
Epithelial‐cadherin Gene Is Not Mutated in Ductal Carcinomas of the Breast
Author(s) -
Kashiwaba Masahiro,
Tamura Gen,
Suzuki Yasushi,
Maesawa Chihaya,
Ogasawara Satoshi,
Sakata Ken,
Satodate Ryoichi
Publication year - 1995
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1995.tb03020.x
Subject(s) - loss of heterozygosity , cadherin , biology , cancer research , gene , tumor suppressor gene , exon , pathology , ductal carcinoma , breast cancer , cancer , carcinogenesis , cell , genetics , allele , medicine
We investigated mutations of the epithelial (E)‐cadherin gene and loss of heterozygosity (LOH) at flanking loci using three microsatellite markers on the long arm of chromosome 16 in 25 ductal carcinomas of the breast. Expression of E‐cadherin was also investigated immunohistochemically. No mutations were detected in exons 6 through 9 of the E‐cadherin gene. LOH was observed more frequently (42%) at D16S402 (16q‐ter) than at D16S421 (16q22.3‐q23.1) (17%), which is located near the E‐cadherin gene. Expression of E‐cadherin was observed at the cell borders in 92% (11/12) of the tumors examined. The absence of mutations in the E‐cadherin gene and its conserved expression suggest that inactivation of E‐cadherin does not contribute significantly to the invasion or metastatic potential of ductal carcinomas of the breast. Furthermore, the high frequency of LOH at 16q‐ter suggests the existence of another tumor suppressor gene which may play a crucial role in the genesis of ductal carcinomas of the breast.