Selective COX-2 inhibition affects fatty acids, but not COX mRNA expression in patients with FAP

Familial adenomatous polyposis (FAP) provides a model for sporadic colorectal cancer development. Cyclooxygenase (COX) inhibition may ameliorate polyp development, but rofecoxib was withdrawn due to cardiovascular side effects. Although this selective COX-2 inhibitor, like diet, may alter the fatty acid and eicosanoid pattern, data on the potential alteration in tissues after use, are scarce. The aims were to study if rofecoxib might influence the fatty acid distribution in serum phospholipids and duodenal lesions, mRNA for COX-1 and COX-2 in leucocytes and duodenal lesions, and finally plasma levels of PGE2 in a randomized, double-blind, placebo controlled study (n = 38). Significant reductions were found for essential fatty acid index both in serum phospholipids (P = 0.01, 95% CI = −0.9; −0.1), and in duodenal lesions (P = 0.04, 95 CI % = −0.9; −0.1) after treatment. No treatment effects were found on the COX mRNA expression, or in the plasma PGE2 levels. Dietary AA/EPA ratio was inversely associated with all the indicators of EFA status (all P < 0.01). These findings suggest that the effects of COX chemoprevention should be further investigated in FAP and that dietary needs should be included in the treatment of FAP

Development and Structure of Pancreas

The goal of this short chapter is to introduce the reader to fundamental concepts on the fine structure of the pancreas and its developmental pattern. This is of paramount importance for any individual that enters the field of pancreatology. In addition, this information is fundamental for understanding issues of histogenesis of pancreatic cancer, animal models, the histopathology of different forms of pancreatitis, pancreatic cysts and pancreatic cancer. The fine structure of the pancreas, as described here, is also essential as a foundation building block where to integrate, at the cellular level, the concepts from cell signaling, transcriptional regulation, secretion, proliferation, apoptosis, and senescence; all cancer-associated mechanisms. Thus, this is a basic, conceptual chapter that will serve as a compass for the reader of this book and in the field.Fil: Rovasio, Roberto Americo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones Biológicas y Tecnológicas. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales. Instituto de Investigaciones Biológicas y Tecnológicas; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales. Centro de Biología Celular y Molecular; Argentin