Latil A, Baron J C, Cussenot O, Fournier G, Soussi T, Boccon-Gibod L, Le Duc A, Rouëssé J, Lidereau R
Laboratoire d'oncogénétique, centre René-Huguenin, Saint-Cloud, France.
Bull Cancer. 1995 Jul;82(7):589-97.
Prostate cancer is one of the most common malignancies in men. Few authors have attempted to identify consistent genetic alterations at the molecular level in adenocarcinoma of the prostate, but those most frequently reported are loss of heterozygosity (LOH) involving chromosome arms 8p, 10q, 16q, and 18q and inactivation of the TP53 tumor suppressor gene. In order to determine if alterations frequently found in other adenocarcinomas (breast, ovarian, colorectal), including losses of genetic material from chromosome arms 1p, 3p, 7q, 8p, 11p, 17p, 17q, and 18q, are also involved in prostate cancer, we examined 20 localized early-stage prostate tumors. We detected no mutations of the TP53 gene. Allelic losses were found from 7q (33%), 8p (50%), 10q (20%), and 18q (33%). Furthermore, as the first step toward isolating tumor suppressor genes on 18q, we used six polymorphic markers and identified a small common deleted region between the chromosome 18 centromere and the D18S19 locus.
前列腺癌是男性中最常见的恶性肿瘤之一。很少有作者尝试在前列腺腺癌的分子水平上鉴定一致的基因改变,但最常报道的是涉及染色体臂8p、10q、16q和18q的杂合性缺失(LOH)以及TP53肿瘤抑制基因的失活。为了确定在其他腺癌(乳腺癌、卵巢癌、结直肠癌)中经常发现的改变,包括来自染色体臂1p、3p、7q、8p、11p、17p、17q和18q的遗传物质丢失,是否也与前列腺癌有关,我们检查了20例局限性早期前列腺肿瘤。我们未检测到TP53基因的突变。发现7q(33%)、8p(50%)、10q(20%)和18q(33%)存在等位基因缺失。此外,作为在18q上分离肿瘤抑制基因的第一步,我们使用了六个多态性标记,并在18号染色体着丝粒和D18S19位点之间鉴定出一个小的常见缺失区域。