The majority of the adenocarcinomas arising in Barrett esophagus manifest clinically at an advanced stage and have a poor prognosis. As a result of this poor prognosis, much attention has been directed toward the exploration of markers for neoplastic progression in Barrett esophagus. The objective of the present study was to determine the expression of beta-catenin by immunohistochemical analysis in 70 adenocarcinomas developed in Barrett esophagus and to examine its relationship to various prognostic factors currently in use. Abnormal beta-catenin expression, consisting of the loss of membranous staining and the appearance of the nuclear staining, was found in 43 cases (61%). Of patients with the 43 tumors showing abnormal beta-catenin expression, 25 (58%) survived more than 1 year. In contrast, only 7 (26%) of 27 patients with tumors showing normal beta-catenin expression survived longer than 1 year. Most of the superficial (Tis-T1) tumors (83% [10/12]) exhibited abnormal beta-catenin expression compared with only 53% (31/58) in the T2-T3 group. These results suggest a possible correlation among beta-catenin expression, tumor stage, and length of survival as prognostic factors in patients with adenocarcinoma in Barrett esophagus.
Although inhibition of adenosine deaminase effectively enhances ISF adenosine before and during ischaemia, the increase before ischaemia does not "precondition" the myocardium, nor does the augmentation of adenosine during and after ischaemia attenuate necrosis in this model of ischaemia. Therefore, the enhancement of ISF adenosine to the extent provided by adenosine deaminase inhibition alone is not sufficient to protect the heart in the way seen with ischaemic preconditioning.
Recent studies have shown that type II pneumocytes, at birth and day 3 postnatally, have a diffuse distribution and localize at alveolar 'corners' between 3 and 7 days. Since alpha 3 beta 1 and alpha 6 beta 1 are laminin-binding receptors that are well expressed by rat type II alveolar epithelial cells, we postulated that they may play a role in the localization of the cells in the alveolus. To begin the evaluation of this hypothesis, we studied the temporal and spatial expression of the alpha 3, alpha 6, and beta 1 integrin subunit protein and mRNA in whole rat lungs during postnatal development by immunofluorescence, confocal microscopy, and Northern blot analysis. The temporal expression of proteins analyzed by immunochemistry, with integrin subunit specific antibodies, increased during the 3- to 7-day postnatal period and in adult lungs. Densitometric values of the alpha 3, alpha 6, and beta 1 mRNA expression, normalized to 28S rRNA, quadrupled from day 1 to day 3 postnatally. The mRNA expression of different integrin chains was elevated 1.5- to threefold from days 5 to 7 postnatally compared to day 1 levels. The alpha 3 and alpha 6 integrin subunit mRNA decreased to newborn levels in adult lungs, whereas the beta 1 integrin mRNA in adult lungs was expressed at approximately 50% of its level in newborn lungs. We postulate that the increases in alpha 3, alpha 6, and beta 1 integrin mRNA expression during the early neonatal period may be important for the spatial distribution of type II pneumocytes.
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