Mapping an endometrial cancer tumor suppressor gene at 10q25 and development of a bacterial clone contig for the consensus deletion interval

被引:26
作者
Peiffer-Schneider, S
Noonan, FC
Mutch, DG
Simpkins, SB
Herzog, T
Rader, J
Elbendary, A
Gersell, DJ
Call, K
Goodfellow, PJ
机构
[1] Washington Univ, Sch Med, Dept Surg, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Dept Gynecol & Obstet, St Louis, MO 63110 USA
[3] Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA
[4] Genome Therapeut Corp, Waltham, MA 02154 USA
关键词
D O I
10.1006/geno.1998.5399
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Frequent loss of chromosome 10q sequences in endometrial cancers suggests the involvement of a tumor suppressor gene. Previous loss-of-heterozygosity (LOH) studies have pointed to the 10q25-q26 region as the likely site of a tumor suppressor involved in endometrial tumorigenesis (S. L. Peiffer et al,, 1995, Cancer Res. 55: 1922-1926; S. Nagase et nl,. 1996, Br. J. Cancer 74: 1979-1983; 1997, Cancer Res. 57: 1630-1633). In an attempt to define further the localization of a tumor suppressor gene at 10q25, we screened a panel of 123 endometrioid adenocarcinomas for loss of heterozygosity of 10q25.3 sequences. Forty-three (35%) revealed LOH at one or more loci, The observed patterns of allelic loss define a minimum consensus region of deletion between D10S221 and D10S610, A sequence-ready bacterial clone contig and a long-range restriction map for a 1-Mb interval spanning the deletion region were developed as the first step in experiments directed toward the discovery the 10q25 tumor suppressor. (C) 1998 Academic Press.
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页码:9 / 16
页数:8
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