,但两地均为我国食管癌、贲门癌高发区;遗传易感性可能在食管癌、贲门癌发病中发挥了不可忽视的作用。p53基因与多种恶性肿瘤发生、发展密切相关,其第72位密码子存在单核苷酸多态性(p53 Pro72Arg,rs1042522),表达产生两种野生型p53蛋白。该多态在不同地域、种族中分布不同,与肿瘤易感性关系研究结果存在差异。本研究分别检测潮汕、太行山两高发区病例与对照人群p53 Pro72Arg基因型,观察该多态在两高发人群中的分布特征及与其它地区、人群比较的差异;比较分析等位基因及基因型频率在病例与对照中的分布差异,初步探讨p53 Pro72Arg多态与食管癌、贲门癌遗传易感性的关联。
     材料与方法
     标本来源:选取本课题组2002年以来收集的潮汕及太行山高发区人群外周血样。病例组来自当地医院确诊为食管癌或贲门癌的患者,对照组来自两地肿瘤高危人群普查的健康人。其中潮汕病例461例、对照499例;太行山病例421例、对照500例。所有病例及对照均为籍贯在两高发区的中国汉族人。
     实验方法:采用UltraPureTM基因组DNA快速提取试剂盒提取基因组DNA; PCR扩增包含p53 Pro72Arg位点的基因片段;应用高通量基于凝胶基因芯片的SNP分型技术检测p53 Pro72Arg基因型并测序验证。
     统计分析方法:将本研究结果与文献及公共数据库数据比较;分别以地域、性别、年龄、是否吸烟、有无消化道肿瘤家族史逐一分层进行病例-对照比较。采用卡方检验比较基因型及等位基因频率;非条件logistic回归计算发病风险(用性别、年龄校正)。
     结果
     1. p53 Pro72Arg等位基因在潮汕、太行山高危人群中分布差别无统计学意义(χ2 =0.67, P=0.41),与中国其他地区汉族及壮族比较差别无统计学意义;在两高危人群总体中的分布与世界其他地区、种族人群比较,差别具有显著性;
     2. p53 Pro72Arg基因型在两高发区人群食管癌病例组与高危人群对照组间总体分布差异具有显著性(P=0.03)。与携带Arg/Arg比较,Pro/Arg和(Pro/Arg+Pro/Pro)可增加两高发区人群食管癌的发病风险,校正比值比(odds ratio, OR)分别为1.37和1.38,95%置信区间(confidengce interval, CI)分别为(1.04-1.80)和(1.06-1.79);携带Pro/Pro可增加较低年龄段(≤50岁)人群食管癌的发病风险,OR值为1.89(95%CI=1.03-3.45)。未发现该多态与贲门癌发病风险明显相关。
     结论
     1.中国南北两大食管癌高发区潮汕地区及太行山区人群具有相同的p53 Pro72Arg多态遗传背景;且同我国其他汉族人群及少数民族壮族一致。
     2.两高发区高危人群中,携带p53 Pro72Arg Pro等位基因可能与食管癌易感性有关;携带Pro/Pro基因型尤可增加较低年龄人群的食管癌发病风险。
     3. p53 Pro72Arg Pro/Pro有可能作为中国食管癌低年龄段高危人群易感个体筛选的遗传学标记。
Background and Objective
     Esophageal cancer (EC) and Cardiac cancer (CC) are common cancers globally with great diversity in their incidences. Chaoshan littoral and Taihang mountains both belong to the six EC&CC high risk areas in China. Although the two areas are completely different in environment and people’s lifestyle, they are almost the same in incidences, family aggregation and pathology types of EC&CC. It is a clue show the hereditary susceptibility may play an important role in the carcinogenesis of EC&CC. Tumor suppressor gene p53 has a tight relationship with almost all kinds of human malignancies. p53 gene codon72 polymorphism (p53 Pro72Arg,rs1042522) results from a single base change (from CGC to CCC). The p53 Pro72Arg polymorphism genotype distribution has geographical and ethnical diverse. Previous studies have shown its association with many kinds of human cancer, however, its significance as a genetic susceptibility factor of cancer is still a matter of controversy. We detecte p53 Pro72Arg polymorphism genotype on cases and controls from Chaoshan littoral and Taihang mountains, observe the distribution of p53 Pro72Arg polymorphism genotype in the two high risk populations and compare our results with other population from other races or areas in the world and other areas in China using references and public data. And we also compare the results of cases with controls in order to investigate the relationship between Pro72Arg polymorphism and EC& CC susceptibility in the two high incidence areas.
