MOLECULAR GENETIC EVENTS IN LUNG CANCER

A. p16或多肿瘤抑制基因（MTS）1是同源的， 在从非小细胞肺癌患者建立的19/78（24%）细胞系中缺失 细胞肺癌相比，193个细胞系中的3个（3%）， 小细胞肺癌组（P <0.001），正常对照组（P <0.001 来自同一个病人的组织p16或多肿瘤抑制因子1 mRNA， 在具有纯合子的细胞系中未检测到蛋白质 删除。纯合子缺失存在于57例（30%）非- 研究的小细胞肺癌细胞系具有正常的视网膜母细胞瘤 蛋白 B。我们研究了6例乳腺癌患者TP 53基因突变的模式， 使用聚合酶链反应-单链 外显子5-8的构象多态性（PCR-SSCP）分析和 免疫组化分析p53蛋白过度表达。三 13个肿瘤（一个病人有三个原发性肿瘤）表现出移动性， 在SSCP分析上发生偏移，并通过 DNA测序免疫组化分析显示13个肿瘤中有7个（54%） 对于10%或更多的肿瘤具有中度至强烈的TP 53菌株 细胞这七个肿瘤中的三个也有TP 53突变。

A. The p16 or multiple tumor suppressor (MTS) 1 gene is homozygously deleted in 19/78 (24%) cell lines established from patients with non-small cell lung cancer compared to 3 of 193 (3%) cell lines established from patients with small cell lung cancer (p <0.001) but not n the normal tissue from the same patients. p16 or multiple tumor suppressor 1 mRNA and protein were not detectable among cell lines which have homozygous deletions. Homozygous deletions are present in 17 of the 57 (30%) non- small cell lung cancer cell lines studied which have normal retinoblastoma protein. B. We studied patterns of TP53 gene mutations in six patients with multiple primary cancers using polymerase chain reaction-single strand conformation polymorphisms (PCR-SSCP) analysis of exons 5-8 and overexpression of p53 protein by immunohistochemical analyses. Three of the 13 tumors (one patient had three primary tumors) exhibited a mobility shift on SSCP analysis and were confirmed to have missense mutations by DNA sequencing. Immunohistochemical analysis showed 7 of 13 (54%) tumors had moderate to strong straining for TP53 for 10% or more of the tumor cells. Three of these seven tumors also had TP53 mutations.