title: Nicotine as a mitogenic stimulus for pancreatic acinar cell proliferation.
abstract: Cell proliferation is an important process in life for growth of normal and cancer cells. The signal transduction pathways activated during this process are strictly regulated. This editorial focuses on the role of nicotine, a mitogen, in the induction of signaling pathways resulting in proliferation of pancreatic tumor cells and compares these events with those in normal acinar cells isolated from the rat pancreas. The data shows striking similarities between these two cellular systems. In addition, the editorial reviews very recent literature of the contribution of MAPK signaling in cell lines associated with human diseases. A prospective cellular model of nicotine induced activation of MAPK cascade is presented.
authors.affiliation: Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, Arkansas 72205, United States. pchowdhury@uams.edu
authors.forename: Parimal
authors.initials: P
authors.lastname: Chowdhury
authors.forename: Kodetthoor-B
authors.initials: KB
authors.lastname: Udupa
mesh_terms: D000818:Animals; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D006801:Humans; D066298:In Vitro Techniques; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008934:Mitogens / Q000633:toxicity*; D008954:Models, Biological; D009538:Nicotine / Q000633:toxicity*; D010179:Pancreas / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051381:Rats
chemical_list: D008934:Mitogens; D009538:Nicotine