Several www.selleckchem.com/products/Cisplatin.html studies have indicated that the intestinal type with metaplasia is more likely to undergo neoplastic progression than the fundic and cardiac form (Hamilton and Smith, 1987; Filipe and Jankowski, 1993). Interestingly, goblet cells show intense immunostaining for MT (Ebert et al, 2000) and may contribute to the higher MT content of the specialised mucosa. In addition, in rats we have shown that MT immunostaining of small intestinal segments is localised to crypt cells and in particular, Paneth cells (Tran et al, 1999). Barrett’s epithelium is often complex and may contain multiple histological patterns. The finding of high-grade dysplasia in metaplastic epithelium remains the best predictor of increased risk of cancer. Whether MT might prove useful in predicting histological types of columnar change warrants investigation.

Immunohistochemical studies will be required to fully identify the specialised cells involved in the increased MT expression. In addition, longitudinal studies on patients with oesophageal reflux without Barrett’s epithelium, is required to determine whether MT is a predictor of progression from normal stratified squamous epithelium into Barrett’s oesophagus. The level of MT in Barrett’s epithelium also might prove relevant to the responsiveness of the oesophagus to pre-surgical radiotherapy and chemotherapy but again this remains to be investigated. For the present we believe the high levels of MT found in columnar metaplastic tissues is an interesting finding which warrants further investigation.

Tight junctions (TJs) are important structural components of the apical junctional complex in the epithelium, where they regulate various intracellular processes such as the establishment of apical-basal polarity and the flow of substances across the intercellular space [1]. Claudins are the main proteins that regulate the functions of TJs and are classified as a family of tetraspan integral membrane proteins, which currently comprises 27 members [2]. A myriad of diseases, including Entinostat cancer, have been associated with alterations in the expression, stability and subcellular localization of claudin family members [3], [4], [5], [6]. However, the precise molecular mechanisms that regulate the expression and function of these proteins, particularly in colorectal cancer, are poorly understood. The epidermal growth factor receptor (EGFR) is dimerized and activated by its extracellular ligand, EGF, which triggers a signaling cascade that leads to the activation of cytoplasmic pathways such as MAPK and PI3K-Akt [7], [8]; these pathways are known to modulate proliferation, differentiation and resistance to cell death [9], [10].