     Materials and Methods
     Sample Resources: Peripheral blood samples from Chaoshan and Taihang had been collected by our group since 2002. Cases were the EC or CC patients from hospitals of these two areas including 461 samples from Chaoshan and 421 samples from Taihang. Controls were the healthy subjects who took part in the survey of EC high risk group in these two areas, including 499 samples from Chaoshan and 500 samples from Taihang. All the samples were Chinese Han nationality with their native place in these two high risk areas.
     Experiment Methods: Genomic DNA was extracted from peripheral blood leukocytes using the UltraPureTM DNA extraction kit (Beijing SBS Genetech C0.,Ltd.); PCR was conducted to amplificate DNA squencece including p53 codon 72. Primers were designed by Primer Primier 5.0 software. The genotypes were evaluated separately by DNA microarray using a method called gel-based microarray for SNP genotyping and a verification of sample drawing DNA sequencing was followed.
     Statistic Methods: Other data from references and public data were collected for comparing with our results. Area, sex, age, smoking habit and digestive tract tumor family history are used as layers in case-control study. Chi square test was used for the comparison of the frequencies of genotypes and alleles. Unconditional logistic regression was used to evaluate the risk of EC or CC (adjusted by sex and age).
     Results
     1. The p53 Pro72Arg allele frequence distribution in our control populations was identical(χ2 =0.67, P=0.41). When compared with other normal populations in different areas of China published in other studies including Zhuang nationality, the p53 Pro72Arg allele frequence distributions were identical too, while with other races in the world, the results showed some significant differences.
     2. The genotypes distribution of p53 Pro72Arg polymorphism was significantly different between EC patients and healthy subjects (P=0.03). When Compared with p53 Pro72Arg Arg/Arg genotype, carrying Pro/Arg and (Pro/Pro+Pro/Arg) genotype increased the risk of EC, the age, sex adjusted OR=1.37(95%CI 1.04-1.80)and 1.38(95%CI 1.06-1.79). Furthermore, the risk associated with the Pro/Pro variant genotype was more pronounced in younger patients (≤50 years) (OR, 1.89; 95% CI, 1.03-3.45).
     Conclusions
     1. The two high incidence areas of esophageal cancer and cardiac cancer—Chaoshan Littoral in south China and the Taihang Mountains in north China shared same p53 Pro72Arg genetic background. Compared with other reports, it’s identical in Han nationality from different parts of China and Zhuang nationality, too.
     2. Pro allele might be correlated with EC carcinogenesis in our objective population. The Pro/Pro genotype was significantly associated with the increased risk of EC in younger population.
     3. p53 Pro72Arg polymorphism Pro/Pro homozygote could be a biomarker associated with EC susceptibility.
引文
[1]. Parkin DM, Bray F, Ferlay J, Pisani P: Global cancer statistics, 2002. CA Cancer J Clin 2005, 55(2):74-108.
    [2]. Vizcaino AP, Moreno V, Lambert R, Parkin DM: Time trends incidence of both major histologic types of esophageal carcinomas in selected countries, 1973-1995. Int J Cancer 2002, 99(6):860-868.
    [3]. Pakin. Cancer incidence in Five Continent s [M] . Lyon : IARC Scientific Publication , 2002 :543-545.
    [4].苏敏,刘敏,李晓昀,张国红,杨合麟:潮汕地区南澳岛食管癌的遗传流行病学研究.中国首届国际食管癌学术会议暨第七届全国食管癌学术会议论文集2005:149-154.
    [5]. Li Dong Wang, QZ, Chung S. Yang: Esophageal and gastric cardia epithelial cell proliferation in northern Chinese subjects living in a high-incidence area. Journal of Cellular Biochemistry 1998, 67(S28-29 ):159 - 165.
    [6]. Lu JB, Yang WX, Zu SK, Chang QL, Sun XB, Lu WQ, Quan PL, Qin YM: Cancer mortality and mortality trends in Henan, China, 1974-1985. Cancer Detect Prev 1988, 13(3-4):167-173.
    [7]. Correa P: Precursors of gastric and esophageal cancer. Cancer 1982, 50(11 Suppl):2554-2565.
    [8]. Henan Medical College, Esophageal cancer [in Chinese]. Beijing:People’s Medical Publishing House 1983:39–63.
    [9]. Lin K, Cai S, Zhuang R. Analysis of the indicator of potential years of life lost of esophageal carcinoma in Nan’ao County [in Chinese].Chin J Cancer 1994;13:41–3.
    [10]. Su M, Liu M, Tian DP, Li XY, Zhang GH, Yang HL, Fan X, Huang HH, Gao YX: Temporal trends of esophageal cancer during 1995-2004 in Nanao Island, an extremely high-risk area in China. Eur J Epidemiol 2007, 22(1):43-48.
