Laparoscopic pancreatic surgery (LPS) has seen significant development but much of the knowledge refers to small and benign pancreatic tumors. This study aims to evaluate the feasibility, safety, and long-term outcome of the laparoscopic approach in patients with benign, premalignant, and overt malignant lesions of the pancreas. This study, currently, is the largest single center experience worldwide. One hundred twenty-three consecutive patients underwent laparoscopic pancreatic surgery from April 1998 to April 2007, 20 patients with cysts or pseudocysts for acute and chronic pancreatitis, laparoscopic pancreatic drainage was performed, and were excluded from the analysis. The 103 patients were divided based on preoperative diagnosis: group I, inflammatory tumors for chronic pancreatitis (eight patients); group II, cystic pancreatic neoplasms (29 patients); group III, intraductal papillary mucinous neoplasms (10 patients); group IV, neuroendocrine pancreatic tumors (NETs) (43 patients); and group V ductal adenocarcinoma (13 patients).
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Harbor-University of California Los Angeles Research and Education Institute, UCLA School of Medicine, Torrance, California 90502, USA. boros@gcrc.rei.edu

INTRODUCTION: Tumor cells, just as other living cells, possess the potential for proliferation, differentiation, cell cycle arrest, and apoptosis. There is a specific metabolic phenotype associated with each of these conditions, characterized by the production of both energy and special substrates necessary for the cells to function in that particular state. Unlike that of normal living cells, the metabolic phenotype of tumor cells supports the proliferative state. AIM: To present the metabolic hypothesis that (1) cell transformation and tumor growth are associated with the activation of metabolic enzymes that increase glucose carbon utilization for nucleic acid synthesis, while enzymes of the lipid and amino acid synthesis pathways are activated in tumor growth inhibition, and (2) phosphorylation and allosteric and transcriptional regulation of intermediary metabolic enzymes and their substrate availability together mediate and sustain cell transformation from one condition to another. CONCLUSION: Evidence is presented that demonstrates opposite changes in metabolic phenotypes induced by TGF-beta, a cell-transforming agent, and tumor growth-inhibiting phytochemicals such as genistein and Avemar, or novel synthetic anti-leukemic drugs such as STI571 (Gleevec). Intermediary metabolic enzymes that mediate the growth signaling pathways and promote malignant cell transformation may serve as high-efficacy nongenetic novel targets for cancer therapies.

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