Papp J, Csokay B, Bosze P, Zalay Z, Toth J, Ponder B, Olah E
National Institute of Oncology, Department of Molecular Biology, Budapest, Hungary.
Br J Cancer. 1996 Nov;74(10):1592-7. doi: 10.1038/bjc.1996.594.
Using a panel of ten polymorphic markers, we examined the frequency of loss of heterozygosity (LOH) on chromosome 17 in 55 sporadic ovarian tumours. LOH on 17p and 17q was observed to be 50% and 62% respectively. LOH at D17S5 was detected in 24/36 (67%) of malignant cases and in 19/43 (44%) at TP53; the marker D17S855 intragenic to the BRCA1 gene showed allele loss in 50% (20/40) cases. The data presented here suggest that loss of the whole chromosome 17 is a relatively frequent event (30%) in ovarian carcinomas and this observation is especially frequent for serous, transitional cell and anaplastic histological subtypes. Mucinous and endometrioid ovarian tumours showed only short interstitial deletions (4/11, 36%). The overall frequency of the short deletions was relatively low (7/43, 16%) in our panel of carcinomas. Amplification of c-erbB-2/neu oncogene was detected in 32% (11/34) of the carcinomas tested; the gene was amplified only in those histological subtypes in which high incidence of LOH on chromosome 17 was observed, and was associated with advanced stages of the disease. We conclude that different histological types of tumour may have different aetiological mechanisms, and tumour-suppressor genes on chromosome 17 might be associated specifically with serous and transitional cell ovarian carcinomas.
我们使用一组十个多态性标记,检测了55例散发卵巢肿瘤中17号染色体杂合性缺失(LOH)的频率。观察到17p和17q上的LOH分别为50%和62%。在24/36(67%)的恶性病例中检测到D17S5处存在LOH,在TP53处为19/43(44%);位于BRCA1基因内的标记D17S855在50%(20/40)的病例中显示等位基因缺失。此处呈现的数据表明,在卵巢癌中,整条17号染色体的缺失是一个相对常见的事件(30%),并且这一现象在浆液性、移行细胞和间变性组织学亚型中尤为常见。黏液性和子宫内膜样卵巢肿瘤仅显示短的间质缺失(4/11,36%)。在我们的癌组织样本中,短缺失的总体频率相对较低(7/43,16%)。在32%(11/34)检测的癌组织中检测到c-erbB-2/neu癌基因的扩增;该基因仅在那些观察到17号染色体上LOH发生率高的组织学亚型中扩增,并且与疾病的晚期阶段相关。我们得出结论,不同组织学类型的肿瘤可能具有不同的病因机制,并且17号染色体上的肿瘤抑制基因可能与浆液性和移行细胞性卵巢癌特异性相关。