    [11].文焕然:中国古代文献中有关食管癌记载初探.三省一市食管癌协作会议资料1975。
    [12].林东昕:中国食管癌分子流行病学研究.中华流行病学杂志2003, 24 (10):939-943。
    [13]. Garavello W, Negri E, Talamini R, Levi F, Zambon P, Dal Maso L, Bosetti C, Franceschi S, La Vecchia C: Family history of cancer, its combination with smoking and drinking, and risk of squamous cell carcinoma of the esophagus. Cancer Epidemiol Biomarkers Prev 2005, 14(6):1390-1393.
    [14]. Yang CS: Research on esophageal cancer in China: a review. Cancer Res 1980, 40(8 Pt 1):2633-2644.
    [15]. Su M, Li XY, Tian DP, Wu MY, Wu XY, Lu SM, Huang HH, Li DR, Zheng ZC, Xu XH: Clinicopathologic analysis of esophageal and cardiac cancers and survey of molecular expression on tissue arrays in Chaoshan littoral of China. World J Gastroenterol 2004, 10(15):2163-2167.
    [16]. Li XY, Su M, Huang HH, Li H, Tian DP, Gao YX: mtDNA evidence: genetic background associated with related populations at high risk for esophageal cancer between Chaoshan and Taihang Mountain areas in China. Genomics 2007, 90(4):474-481.
    [17]. Zhang W, Bailey-Wilson JE, Li W, Wang X, Zhang C, Mao X, Liu Z, Zhou C, Wu M: Segregation analysis of esophageal cancer in a moderately high-incidence area of northern China. Am J Hum Genet 2000, 67(1):110-119.
    [18]. Lane DP: Cancer. p53, guardian of the genome. Nature 1992, 358(6381):15-16.
    [19]. Levine AJ: p53, the cellular gatekeeper for growth and division. Cell 1997, 88(3):323-331.
    [20]. Jin S, Levine AJ: The p53 functional circuit. J Cell Sci 2001, 114(Pt 23):4139-4140.
    [21]. Friend S: p53: a glimpse at the puppet behind the shadow play. Science 1994, 265(5170):334-335.
    [22]. Levine AJ, Momand J, Finlay CA: The p53 tumour suppressor gene. Nature 1991, 351(6326):453-456.
    [23]. Hollstein M, Sidransky D, Vogelstein B, Harris CC: p53 mutations in human cancers. Science 1991, 253(5015):49-53.
    [24]. Cho Y, Gorina S, Jeffrey PD, Pavletich NP: Crystal structure of a p53 tumor suppressor-DNA complex: understanding tumorigenic mutations. Science 1994,265(5170):346-355.
    [25]. Law JC, Strong LC, Chidambaram A, Ferrell RE: A germ line mutation in exon 5 of the p53 gene in an extended cancer family. Cancer Res 1991, 51(23 Pt 1):6385-6387.
    [26]. Thomas M, Kalita A, Labrecque S, et al. Two polymorphic variants of wild-type p53differ biochemically and biologicall.Mol Cell boil 1999, 19: 1092-1100.
    [27]. Pim D, Banks L: p53 polymorphic variants at codon 72 exert different effects on cell cycle progression. Int J Cancer 2004, 108(2):196-199.
    [28]. Dumont P, Leu JI, Della Pietra AC, 3rd, George DL, Murphy M: The codon 72 polymorphic variants of p53 have markedly different apoptotic potential. Nat Genet 2003, 33(3):357-365.
    [29]. Zhang ZW, Newcomb P, Hollowood A, Feakins R, Moorghen M, Storey A, Farthing MJ, Alderson D, Holly J: Age-associated increase of codon 72 Arginine p53 frequency in gastric cardia and non-cardia adenocarcinoma. Clin Cancer Res 2003, 9(6):2151-2156.
    [30]. Sakamuro D, Sabbatini P, White E, Prendergast GC: The polyproline region of p53 is required to activate apoptosis but not growth arrest. Oncogene 1997, 15(8):887-898.
    [31]. Shao Y, Tan W, Zhang S: P53 gene codon 72 polymorphism and risk of esophageal squamous cell carcinoma: a case/control study in a Chinese population. In: Dis Esophagus. vol. 21; 2008: 139-143.
    [32]. Chung W C LKM, Lee B I, et al.: P53 genetic polymorphism of gastric cancer in Korea Korean J Intern Med 2006, 21(1):28- 32.
    [33]. Buyru N, Tigli H, Dalay N: P53 codon 72 polymorphism in breast cancer. Oncol Rep 2003, 10(3):711-714.
    [34]. Fan R, Wu MT, Miller D, Wain JC, Kelsey KT, Wiencke JK, Christiani DC: The p53 codon 72 polymorphism and lung cancer risk. Cancer Epidemiol Biomarkers Prev 2000, 9(10):1037-1042.
