Differential loss of E-cadherin expression in infiltrating ductal and lobular breast carcinomas.

The epithelial-specific cell-cell adhesion molecule E-cadherin was analyzed immunohistochemically on tissue sections of 89 human primary infiltrating breast carcinomas, using monoclonal antibodies 6F9 (for cryostat sections) and 5H9 (for cryostat and paraffin sections). The tumors included 41 well and moderately differentiated infiltrating ductal carcinomas (IDCs) most of which (78%) showed strong linear staining at the cell borders at a level, as high as luminal cells of normal mammary glands. The 26 poorly differentiated, more highly malignant IDCs examined also were all positive for E-cadherin, although a higher proportion of them (54%) showed reduced staining, which was heterogeneous and dotted over the cell borders.

Stimulation of urokinase-type plasminogen activator expression by blockage of E-cadherin-dependent cell-cell adhesion.

Decreased expression of the cell-cell adhesion molecule, E-cadherin, promotes dedifferentiation and invasiveness of human carcinoma cells, whereas this process can be reversed by reexpression of E-cadherin (U. H. Frixen et al.

Cell adhesion in invasion and metastasis.

Metastatic cells exhibit considerable flexibility in their adhesive interactions with other cells or components of the extracellular matrix. This review will describe the involvement of specific adhesion receptors, extracellular matrix molecules and cell dissociating cytokines in the metastatic cascade. We will particularly focus on disturbance of intercellular adhesion as a prerequisite for the release of invasive cells from carcinomas.

E-cadherin expression in squamous cell carcinomas of head and neck: inverse correlation with tumor dedifferentiation and lymph node metastasis.

Tissue sections of 32 squamous cell carcinomas (SCCs) of the head and neck were investigated for the expression of the epithelium-specific cell adhesion molecule E-cadherin. We found that E-cadherin expression is inversely correlated both with the loss of differentiation of the tumor and with lymph node metastasis. The well-differentiated SCCs expressed E-cadherin, often as strongly as the normal stratified epithelium (12 cases were tested); the moderately differentiated SCCs expressed intermediate amounts of E-cadherin or were heterogeneous (15 cases were analyzed); whereas the poorly differentiated SCCs were all E-cadherin-negative (five cases were investigated).

Dominant and recessive genes involved in tumor cell invasion.

The past year has been the discovery and further analysis of several genes and protein products that are critically involved in the generation of invasive and metastatic tumor cells. Like oncogenes and tumor suppressor genes, the genes responsible for invasive and metastatic phenotypes can function in a dominant or recessive fashion. In this review, particular emphasis will be given to the dominantly acting genes encoding the cell adhesion molecule CD44 and the motility factor scatter factor, and the recessively acting genes encoding the cell adhesion molecule E-cadherin and nm23.