Abstract
Background: Stomach diseases are an important sector of gastroenterology, including proliferative benign; premalignant; and malignant pathologies of the gastric mucosa, such as gastritis, hyperplastic polyps, metaplasia, dysplasia, and adenocarcinoma. There are data showing quantitative changes in chaperone system (CS) components in inflammatory pathologies and tumorigenesis, but their roles are poorly understood, and information pertaining to the stomach is scarce. Here, we report our findings on one CS component, the chaperone Hsp60, which we studied first considering its essential functions inside and outside mitochondria. Methods: We performed immunohistochemical experiments for Hsp60 in different samples of gastric mucosa. Results: The data obtained by quantitative analysis showed that the average percentages of Hsp60 were of 32.8 in normal mucosa; 33.5 in mild-to-moderate gastritis; 51.8 in severe gastritis; 58.5 in hyperplastic polyps; 67.0 in intestinal metaplasia; 89.4 in gastric dysplasia; and 92.5 in adenocarcinomas. Noteworthy were: (i) the difference between dysplasia and adenocarcinoma with the other pathologies; (ii) the progressive increase in Hsp60 from gastritis to hyperplastic polyp, gastric dysplasia, and gastric carcinoma; and (iii) the correlation of Hsp60 levels with histological patterns of cell proliferation and, especially, with tissue malignancy grades. Conclusions: This trend likely reflects the mounting need for cells for Hsp60 as they progress toward malignancy and is a useful indicator in differential diagnosis, as well as the call for research on the mechanisms underpinning the increase in Hsp60 and its possible roles in carcinogenesis.
Highlights
Quantitative variations of molecular chaperones in cells and tissues during carcinogenesis have been recognized for a long time
We found that the number of cells positive for Hsp60 and the positivity of the individual cells in gastric adenocarcinoma (GC) are high compared to the normal mucosa (NM)
The highest levels of Hsp60 positivity were found in GC, but they were high in gastric dysplasia (GD) in comparison with all the other pathologies studied, which reaffirms the close relationship between GC and GD, with the latter being a prelude to malignant transformation with the atypical alteration of epithelial cells
Summary
Quantitative variations of molecular chaperones in cells and tissues during carcinogenesis have been recognized for a long time. We present data from a recent study of Hsp levels in gastric mucosa obtained with immunohistochemistry, comparing cancer with other gastric pathologies These pathologies cause tissue disorganization and remodeling as exemplified by benign inflammatory, benign proliferation (e.g., hyperplastic polyps), metaplastic and dysplastic conditions, and malignant proliferations. In the study reported here, we performed an immunomorphological evaluation of the tissue levels of Hsp in specimens of gastric mucosa with inflammation (mild or moderate/severe gastritis), hyperplastic polyps, metaplasia, dysplasia, or cancer. Noteworthy were: (i) the difference between dysplasia and adenocarcinoma with the other pathologies; (ii) the progressive increase in Hsp from gastritis to hyperplastic polyp, gastric dysplasia, and gastric carcinoma; and (iii) the correlation of Hsp levels with histological patterns of cell proliferation and, especially, with tissue malignancy grades. Conclusions: This trend likely reflects the mounting need for cells for Hsp as they progress toward malignancy and is a useful indicator in differential diagnosis, as well as the call for research on the mechanisms underpinning the increase in Hsp and its possible roles in carcinogenesis
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