    [35]. Garcia-Closas M, Kristensen V, Langerod A, Qi Y, Yeager M, Burdett L, Welch R, Lissowska J, Peplonska B, Brinton L et al: Common genetic variation in TP53 and its flanking genes, WDR79 and ATP1B2, and susceptibility to breast cancer. Int J Cancer 2007, 121(11):2532-2538.
    [36]. Huang XE, Hamajima N, Katsuda N, Matsuo K, Hirose K, Mizutani M, Iwata H, Miura S,Xiang J, Tokudome S et al: Association of p53 codon Arg72Pro and p73 G4C14-to-A4T14 at exon 2 genetic polymorphisms with the risk of Japanese breast cancer. Breast Cancer 2003, 10(4):307-311.
    [37]. Baynes C, Healey CS, Pooley KA, Scollen S, Luben RN, Thompson DJ, Pharoah PD, Easton DF, Ponder BA, Dunning AM: Common variants in the ATM, BRCA1, BRCA2, CHEK2 and TP53 cancer susceptibility genes are unlikely to increase breast cancer risk. Breast Cancer Res 2007, 9(2):R27.
    [38]. Ottman R: Gene-environment interaction: definitions and study designs. Prev Med 1996, 25(6):764-770.
    [39]. Ji M, Hou P, Li S, He N, Lu Z: Microarray-based method for genotyping of functional single nucleotide polymorphisms using dual-color fluorescence hybridization. Mutat Res 2004, 548(1-2):97-105.
    [40]. Hou P, Ji M, Li S, Lu Z: Microarray-based approach for high-throughput genotyping of single-nucleotide polymorphisms with layer-by-layer dual-color fluorescence hybridization. Clin Chem 2004, 50(10):1955-1957.
    [41]. Mechanic LE, Bowman ED, Welsh JA, Khan MA, Hagiwara N, Enewold L, Shields PG, Burdette L, Chanock S, Harris CC: Common genetic variation in TP53 is associated with lung cancer risk and prognosis in African Americans and somatic mutations in lung tumors. Cancer Epidemiol Biomarkers Prev 2007, 16(2):214-222.
    [42]. Tommiska J, Eerola H, Heinonen M, Salonen L, Kaare M, Tallila J, Ristimaki A, von Smitten K, Aittomaki K, Heikkila P et al: Breast cancer patients with p53 Pro72 homozygous genotype have a poorer survival. Clin Cancer Res 2005, 11(14):5098-5103.
    [43]. Tandle AT, Sanghvi V, Saranath D: Determination of p53 genotypes in oral cancer patients from India. Br J Cancer 2001, 84(6):739-742.
    [44]. Pierce LM, Sivaraman L, Chang W, Lum A, Donlon T, Seifried A, Wilkens LR, Lau AF, Le Marchand L: Relationships of TP53 codon 72 and HRAS1 polymorphisms with lung cancer risk in an ethnically diverse population. Cancer Epidemiol Biomarkers Prev 2000, 9(11):1199-1204.
    [45]. Yang Y, Xiao Z, Chen W, Sang H, Guan Y, Peng Y, Zhang D, Gu Z, Qian M, He G et al: Tumor suppressor gene TP53 is genetically associated with schizophrenia in the Chinesepopulation. Neurosci Lett 2004, 369(2):126-131.
    [46]. LI Jun ZQ-Q, WANG Ping: Relationship between p53 codon 72 polymorphism and liability of squamous cervical cancer in Han popula tion of Shanxi province: Case-control study. J FourthMilMed Univ 2006; 27 (16):1499-1501.
    [47]. Ma H, Hu Z, Zhai X, Wang S, Wang X, Qin J, Chen W, Jin G, Liu J, Gao J et al: Joint effects of single nucleotide polymorphisms in P53BP1 and p53 on breast cancer risk in a Chinese population. Carcinogenesis 2006, 27(4):766-771.
    [48]. Xi Mingrong HY, Yang Xiaoyun,Hou Minmin,and Cao Zeyi: The preliminary Study on the Relationship between HPV-associated Cervical Cancer and p53 Condon 72 Polymorphism in Sichuan Province. The Chinese-German Journal of Clinical Oncology 2003, 2(3):160-163.
    [49].卓阳,高建华,赵永忠等:瘢痕疙瘩发病风险与p53基因第72位密码子多态性的关系.中华整形外科杂志2005, 21(3):201-203。
    [50]. Lee JM, Lee YC, Yang SY, Shi WL, Lee CJ, Luh SP, Chen CJ, Hsieh CY, Wu MT: Genetic polymorphisms of p53 and GSTP1,but not NAT2,are associated with susceptibility to squamous-cell carcinoma of the esophagus. Int J Cancer 2000, 89(5):458-464.
