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原发性肺癌肿瘤组织染色体变异比较基因组杂交分析 被引量:1

Chromosome Analysis of Primary Lung Cancer Using Comparative Genomic Hybridization
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摘要 目的:分析原发性肺癌肿瘤组织染色体异常变化,了解肺癌组织染色体畸变规律。方法:应用比较基因组杂交技术分析55例原发性肺癌患者肿瘤组织染色体。结果:原发性肺鳞癌常见染色体扩增区是2q、5p、11q、22q,常见缺失区是1p、4q、5q、6q、8p、9p、10q、11p、13q、18q、21q。肺腺癌常见扩增区是5p、8q、11q,常见缺失区是10p、19。腺鳞癌、肺泡细胞癌、小细胞癌等染色体变化各有不同。结论:原发性肺癌存在广泛的遗传物质不平衡现象,不同病理分型的染色体基因扩增和缺失可能是其发生、发展的基础。 Objective: To analyze the unbalanced state of hereditary material of squamous cell carcinoma, adenocarcinoma and other types of lung cancer and to provide data for study of the mechanism of lung cancer. Methods: Fifty-five patients suffered from lung cancer were included in this study. The technology of comparative genomic hybridization (CGH) was used. Results: The common extension regions of squamous carcinoma were 2q, 5p, 11q and 22q. The common deletion regions were lp, 4q, 5q, 6q, 8p, 9p, 10q, 11p, 13q, 18q and 21q. The common extension regions of adenocarcinoma were 5p, 8q and 11q. The common deletion regions were 10p and 19. Conclusion: The hereditary material of lung cancer is unbalanced. The extension and deletion of chromatosome are the base of the occurrence of different lung cancer.
出处 《中国肿瘤临床》 CAS CSCD 北大核心 2006年第7期395-398,共4页 Chinese Journal of Clinical Oncology
基金 国家自然科学基金面上项目资助(编号:30270591)
关键词 原发性肺癌 比较基因组杂交 染色体 Primary lung cancer Comparative hybridization Chromosome
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参考文献10

  • 1Shan Z,Parker T,Wiest JS.Identifying novel homozygous deletions by microsatellite analysis and characterization of tumor suppressor candidate 1 gene,TUSC1,on chromosome 9p in human lung cancer[J].Oncogene,2004,23(39):6612~6620
  • 2Tchinda J,Dijkhuizen T,Vlies PP,et al.Translocations involving 6p22 in acute myeloid leukaemia at relapse:breakpoint characterization using microarray-based comparative genomic hybridization[J].BrJ Haematol,2004,126(4):495~500
  • 3Park SY,Kim YH,Chun YH,et al.Chromosomal aberrations in Korean nonsmall cell lung carcinomas:degenerate oligonucleotide primed polymerase chain reaction comparative genomic hybridization studies[J].Cancer Genet Cytogenet,2004,152 (2):153~157
  • 4Roque L,Rodrigues R,Martins G,et al.Comparative genomic hybridization analysis of a pleuropulmonary blastoma[J].Cancer Genet Cytogenet,2004,149(1):58~62
  • 5Chujo M,Noguchi T,Miura T,et al.Comparative genomic hybridization analysis detected frequent overrepresentation of chromosome 3q in squamous cell carcinoma of the lung[J].Lung Cancer,2002,38(1):23~29
  • 6Zhou X,Kemp BL,Khuri FR,et al.Prognostic implication of microsatellite alteration profiles in early-stage non-small cell lung cancer[J].Clin Cancer Res,2000,6(2):559~565
  • 7Rosell R,Pifarre A,Monzo M,et al.Reduced survival in patients with stage-I non-small-cell lung cancer associated with DNA-replication errors[J].Int J Cancer,1997,74(3):330~334
  • 8Petersen S,Aninat MM,Schluns K,et al.Chromosomal alterations in the clonal evolution to the metastatic stage of squamous cell carcinomas of the lung[J].BrJ Cancer,2000,82(1):65~73
  • 9Lott ST,Chandler DS,Curley SA,et al.High frequency loss of heterozygosity in von Hippel-Lindau (VHL)-associated and sporadic pancreatic islet cell tumors:evidence for a stepwise mechanism for malignant conversion in VHL tumorigenesis[J].Cancer Res,2002,62(7):1952~1955
  • 10Kamada M,Suzuki K,Kato Y,et al.von Hippel-Lindau protein promotes the assembly of actin and vinculin and inhibits cell motility[J].Cancer Res,2001,61(10):4184~4189

同被引文献16

  • 1Kallioniemi A, Kallioniemi OP, Sudar D, et al. Comparative genomic hybridization for molecular cytogenetic analysis of solid tumors [J]. Science,1992, 258(5083):818-821.
  • 2Han S, Semba S, Abe T, et al. Infrequent somatic mutations of the p73 gene in various human cancers [ J ] . Eur J Surg Oncol,1999, 25(2): 194-198.
  • 3Henderson LJ, Coe BP, Lee E, et al. Genomic and gene expression profiling of minute alterations of chromosome arm 1p in small cell lung carcinoma cells [J]. B J Cancer, 2005, 92(8):1553-1560.
  • 4Dang TP, Eichenberger S, Gonzalez A, et al. Constitutive activation of Notch3 inhibits terminal epithelial differentiation in lungs of transgenic mice [J]. Oncogene, 2003, 22(13):1988-1997.
  • 5Haruki N, Kawaguchi KS, Eichenberger S, et al. Dominantnegative Notch3 receptor inhibits mitogen-activated protein kinase pathway and the growth of human lung cancers [ J ] . Cancer Res, 2005, 65(9):3555-3561.
  • 6Daniel VC, Peacock CD, Watkins DN. Developmental signalling pathways in lung cancer [ J ] . Respirology, 2006,11(3):234-240.
  • 7Cathie G, Jennifer C, Jonathan J, et ah Involvement of multiple developmental genes on chromosome 1p in lung tumorigenesis [ J ] . Hum Mol Genet, 2005, 14(4):475-482.
  • 8Yokoi S, Yasui K, Saito-Ohara F, et al. A novel target gene SKP2, within the 5p13 amplication that is frequently detected in small cell lung cancers [J]. Am J Pathol, 2002, 161(1):207-216.
  • 9Yokoi S, Yasui K, Mori M, et al. Amplification and overexpression of SKP2 are associated with metastasis of non- small cell lung cancers to lymph nodes [ J ] . Am J Pathol,2004, 165(1):175-180.
  • 10Yang G, Ayala G, De Marzo A, et al. Elevated Skp2 protein expression in human prostate cancer: association with loss of the cyclin-dependent kinase inhibitor p27 and PTEN and with reduced recurrence-free survival [ J ] . Clin Cancer Res, 2002, 8(11):3419-3426.

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