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

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