Massion Pierre P, Taflan Peter M, Jamshedur Rahman S M, Yildiz Pinar, Shyr Yu, Edgerton Mary E, Westfall Matthew D, Roberts John R, Pietenpol Jennifer A, Carbone David P, Gonzalez Adriana L
Department of Medicine, The Vanderbilt Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, 2200 Pierce Avenue, PRB 640, Nashville, Tennessee 37232-6838, USA.
Cancer Res. 2003 Nov 1;63(21):7113-21.
The fight against lung cancer is greatly compromised by the lack of effective early detection strategies. Genomic abnormalities and specifically the amplification of chromosomal region 3q26-3qter in lung cancer represent a major signature of neoplastic transformation. Here, we address the significance of p53 homologue p63 mapping to 3q27 in lung tumorigenesis. We analyzed p63 gene copy number (CN) by fluorescence in situ hybridization and expression by immunohistochemistry in tissue microarrays of 217 non-small cell lung cancers (NSCLCs) and correlated them with survival. We additionally characterized our findings in a subset of 24 NSCLCs by reverse transcription-PCR and Western blotting. We analyzed p63 CN and protein expression in 41 preinvasive squamous lesions. The p63 genomic sequence was amplified in 88% of squamous carcinomas, in 42% of large cell carcinomas, and in 11% of adenocarcinomas of the lung. The predominant splice variant of p63 expressed was DeltaNp63alpha. Western analyses revealed DeltaNp63alpha expression in normal bronchus and squamous carcinomas but not in normal lung or in adenocarcinomas. Furthermore, p63genomic amplification and protein staining intensity associated with better survival. We found a significant increase in CN in preinvasive lesions graded severe dysplasia or higher. Our data demonstrate that there is early and frequent genomic amplification of p63 in the development of squamous carcinoma of the lung and that patients with NSCLC showing amplification and overexpression of p63 have prolonged survival. These observations suggest that p63 genomic amplification has an early role in lung tumorigenesis and deserves additional evaluation as a biomarker for lung cancer progression.
缺乏有效的早期检测策略严重阻碍了肺癌的防治工作。基因组异常,尤其是肺癌中染色体区域3q26 - 3qter的扩增,是肿瘤转化的主要特征。在此,我们探讨了定位于3q27的p53同源物p63在肺癌发生中的意义。我们通过荧光原位杂交分析了217例非小细胞肺癌(NSCLC)组织芯片中p63基因拷贝数(CN),并通过免疫组织化学分析了其表达情况,并将这些结果与生存率相关联。我们还通过逆转录PCR和蛋白质印迹法对24例NSCLC亚组的研究结果进行了进一步表征。我们分析了41例浸润前鳞状病变中的p63 CN和蛋白表达。p63基因组序列在88%的肺鳞状细胞癌、42%的大细胞癌和11%的肺腺癌中发生扩增。p63表达的主要剪接变体是DeltaNp63alpha。蛋白质印迹分析显示DeltaNp63alpha在正常支气管和鳞状细胞癌中表达,但在正常肺组织或腺癌中不表达。此外,p63基因组扩增和蛋白染色强度与更好的生存率相关。我们发现,在重度发育异常或更高级别的浸润前病变中,CN显著增加。我们的数据表明,在肺鳞状细胞癌的发生过程中,p63存在早期且频繁的基因组扩增,并且显示p63扩增和过表达的NSCLC患者生存期延长。这些观察结果表明,p63基因组扩增在肺癌发生中起早期作用,值得作为肺癌进展的生物标志物进行进一步评估。