ALLELIC LOSS ON CHROMOSOME-17 IN HUMAN OVARIAN-CANCER

ALLELIC LOSS ON CHROMOSOME-17 IN HUMAN OVARIAN-CANCER
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DOI:
10.1002/ijc.2910540115
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发表时间:
1993-04-22
影响因子:
6.4
通讯作者:
XYNOS, F
XYNOS, F
中科院分区:
医学1区
文献类型:
--
作者:
PHILLIPS, N;ZIEGLER, M;XYNOS, F

文献摘要

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为寻找17号染色体上可能含有抑癌基因的共同缺失区,对27例卵巢癌和3例卵巢低恶性潜能肿瘤(LMP)进行了6个p臂和10个q臂位点的杂合性丢失(洛)检测。90%的肿瘤在一个或多个位点上有缺失。在p臂上,在17p13.3上存在单个接近共同的缺失区域(D17 S30/pYNZ 22)。1; 86%洛),一个低洛率的中间位点,和一个高洛率的位于17 p11.2的更近端位点(D17 S58/pEW 301; 82%洛)。在侵袭性较低的肿瘤中,D17 S30的洛不伴有p53的洛缺失。q臂在q21上的D17 S579(Mfd 188; 74%洛)处有一个高阶段癌的共同缺失区域,该位点与家族性乳腺卵巢癌综合征(BRCAI)位点紧密连锁。D17 S579在所有有信息的高阶段癌中丢失,在所有低阶段癌和LMP肿瘤中保留。可能存在至少2个肿瘤抑制基因,p臂上的早期作用基因和q臂上的基因参与肿瘤进展和转移。
In order to identify a common region of deletion on chromosome 17 potentially containing a tumor-suppressor gene, 27 ovarian carcinomas and 3 ovarian tumors of low malignant potential (LMP) were examined for loss of heterozygosity (LOH) at 6 p arm and 10 q arm loci. Ninety percent of all tumors had deletions at one or more loci. On the p arm, there was a single near-common region of deletion on 17p13.3 (D17S30/pYNZ22. 1; 86% LOH), an intervening locus with a low LOH rate, and a more proximal locus on 17p 11.2 (D17S58/pEW301; 82% LOH) with a high LOH rate. In less aggressive tumors, LOH at D17S30 was not accompanied by LOH at p53. The q arm had a common region of deletion for high-stage carcinoma at D17S579 (Mfd188; 74% LOH) on q21, a locus tightly linked to the familial breast-ovarian-cancer syndrome (BRCAI) locus. D17S579 was lost in all informative high-stage carcinomas and retained in all low-stage carcinomas and tumors of LMP. There may be at least 2 tumor-suppressor genes, an early-acting gene on the p arm and a gene on the q arm involved in tumor progression and metastasis.