Document Detail


Primers on molecular pathways - cycling toward pancreatic cancer.
MedLine Citation:
PMID:  20299817     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Human cells divide and proliferate during the early stages of life to support development, and throughout adult life to support normal cellular turnover. Each dividing cell follows an orderly and tightly regulated series of events known as the cell cycle. This process ensures proper cellular division that maintains DNA and chromosomal integrity and responds appropriately to external signals which communicate the level of demand for new cells. In cancer, genetic mutations leading to the overexpression of proteins which support cell cycle progression, or the downregulation of proteins involved in cell cycle inhibition contributes to the dysregulated cellular division and proliferation of malignant cells. The resulting uninhibited cellular proliferation provides ample opportunity for additional genetic mutations that lead to tumor progression. In the following review, we provide a brief introduction to the cell cycle and a discussion of the mechanism underlying the dysregulation of the cell cycle in human cancer. We pay particular attention to pancreatic adenocarcinoma, an aggressive tumor that has a 5-year survival rate of 3-5%, and is the fourth leading cause of cancer mortality in the US. and IAP.
Authors:
Yang Liu; Sherine F Elsawa; Luciana L Almada
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Publication Detail:
Type:  Journal Article; Review     Date:  2010-03-19
Journal Detail:
Title:  Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]     Volume:  10     ISSN:  1424-3911     ISO Abbreviation:  Pancreatology     Publication Date:  2010  
Date Detail:
Created Date:  2010-04-21     Completed Date:  2010-07-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100966936     Medline TA:  Pancreatology     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  6-13     Citation Subset:  IM    
Affiliation:
Schulze Center for Novel Therapeutics, Mayo Clinic, Rochester, Minn., USA.
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MeSH Terms
Descriptor/Qualifier:
Adenocarcinoma / genetics
Adult
Cell Cycle / physiology*
Cyclin-Dependent Kinase Inhibitor p27 / metabolism
Cyclin-Dependent Kinases / physiology
Cyclins / metabolism
DNA Damage / physiology
Epigenesis, Genetic
Humans
Pancreatic Neoplasms / genetics*,  physiopathology
Tumor Suppressor Protein p53 / metabolism
Chemical
Reg. No./Substance:
0/Cyclins; 0/Tumor Suppressor Protein p53; 147604-94-2/Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.22/Cyclin-Dependent Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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