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非小细胞肺癌3p染色体多区域杂合性缺失检测的研究 被引量：3

Research of loss of heterozygaity on chromosome 3p in non-small cell lung cancer
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摘要 背景与目的已有研究表明,3号染色体短臂(3p)等位基因的杂合性缺失(loss of heterozygaity,LOH)是非小细胞肺癌(non-small cell lung cancer,NSCLC)发生中常见且早期发生的分子生物学改变,可以造成该染色体所包含的多种抑癌基因的失活。本研究的目的是探讨人3pLOH在非小细胞肺癌(NSCLC)临床检测中的意义。方法采用荧光定量PCR方法分别对32例非小细胞肺癌肿瘤组织及8例非恶性肿瘤肺组织和外周血有核细胞进行3p位点LOH检测,对试验结果进行非参数检验。结果32例肺癌标本中LOH联合检出率为78.125%,外周血有核细胞LOH联合检出率为65.625%,其中肺癌组织标本各位点LOH检出率分别为43.75%(3p25)、56.25%(3p14)、56.25%(3p21.3),外周血有核细胞检出率分别为18.75%、31.25%、50%,相比对照组结果具有差异,组织及外周血有核细胞联合检出率高于各位点单纯检出率,差别具有统计学意义;同一患者的肺癌肿瘤组织与外周血有核细胞3p基因LOH联合检测结果存在一致性。结论肺癌组织及外周血有核细胞3p基因LOH检测对于肺癌的无创诊断具有较好的临床意义,且多位点联合检测有助于提高检测的敏感性。 Background and objective It has been proven that allelic loss of chromosome region 3p occurs early and frequently in non-small-cell lung cancer, and numerous tumor suppressor genes at this locus may be targets of inactivation. The aim of this study is to investigate the relationship between loss of heterozygosity (LOH) of the allele genes on 3p and the diagnostic value of NSCLC. Methods A total of 32 NSCLC samples and 8 tissues of the pulmonary benign disease have been analyzed by fluorescent quantitative P...
作者 梅新宇 孙余婕 徐美青 马冬春 魏大中 田界勇 任自学
机构地区 安徽医科大学附属省立医院胸外科 安徽医科大学附属省立医院临床检验中心
出处 《中国肺癌杂志》 CAS 2008年第4期534-537,共4页 Chinese Journal of Lung Cancer
基金 安徽省自然科学基金(No.050430703)资助~~
关键词 肺肿瘤 等位基因位点杂合性缺失 有核细胞 Lung neoplasms Loss of heterozygosity Nucleated cell
分类号 R734.2 [医药卫生—肿瘤]
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参考文献9

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同被引文献23

  • 1Zabarovsky ER, Lerman MI, Minna JD. Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers. Oncogene, 2002, 21 (45): 6915-6935.
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  • 5Wang Y, Yu Z, Wang T, et al. Identification of epigenetic aberrant promoter methylation of RASSFIA in serum DNA and its clinicopathological significance in lung cancer. Lung Cancer, 2007, 56(2): 289-294.
  • 6Tomizawa Y, lijima H, Nomoto T, et al. Clinicopathological significance ofaberrant methylation of RARbeta2 at 3p24, RASSFIA at 3p21.3, and FHIT at 3p14.2 in patients with non-small cell lung cancer. Lung Cancer, 2004, 46(3): 305-312.
  • 7Geng X, Wang F, Zhang L, et al. Loss of heterozygosity combined with promoter hypermethylation, the main mechanism of human MutL Homolog (hMLH1) gene inactivation in non-small cell lung cancer in a Chinese population. Tumori, 2009, 95 (4): 488-494.
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  • 9Kwong J, Lee JY, Wong KK, et al. Candidate tumor-suppressor gene DLEC1 is frequently downregulated by promoter hypermethylation and histone hypoacetylation in human epithelial ovarian cancer. Neoplasia, 2006, 8(4): 268-278.
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中国肺癌杂志
2008年 第4期

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