Background: Osteoporosis is a well‐known complication of Crohn's disease (CD). Osteoprotegerin (OPG) concentration is elevated in patients with CD compared to healthy controls. Long‐term infliximab (IFX) maintenance therapy improves the patients' bone mineral density. The effect of IFX on bone metabolism has not yet been clarified. Our aim was to evaluate IFX effects on bone pathology in CD patients. Methods: Twenty‐nine patients were treated with IFX as an induction therapy according to international guidelines at weeks 0, 2, and 6. Serum concentrations of biochemical markers of bone formation (osteocalcin, OC) and bone resorption (beta‐crosslaps, bCL), and serum concentrations of OPG and receptor activator of nuclear factor kappa B ligand (sRANKL) were measured before every treatment at days 1, 14, and 42. Results: Serum levels of OC and sRANKL increased after treatment. OC concentrations were 28.93 ± 14.95 ng/mL versus 36.33 ± 20.05 ng/mL (P < 0.005) at days 1 and 42, respectively; sRANKL concentrations were elevated from 0.0112 ± 0.028 ng/mL to 0.0411 ± 0.123 ng/mL (NS) by the end of the study. The concentrations of both bCL and OPG decreased. bCL concentrations were 0.636 ± 0.594 versus 0.519 ± 0.235 (NS) at days 1 and 42, respectively, while OPG concentration decreased from 3.739 ± 1.485 to 3.491 ± 1.618 (P < 0,05). Conclusions: IFX therapy decreased the OPG concentration in CD patients significantly. In parallel, the serum bone resorption marker (bCL) also decreased. Concentrations of bone formation marker (OC) and sRANKL increased during the same period; however, those changes were not statistically significant. Elevated OPG in CD could be a counter‐regulatory response to inflammatory cytokines or may reflect T‐cell activation. (Inflamm Bowel Dis 2007)

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.

Serum soluble E-cadherin concentrations exhibit a completely different pattern in intestinal-type and diffuse-typegastric cancer. Serum levels are increased in intestinal-type gastric cancer, especially in advanced stages, whereas in diffuse-type gastric cancer E-cadherin levels are decreased in advanced, metastasized cancer.We conclude that soluble E-cadherin concentrations should be interpreted along with Laurén classification and thus might serve as a biological marker in intestinal-type gastric cancer.

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