Expression of cell adhesion molecules in oesophageal carcinoma and its prognostic value

Abstract

Oesophageal carcinoma remains a disease of poor prognosis. Surgical cure rates are compromised by the fact that most patients are diagnosed at a late stage of disease because of the delayed onset of symptoms, by which time metastases and organ infiltration may have already occurred. Thus, invasion and metastases play a key role in influencing patient survival, and the search for novel treatments may therefore hinge on gaining insight into the mechanisms controlling these processes. It has been established that the initial step in the metastatic cascade is the detachment of tumour cells from the primary tumour via dysregulation of normal cell–cell and cell–matrix interactions. Distinct proteins known as cell adhesion molecules (CAMs) mediate these interactions. In recent years, a plethora of information has contributed to the in depth understanding of these molecules. This review provides a brief description of five families of CAMs (cadherins, integrins, CD44, immunoglobulin superfamily, and selectins) and highlights their altered expression in relation both to prognosis and tumour behaviour in squamous cell carcinoma and adenocarcinoma of the oesophagus.

Classification of epithelial–mesenchymal transition phenotypes in esophageal squamous cell carcinoma is strongly associated with patient prognosis

“…Loss of E-cadherin expression is a well-documented condition for invasiveness; [14][15][16][17][18][19][20] however, this result is debatable. 3,4 Our work demonstrated that the loss of E-cadherin itself, without a mesenchymal phenotype, may not be associated with invasive behavior, whereas tumors with a mesenchymal phenotype, regardless of E-cadherin expression, showed aggressive behavior in esophageal squamous cell carcinoma.…”

The functional interplay between EGFR overexpression, hTERT activation, and p53 mutation in esophageal epithelial cells with activation of stromal fibroblasts induces tumor development, invasion, and differentiation

“…Cold Spring Harbor Laboratory Press on May 11, 2018 -Published by genesdev.cshlp.org Downloaded from are not diagnosed until late stages of disease (Nair et al 2005). The development of ESCC is a progressive multistep process, starting with increases in esophageal epithelial cell proliferation, leading to basal cell hyperplasia, dysplasia, carcinoma in situ, and finally advanced carcinoma (Lehrbach et al 2003).…”

“…The development of ESCC is a progressive multistep process, starting with increases in esophageal epithelial cell proliferation, leading to basal cell hyperplasia, dysplasia, carcinoma in situ, and finally advanced carcinoma (Lehrbach et al 2003). At the late stages of disease, tumor invasion plays a key role in influencing patient survival (Nair et al 2005). Interestingly enough, the prognosis of ESCC is poor compared with other squamous cell carcinomas originating at other sites, suggesting that the local tumor microenvironment might be very critical in accounting for these differences.…”

C-terminal binding proteins: Emerging roles in cell survival and tumorigenesis

“…59 EMT and loss of E-cadherin expression is also associated with disease progression, increased malignancy and poor prognosis in many epithelial tumors, including those of the colon, stomach, lung, bladder, oesophagus, prostate and breast. [60][61][62][63][64][65][66] Along with increased invasive properties, one of the key outcomes of EMT is a marked reduction in a cell's susceptibility to pro-apototic stimuli such as loss of cell-cell contact, growth factor withdrawal, and TNF-α. 39,67 Activation of transcription from the E-cadherin promoter is driven by ubiquitously expressed, and constitutively active transcription factors.…”