    [51].彭涛,严律南,李家荃等:广西原发性肝细胞癌与p53基因72密码子单核苷酸多态性密切相关.中华外科杂志2004, 42(5):313-314。
    [52]. Cao YY, Ge H, Chen LQ, Chen ZF, Wen DG, Li Y, Zhang JH: Correlation of 53BP1 and p53 polymorphisms to susceptibility to esophageal squamous cell carcinoma and gastric cardiac adenocarcinoma. Ai Zheng 2007, 26(10):1052-1057.
    [53]. Weston A, Ling-Cawley HM, Caporaso NE, Bowman ED, Hoover RN, Trump BF, Harris CC: Determination of the allelic frequencies of an L-myc and a p53 polymorphism in human lung cancer. Carcinogenesis 1994, 15(4):583-587.
    [54]. Shepherd T, Tolbert D, Benedetti J, Macdonald J, Stemmermann G, Wiest J, DeVoe G, Miller MA, Wang J, Noffsinger A et al: Alterations in exon 4 of the p53 gene in gastric carcinoma. Gastroenterology 2000, 118(6):1039-1044.
    [55]. Beckman G, Birgander R, Sjalander A, Saha N, Holmberg PA, Kivela A, Beckman L: Is p53 polymorphism maintained by natural selection? Hum Hered 1994, 44(5):266-270.
    [56].黄挺.潮汕文化源流.广东高等教育出版社. ISBN7-5361-2076-1.1999年第一版:P1-71。
    [57].黄赞发.潮汕先民与先贤.汕头大学出版社.ISBN7-81036-406-5.2000年第一版:P1-30。
    [58].韩小友,张永贞,闫秀梅等:食管癌和贲门癌遗传特征研究.中华流行病学杂志2002, 23(4):285。
    [59]. Walker KK, Levine AJ: Identification of a novel p53 functional domain that is necessary for efficient growth suppression. Proc Natl Acad Sci U S A 1996, 93(26):15335-15340.
    [60]. Koushik A, Tranah GJ, Ma J, Stampfer MJ, Sesso HD, Fuchs CS, Giovannucci EL, Hunter DJ: p53 Arg72Pro polymorphism and risk of colorectal adenoma and cancer. Int J Cancer 2006, 119(8):1863-1868.
    [61]. Hong WS, Hong SI, Lee DS, Son Y: Effect of non-tumor cell contamination on detection of p53 gene mutations in human gastric cancer cells by polymerase chain reaction single-strand conformation polymorphism analysis. Korean J Intern Med 1994, 9(1):20-24.
    [62]. Peixoto Guimaraes D, Hsin Lu S, Snijders P, Wilmotte R, Herrero R, Lenoir G, Montesano R, Meijer CJ, Walboomers J, Hainaut P: Absence of association between HPV DNA, TP53 codon 72 polymorphism, and risk of oesophageal cancer in a high-risk area of China. Cancer Lett 2001, 162(2):231-235.
    [63]. Lu XM, Zhang YM, Lin RY, Liang XH, Zhang YL, Wang X, Zhang Y, Wang Y, Wen H: p53 polymorphism in human papillomavirus-associated Kazakh's esophageal cancer in Xinjiang, China. World J Gastroenterol 2004, 10(19):2775-2778.
    [64]. Kawaguchi H, Ohno S, Araki K, Miyazaki M, Saeki H, Watanabe M, Tanaka S, Sugimachi K: p53 polymorphism in human papillomavirus-associated esophageal cancer. Cancer Res 2000, 60(11):2753-2755.
    [65]. Yang W, Zhang Y, Tian X, Ning T, Ke Y: p53 Codon 72 polymorphism and the risk of esophageal squamous cell carcinoma. Mol Carcinog 2008, 47(2):100-104.
    [66]. Cao B, Tian X, Li Y, Jiang P, Ning T, Xing H, Zhao Y, Zhang C, Shi X, Chen D et al: LMP7/TAP2 gene polymorphisms and HPV infection in esophageal carcinoma patients from a high incidence area in China. Carcinogenesis 2005, 26(7):1280-1284.
    [67]. Syrjanen KJ: HPV infections and oesophageal cancer. J Clin Pathol 2002,55(10):721-728.
    [68].管立学,李相州,胡德宏,高丽,王敬先,张培良,王瑞丽: P53基因CD72Arg/Pro多态性与贲门腺癌生物学行为的研究.世界肿瘤杂志2004, 3(2):145-147,177。
    [69]. Bloom BS, Iannacone RC: Internet availability of prescription pharmaceuticals to the public. Ann Intern Med 1999, 131(11):830-833.
