Rao J Y, Apple S K, Jin Y, Lin S, Nieberg R K, Hirtschowitz S L
Department of Pathology and Laboratory Medicine, University of California at Los Angeles Medical Center, 90095-1732, USA.
Cancer Epidemiol Biomarkers Prev. 2000 Feb;9(2):175-9.
The oncogene c-myc is a key regulator of cell cycle progression (from G1 to S phase). The amplification of c-myc can either induce cell proliferation or apoptosis. As a part of our ongoing effort to develop methods for multiple tumor marker analysis, this study was carried out to determine whether biomarkers such as c-myc amplification could be analyzed on genetic materials collected from archival fine-needle aspiration (FNA) smears. A novel comparative PCR analysis was used to analyze c-myc amplification semiquantitatively. Genomic DNA was prepared using cells obtained from archival FNA materials that had undergone quantitative fluorescence image analysis (QFIA) for other biomarkers. Of the 72 cases selected from 1995 for this study, 53 had an adequate amount of DNA for analysis. A novel comparative PCR analysis was used to analyze c-myc amplification quantitatively. For each batch of experiments, DNA from the high c-myc expressing cells, HL-60, and DNA from the low expressing cells, K562, were served as positive and negative controls, respectively. c-myc amplification was observed in 16 (94.1%) of 17 malignant lesions, 5 (41.7%) of 12 proliferative breast diseases with nuclear atypia, and 4 (16.7%) of 24 other benign lesions (fibroadenoma or fibrocystic disease). The overall difference of c-myc expression among these groups was highly significant by chi2 analysis (P = 0.0002). We conclude that multiple phenotypic markers and genotypic markers may be combined in a risk assessment biomarker profile on small FNA samples that can be obtained on multiple occasions relatively noninvasively from the patient. The results of this study suggest that c-myc amplification may be a biomarker of breast cancer risk. However, additional large, prospective studies are needed to confirm the current observation.
癌基因c-myc是细胞周期进程(从G1期到S期)的关键调节因子。c-myc的扩增既可以诱导细胞增殖,也可以诱导细胞凋亡。作为我们正在进行的开发多种肿瘤标志物分析方法工作的一部分,本研究旨在确定诸如c-myc扩增等生物标志物是否可以在从存档细针穿刺(FNA)涂片收集的遗传材料上进行分析。采用一种新型比较PCR分析对c-myc扩增进行半定量分析。使用从已对其他生物标志物进行定量荧光图像分析(QFIA)的存档FNA材料中获得的细胞制备基因组DNA。在本研究从1995年选取的72例病例中,53例有足够量的DNA用于分析。采用一种新型比较PCR分析对c-myc扩增进行定量分析。对于每一批实验,分别将高表达c-myc的细胞HL-60的DNA和低表达细胞K562的DNA用作阳性和阴性对照。在17例恶性病变中的16例(94.1%)、12例有核异型性的增殖性乳腺疾病中的5例(41.7%)以及24例其他良性病变(纤维腺瘤或纤维囊性疾病)中的4例(16.7%)观察到c-myc扩增。通过卡方分析,这些组之间c-myc表达的总体差异具有高度显著性(P = 0.0002)。我们得出结论,多种表型标志物和基因型标志物可以组合在一个风险评估生物标志物谱中,用于从小的FNA样本中进行分析,这些样本可以相对无创地从患者身上多次获取。本研究结果表明,c-myc扩增可能是乳腺癌风险的一个生物标志物。然而,需要更多大规模的前瞻性研究来证实目前的观察结果。