E-cadherin Expression in Canine Gastric Carcinomas: Association with Clinicopathological Parameters

Abstract

E-cadherin (E-cad) is a cell-adhesion molecule known for its tumor-invasion suppressor function. E-cad expression was examined immunohistochemically in a series of canine tissue samples, including normal gastric mucosa (NGM; n = 3), gastric carcinomas (GC; n = 33), adjacent non-neoplastic mucosa (NNM; n = 32), neoplastic emboli (n = 16) and metastatic lesions (n = 9). The relationship between E-cad expression and clinicopathological features were investigated. In NGM, epithelial cells showed strong latero-lateral membranous expression of E-cad, and this pattern was considered normal. The membranous staining was preserved in all specimens of NNM (100%), whereas abnormal E-cad expression was found in 87.9% of the GCs. A marked difference in E-cad expression was observed between normal and malignant tissues (p < 0.0002). Abnormal E-cad expression was significantly more frequent in poorly/undifferentiated carcinomas (96%) and diffuse (95%) and indeterminate carcinomas (100%) than in well-differentiated/intestinal ones (62.5%; p = 0.0115 and p = 0.0392, respectively). There was significant association between abnormal E-cad expression and the depth of invasion (p = 0.0117), and the presence neoplastic emboli (p = 0.0194). No statistically significant differences in E-cad expression were observed concerning tumor location, histological type according to WHO classification, and presence of metastatic lesions. Therefore, deregulation of E-cad expression may play a role in canine gastric carcinogenesis and in tumor progression; moreover, it might be a prognostic tool for canine gastric cancer.

Localized chemotherapy approaches and advanced drug delivery strategies: a step forward in the treatment of peritoneal carcinomatosis from ovarian cancer

“…During the development of ovarian carcinoma, tumor cells may detach from the primary tumor site through a process called exfoliation, probably mediated by the downregulation of adhesion molecules, such as E-cadherin, on the surface of tumor cells ( 7 ) and facilitated by the high interstitial fluid pressure common to many solid tumors ( 8 ). These mechanisms have also been confirmed for colon ( 9 ) and gastric ( 10 ) cancer with peritoneal spread. Because of the anatomical location, gravity, peristaltic movement of the gastrointestinal tract, and negative pressure exerted by the movements of the muscles of the diaphragm, exfoliated cells commonly implant in the pelvic and subdiaphragmatic region, and their adhesion to the mesothelial layer of the peritoneum appears to be mediated by glycan-binding proteins expressed by mesothelial cells ( 11 ) and by adhesion molecules such as CD44, integrins, selectins, and a number of other leukocyte-associated adhesion molecules ( 12 ).…”