    [70]. Vaughan TL, Davis S, Kristal A, Thomas DB: Obesity, alcohol, and tobacco as risk factors for cancers of the esophagus and gastric cardia: adenocarcinoma versus squamous cell carcinoma. Cancer Epidemiol Biomarkers Prev 1995, 4(2):85-92.
    [1]. Thomas M, Kalita A, Labrecque S, Pim D, Banks L, Matlashewski G: Two polymorphic variants of wild-type p53 differ biochemically and biologically. Mol Cell Biol 1999, 19(2):1092-1100.
    [2]. Thomas M, Kalita A, Labrecque S, et al. Two polymorphic variants of wild-type p53differ biochemically and biologicall.Mol Cell boil 1999,19: 1092-1100.
    [3]. Pim D, Banks L: p53 polymorphic variants at codon 72 exert different effects on cell cycle progression. Int J Cancer 2004, 108(2):196-199.
    [4]. Dumont P, Leu JI, Della Pietra AC, 3rd, George DL, Murphy M: The codon 72 polymorphic variants of p53 have markedly different apoptotic potential. Nat Genet 2003, 33(3):357-365.
    [5].王瑞,李琰,张健慧:中国人食管癌及肺癌发病风险与p53基因多态性.中华肿瘤杂志2003, 25( 4):365-367。
    [6]. Nagpal JK, Sahni S, Das BR: P53 codon 72 polymorphism and susceptibility to development of human papilloma virus-associated cervical cancer in Indian women. Eur J Clin Invest 2002, 32(12):943-948.
    [7]. Shao Y, Tan W, Zhang S: P53 gene codon 72 polymorphism and risk of esophageal squamous cell carcinoma: a case/control study in a Chinese population. In: Dis Esophagus. vol. 21; 2008: 139-143.
    [8]. Lee JM, Lee YC, Yang SY, Shi WL, Lee CJ, Luh SP, Chen CJ, Hsieh CY, Wu MT: Genetic polymorphisms of p53 and GSTP1,but not NAT2,are associated with susceptibility to squamous-cell carcinoma of the esophagus. Int J Cancer 2000, 89(5):458-464.
    [9]. Yang W, Zhang Y, Tian X, Ning T, Ke Y: p53 Codon 72 polymorphism and the risk of esophageal squamous cell carcinoma. Mol Carcinog 2008, 47(2):100-104. 47
    [10]. Kawaguchi H, Ohno S, Araki K, Miyazaki M, Saeki H, Watanabe M, Tanaka S, Sugimachi K: p53 polymorphism in human papillomavirus-associated esophageal cancer. Cancer Res 2000, 60(11):2753-2755.
    [11]. Pantelis A, Pantelis D, Ruemmele P, Hartmann A, Hofstaedter F, Buettner R, Bootz F, Stoehr R: p53 Codon 72 polymorphism, loss of heterozygosity and high-risk human papillomavirus infection in a low-incidence German esophageal squamous cell carcinoma patient cohort. Oncol Rep 2007, 17(5):1243-1248.
    [12]. Peixoto Guimaraes D, Hsin Lu S, Snijders P, Wilmotte R, Herrero R, Lenoir G, Montesano R, Meijer CJ, Walboomers J, Hainaut P: Absence of association between HPV DNA, TP53 codon 72 polymorphism, and risk of oesophageal cancer in a high-risk area of China. Cancer Lett 2001, 162(2):231-235.
    [13].管立学,李相州,胡德宏,高丽,王敬先,张培良,王瑞丽: P53基因CD72Arg/Pro多态性与贲门腺癌生物学行为的研究.世界肿瘤杂志2004, 3(2):145-147,177。
    [14]. Cao YY, Ge H, Chen LQ, Chen ZF, Wen DG, Li Y, Zhang JH: Correlation of 53BP1 and p53 polymorphisms to susceptibility to esophageal squamous cell carcinoma and gastric cardiac adenocarcinoma. Ai Zheng 2007, 26(10):1052-1057.
    [15]. Shepherd T, Tolbert D, Benedetti J, Macdonald J, Stemmermann G, Wiest J, DeVoe G, Miller MA, Wang J, Noffsinger A et al: Alterations in exon 4 of the p53 gene in gastric carcinoma. Gastroenterology 2000, 118(6):1039-1044.
    [16]. Zhang ZW, Newcomb P, Hollowood A, Feakins R, Moorghen M, Storey A, Farthing MJ, Alderson D, Holly J: Age-associated increase of codon 72 Arginine p53 frequency in gastric cardia and non-cardia adenocarcinoma. Clin Cancer Res 2003, 9(6):2151-2156.
