Assignment of E-cadherin (CDH1) and KSP-cadherin (CDH16) to chromosome 16q22.1 by radiation hybrid mapping.

D Baudry, C Jeanpierre
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引用次数: 1

Abstract

Cadherins are cellular adhesion molecules. Since disturbance of intracellular adhesion is important for invasion and metastasis of tumor cells, cadherins are considered prime candidates for tumor suppressor genes. A variety of solid tumors show loss of heterozygosity for the long arm of chromosome 16 (Austruy et al., 1995; Driouch et al., 1997), which is indicative of the potential localization of tumor suppressor genes. The homophilic cell adhesion molecule E-cadherin (CDH1) has been involved in gastric (Becker et al., 1994), breast (Berx et al., 1995) and gynecologic carcinomas (Risinger et al., 1994). This report refined localization of: (1) E-cadherin (CDH1), previously mapped to 16q22.1 on a panel of somatic cell hybrids (Callen et al., 1995) and between WI-9392 and D16S496 on the Genebridge 4 radiation hybrid panel (Hunstman et al., 1998); (2) KSP-cadherin (CDH16), previously mapped to chromosome 16q21-proximal 16q22 by in situ hybridization (Thomson et al., 1998). A more precise localization of these two genes in a publicly available radiation hybrid map will facilitate marker selection for linkage and loss of heterozygosity analyses. Materials and methods
E-cadherin (CDH1)和KSP-cadherin (CDH16)在16q22.1染色体上的定位
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