Linked Life Data

19308045

Source:http://linkedlifedata.com/resource/pubmed/id/19308045

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2009-4-28
pubmed:abstractText
The pathobiology of chronic pancreatitis (CP) remains enigmatic despite remarkable progress made recently in uncovering key mechanisms involved in the initiation and progression of the disease. CP is increasingly thought of as a multifactorial disorder. Apoptosis plays a role in parenchymal destruction, the pathological hallmark of CP. The apoptotic mechanisms preferentially target the exocrine compartment, leaving endocrine islets relatively intact for a prolonged period. Exocrine cells shed their 'immunoprivileged' status, express death receptors, and are rendered susceptible to apoptosis induced by death ligands on infiltrating lymphocytes, and released locally by activated pancreatic stellate cells. Islet cells retain their 'immunoprivileged' status and activate anti-apoptotic programs through NF-kappaB. Ductal changes, including distortion, dilatation, and pancreatic ductal hypertension in the setting of CP, induce genomic damage and increased cell turnover. In addition, signaling mechanisms that play a role in the development of embryonic pancreas are reinstated, thus, playing a role in repair, regeneration, and transformation. This, in turn, leads to acino-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN). Some of these pathways are activated in pancreatic cancer. We attempt to integrate the current knowledge and major concepts in the pathogenesis of CP and to explain the mechanism of differential cell loss. We also discuss the possible implications of signaling pathway activation in pancreatic inflammation, relevant to the cellular transformation that leads to pancreatic neoplasia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1530-0307
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
489-97
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Mechanisms of parenchymal injury and signaling pathways in ectatic ducts of chronic pancreatitis: implications for pancreatic carcinogenesis.
pubmed:affiliation
Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA. bhanotu@mskcc.org
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't