    [17]. Lin K, Shen W, Shen Z, Cai S, Wu Y: Estimation of the potential for nitrosation and its inhibition in subjects from high- and low-risk areas for esophageal cancer in southern China. Int J Cancer 2003, 107(6):891-895.
    [18]. Zhang L, Xing D, He Z, Lin D: [p53 gene codon 72 polymorphism and susceptibility to esophageal squamous cell carcinoma in a Chinese population]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi 2002, 19(1):10-13.
    [19]. Chung W C LKM, Lee B I, et al.: P53 genetic polymorphism of gastric cancer in Korea Korean J Intern Med 2006, 21(1):28- 32.
    [20]. Wu MT, Chen MC, Wu DC: Influences of lifestyle habits and p53 codon 72 and p21 codon 31 polymorphisms on gastric cancer risk in Taiwan. Cancer Lett 2004, 205(1):61-68.
    [21]. Jung B, Smith EJ, Doctolero RT, Gervaz P, Alonso JC, Miyai K, Keku T, Sandler RS, Carethers JM: Influence of target gene mutations on survival, stage and histology in sporadic microsatellite unstable colon cancers. Int J Cancer 2006, 118(10):2509-2513.
    [22].朱忠政,朱冠山,吴孟超等: p53基因第72密码子多态性与中国人肝细胞癌遗传易感性的相关性.中华医学遗传学杂志2005, 22( 6):632-635。
    [23]. Yu MW, Yang SY, Chiu YH, Chiang YC, Liaw YF, Chen CJ: A p53 genetic polymorphism as a modulator of hepatocellular carcinoma risk in relation to chronic liver disease, familial tendency, and cigarette smoking in hepatitis B carriers. Hepatology 1999, 29(3):697-702.
    [24]. Leveri M, Gritti C, Rossi L, Zavaglia C, Civardi E, Mondelli MU, De Silvestri A, Silini EM: Codon 72 polymorphism of P53 gene does not affect the risk of cirrhosis and hepatocarcinoma in HCV-infected patients. Cancer Lett 2004, 208(1):75-79.
    [25]. Anzola M, Cuevas N, Lopez-Martinez M, Saiz A, Burgos JJ, de Pancorbo MM: Frequent loss of p53 codon 72 Pro variant in hepatitis C virus-positive carriers with hepatocellular carcinoma. Cancer Lett 2003, 193(2):199-205.
    [26]. Buyru N, Tigli H, Dalay N: P53 codon 72 polymorphism in breast cancer. Oncol Rep 2003, 10(3):711-714.
    [27]. Garcia-Closas M, Kristensen V, Langerod A, Qi Y, Yeager M, Burdett L, Welch R, Lissowska J, Peplonska B, Brinton L et al: Common genetic variation in TP53 and its flanking genes, WDR79 and ATP1B2, and susceptibility to breast cancer. Int J Cancer 2007, 121(11):2532-2538.
    [28]. Huang XE, Hamajima N, Katsuda N, Matsuo K, Hirose K, Mizutani M, Iwata H, Miura S, Xiang J, Tokudome S et al: Association of p53 codon Arg72Pro and p73 G4C14-to-A4T14 at exon 2 genetic polymorphisms with the risk of Japanese breast cancer. Breast Cancer 2003, 10(4):307-311.
    [29]. Baynes C, Healey CS, Pooley KA, Scollen S, Luben RN, Thompson DJ, Pharoah PD, Easton DF, Ponder BA, Dunning AM: Common variants in the ATM, BRCA1, BRCA2,CHEK2 and TP53 cancer susceptibility genes are unlikely to increase breast cancer risk. Breast Cancer Res 2007, 9(2):R27.
    [30]. Sifuentes Alvarez A, Reyes Romero M: [Risk factors for cervico-uterine cancer associated to HPV: p53 codon 72 polymorphism in women attending hospital care]. Ginecol Obstet Mex 2003, 71:12-15.
    [31]. Makni H, Franco EL, Kaiano J, Villa LL, Labrecque S, Dudley R, Storey A, Matlashewski G: P53 polymorphism in codon 72 and risk of human papillomavirus-induced cervical cancer: effect of inter-laboratory variation. Int J Cancer 2000, 87(4):528-533.
    [32]. Cenci M, French D, Pisani T, Alderisio M, Lombardi AM, Marchese R, Colelli F, Vecchione A: p53 polymorphism at codon 72 is not a risk factor for cervical carcinogenesis in central Italy. Anticancer Res 2003, 23(2B):1385-1387.
    [33]. Bhattacharya P, Duttagupta C, Sengupta S: Proline homozygosity in codon 72 of p53: a risk genotype for human papillomavirus related cervical cancer in Indian women. Cancer Lett 2002, 188(1-2):207-211.
