Document Detail


Apoptosis pathways and their therapeutic exploitation in pancreatic cancer.
MedLine Citation:
PMID:  19382915     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Resistance to apoptosis (programmed cell death) is a characteristic feature of human malignancies including pancreatic cancer, which is one of the leading causes of cancer deaths in the western world. Defects in this intrinsic cell death program can contribute to the multistep process of tumorigenesis, because too little cell death can disturb tissue homeostasis. Further, blockade of apoptosis pathways can cause treatment failure, because intact apoptosis signalling cascades largely mediate therapy-induced cytotoxicity. The elucidation of apoptosis pathways in pancreatic carcinoma over the last decade has resulted in the identification of various molecular defects. How apoptosis pathways can be exploited for the treatment of pancreatic cancer will be discussed in this review.
Authors:
Simone Fulda
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2009-03-27
Journal Detail:
Title:  Journal of cellular and molecular medicine     Volume:  13     ISSN:  1582-4934     ISO Abbreviation:  J. Cell. Mol. Med.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-08-21     Completed Date:  2009-11-04     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101083777     Medline TA:  J Cell Mol Med     Country:  England    
Other Details:
Languages:  eng     Pagination:  1221-7     Citation Subset:  IM    
Affiliation:
University Children's Hospital, Eythstr., Ulm, Germany. simone.fulda@uniklinik-ulm.de
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis*
Humans
Inhibitor of Apoptosis Proteins / metabolism
Mitochondria / metabolism
Pancreatic Neoplasms / pathology*,  therapy*
Receptors, Death Domain / metabolism
Chemical
Reg. No./Substance:
0/Inhibitor of Apoptosis Proteins; 0/Receptors, Death Domain

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


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