Papillary urothelial hyperplasia is a clonal precursor to papillary transitional cell bladder cancer

Papillary urothelial hyperplasia is a clonal precursor to papillary transitional cell bladder cancer
复制标题

DOI:
10.1002/1097-0215(20001120)89:6
复制
发表时间:
2000-11-20
影响因子:
6.4
通讯作者:
Sidransky, D
Sidransky, D
中科院分区:
医学1区
文献类型:
--
作者:
Chow, NH;Cairns, P;Sidransky, D

文献摘要

被引文献

相似文献

乳头状瘤和乳头状增生(PH)被认为是膀胱乳头状癌的前驱病变。我们在9条染色体上的17个微卫星标记上检测了15个PH病变和4个乳头状瘤的杂合性缺失(LOH)。15例PHS中有8例(53%)为克隆性,至少有1个微卫星标记存在杂合性缺失。相比之下,在测试的标记中,没有一个乳头状瘤显示出任何基因变化。在PH中,染色体9q丢失最多(4/15),其次是9p和18q(n=2),其次是8p、10q、11p和17p(n=1)。此外,2个增生性病变仅在9q出现杂合性缺失,证实了染色体9q上的等位基因Tass是膀胱癌进展的最早事件之一。在1例患者中,在PH和复发的移行细胞癌之间观察到相同的杂合性缺失模式。我们的分子数据表明,至少有一部分PHS代表膀胱癌前病变,这些病变随后发展为乳头状膀胱癌。此外,染色体臂9q可能含有一个肿瘤抑制基因(S),该基因在人类膀胱癌发生的早期阶段就失活了。内部J·癌症(Pred.昂科尔,)89:5 14-518,2000。(C)Wiley-Liss公司
Papilloma and papillary hyperplasia (PH) have been proposed to be the putative precursor lesions of papillary transitional-cell carcinoma of the urinary bladder. We examined 15 PH lesions and 4 papillomas for loss of heterozygosity (LOH) at 17 microsatellite markers on 9 chromosomal arms. Eight of 15 (53%) PHs were clonal, demonstrating LOH of at least 1 microsatellite marker. In contrast, none of the papillomas showed any genetic changes among the markers tested. In PH, chromosomal arm 9q was the most frequently lost (4/15), followed by 9p and 18q (n = 2) and, less frequently, 8p, 10q, 11p and 17p(n = 1). Furthermore, 2 hyperplastic lesions demonstrated LOH at 9q only, confirming the notion that allelic tass on chromosomal arm 9q is among the earliest events in bladder-cancer progression. In I patient, identical LOH patterns were observed between PH and a recurrent transitional-cell carcinoma. Our molecular data demonstrate that at least a proportion of PHs represent pre cancerous lesions of the bladder that subsequently progress to papillary bladder cancer. Moreover, chromosomal arm 9q may harbor a tumor-suppressor gene(s) inactivated in the earliest stages of human bladder tumorigenesis. Int. J. Cancer (Pred. Oncol,) 89:5 14-518, 2000. (C) Wiley-Liss, Inc.