Mapping an endometrial cancer tumor suppressor gene at 10q25 and development of a bacterial clone contig for the consensus deletion interval.
Mapping an endometrial cancer tumor suppressor gene at 10q25 and development of a bacterial clone contig for the consensus deletion interval.
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DOI:
10.1006/geno.1998.5399
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发表时间:
1998-08
期刊:
影响因子:
4.4
通讯作者:
Stacia Peiffer-Schneider;F. Noonan;D. Mutch;Sally B. Simpkins;T. Herzog;J. Rader;A. Elbendary;D. Gersell;K. Call;P. Goodfellow
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文献类型:
--
作者:
Stacia Peiffer-Schneider;F. Noonan;D. Mutch;Sally B. Simpkins;T. Herzog;J. Rader;A. Elbendary;D. Gersell;K. Call;P. Goodfellow
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 al., 1996, Br. J. Cancer 74: 1979-1983; S. Nagase et al.,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.