PTEN is a candidate tumour suppressor gene and frequently mutated in multiple cancers, however, not in pancreatic cancer.Recently, it has been demonstrated that PTEN expression is regulated by TGF-b1. Using TGF-b1 transgenic mice (n=7) and wildtype littermates (n=6), as well as pancreatic tissues obtained from organ donors (n=10) and patients with pancreatic cancer (n=10), we assessed the expression of PTEN by means of immunohistochemistry and semiquantitative PCR analysis. In addition, PANC-1 cells were treated with TGF-b1 in vitro and the levels of PTEN mRNA were determined in these cells. In human pancreatic cancers PTEN mRNA levels were significantly decreased (P50.05). In addition, in the pancreas of TGF-b1 transgenic mice the expression of PTEN was significantly reduced (P50.01), as compared to wildtype littermates and incubation of PANC-1 cells with TGF-b1 decreased PTEN mRNA levels after 24 h. Inasmuch as TGF-b1 decreases PTEN expression in human pancreatic cancer cells and human pancreatic cancers overexpress TGF-b1, the reduced expression of PTEN in pancreatic cancer may be mediated by TGF-b1 overexpression. Thus, although PTEN is not mutated in pancreatic cancers, the reduction of its expression may give pancreatic cancer cells an additional growth advantage.

The prevalence of H. pylori compared to the age-matched controls is significantly lower in patients with inflammatory bowel disease but not in those with chronic obstructive pulmonary disease. Antibiotic use is not responsible for the lower prevalence of H. pylori infection in patients with inflammatory bowel disease.

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Chronic pancreatitis is an inflammatory disease of the pancreas, characterized by a progressive destruction of the exocrine and endocrine pancreas, leading both to exocrine and endocrine insufficiency. In recent years, our knowledge of this disease has improved, an epidemiological link between chronic pancreatitis and pancreatic cancer has been established, and the molecular alterations underlying their pathogenesis have been partly revealed. Nevertheless, the differentiation of chronic inflammation of the pancreas from cancer of the pancreas remains a great challenge. This overview will point out the present knowledge of the molecular pathogenesis of chronic pancreatitis and pancreatic cancer and will focus on the role of molecular markers for differentiating chronic pancreatitis from pancreatic cancer.

Background: Recent research has revealed a rapid increase in the number of alterations underlying oncogenesis and the proteins which regulate the cell cycle. p16 is a cell cycle regulatory protein acting as a cyclin-dependent kinase inhibitor (CDKI). Because of its antiproliferative effect, p16 has been suggested to be a tumor suppressor gene. Deletions, mutations and functional inactivation of p16 occur with a frequency second only to p53 in most human malignancies. Aim: to evaluate the p16 protein expression in primary gastric cancer in order to understand the possible differences in relation to histotype and grade of tumors. Material and Methods: Immunohistochemical expression of p16 was investigated in matched normal and cancerous tissues from 70 patients with gastric cancer (52 intestinal and 18 diffuse type). Results: In non-cancerous gastric tissues the immunostaining of p16 was weak and limited to antral glands. In gastric cancer tissues, the enhanced immunoreactivity of p16 was not significantly different in intestinal and diffuse type of gastric cancer. However, the intensity of immunostaining was inversely related to the grade of differentiation of these tumours. Conclusions: The overexpression of p16 seems to be a common event in the development of both intestinal and diffuse type of gastric cancer and it is likely that it may be driven by features of the neoplastic state. Likewise, the absence of p16 in the lowest grade of differentiation may reflect increased selection pressure and clonal expansion of the cells with a more aggressive phenotype.