    [34].郑兴征,杨安强,潘晓琳,郑莉莉,周秋媛,李新敏,王晓凌,严丽华,李洪安: p53 Arg72Pro多态性与新疆维吾尔族和汉族妇女宫颈癌的相关性.中华病理学杂志2007, 36(8):511-515。
    [35]. Pegoraro RJ, Moodley M, Rom L, Chetty R, Moodley J: P53 codon 72 polymorphism and BRCA 1 and 2 mutations in ovarian epithelial malignancies in black South Africans. Int J Gynecol Cancer 2003, 13(4):444-449.
    [36]. Hogdall EV, Hogdall CK, Christensen L, Glud E, Blaakaer J, Bock JE, Vuust J, Norgaard-Pedersen B, Kjaer SK: Distribution of p53 codon 72 polymorphisms in ovarian tumour patients and their prognostic significance in ovarian cancer patients. Anticancer Res 2002, 22(3):1859-1864.
    [37].康山,张健慧等: p53基因多态性与卵巢上皮性癌发病风险的关系.中华妇产科杂志2004, 39(11):754-758。
    [38]. Fan R, Wu MT, Miller D, Wain JC, Kelsey KT, Wiencke JK, Christiani DC: The p53 codon 72 polymorphism and lung cancer risk. Cancer Epidemiol Biomarkers Prev 2000, 9(10):1037-1042.
    [39]. Irarrazabal CE, Rojas C, Aracena R, Marquez C, Gil L: Chilean pilot study on the risk of lung cancer associated with codon 72 polymorphism in the gene of protein p53. Toxicol Lett 2003, 144(1):69-76.
    [40]. Papadakis ED, Soulitzis N, Spandidos DA: Association of p53 codon 72 polymorphism with advanced lung cancer: the Arg allele is preferentially retained in tumours arising in Arg/Pro germline heterozygotes. Br J Cancer 2002, 87(9):1013-1018.
    [41]. Tagawa M, Murata M, Kimura H: Prognostic value of mutations and a germ line polymorphism of the p53 gene in non-small cell lung carcinoma: association with clinicopathological features. Cancer Lett 1998, 128(1):93-99.
    [42]. Pierce LM, Sivaraman L, Chang W, Lum A, Donlon T, Seifried A, Wilkens LR, Lau AF, Le Marchand L: Relationships of TP53 codon 72 and HRAS1 polymorphisms with lung cancer risk in an ethnically diverse population. Cancer Epidemiol Biomarkers Prev 2000, 9(11):1199-1204.
    [43]. Matakidou A, El Galta R, Webb EL, Rudd MF, Bridle H, Eisen T, Houlston RS: Lack of evidence that p53 Arg72Pro influences lung cancer prognosis: an analysis of survival in 619 female patients. Lung Cancer 2007, 57(2):207-212.
    [44]. Xu Y, Yao L, Ouyang T, Li J, Wang T, Fan Z, Lin B, Lu Y, Xie Y: p53 Codon 72 polymorphism predicts the pathologic response to neoadjuvant chemotherapy in patients with breast cancer. Clin Cancer Res 2005, 11(20):7328-7333.
    [45]. Tommiska J, Eerola H, Heinonen M, Salonen L, Kaare M, Tallila J, Ristimaki A, von Smitten K, Aittomaki K, Heikkila P et al: Breast cancer patients with p53 Pro72 homozygous genotype have a poorer survival. Clin Cancer Res 2005, 11(14):5098-5103.
    [46]. Santos AM, Sousa H, Portela C, Pereira D, Pinto D, Catarino R, Rodrigues C, Araujo AP, Lopes C, Medeiros R: TP53 and P21 polymorphisms: response to cisplatinum/paclitaxel-based chemotherapy in ovarian cancer. Biochem Biophys Res Commun 2006, 340(1):256-262.
    [47]. Sullivan A, Syed N, Gasco M, Bergamaschi D, Trigiante G, Attard M, Hiller L, Farrell PJ, Smith P, Lu X et al: Polymorphism in wild-type p53 modulates response to chemotherapy in vitro and in vivo. Oncogene 2004, 23(19):3328-3337.
    [48]. Wang YC, Chen CY, Chen SK, Chang YY, Lin P: p53 codon 72 polymorphism inTaiwanese lung cancer patients: association with lung cancer susceptibility and prognosis. Clin Cancer Res 1999, 5(1):129-134.
    [49]. Olschwang S, Laurent-Puig P, Vassal A, Salmon RJ, Thomas G: Characterization of a frequent polymorphism in the coding sequence of the Tp53 gene in colonic cancer patients and a control population. Hum Genet 1991, 86(4):369-370.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700