Document Detail


Regulation of tumor cell dormancy by tissue microenvironments and autophagy.
MedLine Citation:
PMID:  23143976     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The development of metastasis is the major cause of death in cancer patients. In certain instances, this occurs shortly after primary tumor detection and treatment, indicating these lesions were already expanding at the moment of diagnosis or initiated exponential growth shortly after. However, in many types of cancer, patients succumb to metastatic disease years and sometimes decades after being treated for a primary tumor. This has led to the notion that in these patients residual disease may remain in a dormant state. Tumor cell dormancy is a poorly understood phase of cancer progression and only recently have its underlying molecular mechanisms started to be revealed. Important questions that remain to be elucidated include not only which mechanisms prevent residual disease from proliferating but also which mechanisms critically maintain the long-term survival of these disseminated residual cells. Herein, we review recent evidence in support of genetic and epigenetic mechanisms driving dormancy. We also explore how therapy may cause the onset of dormancy in the surviving fraction of cells after treatment and how autophagy may be a mechanism that maintains the residual cells that are viable for prolonged periods.
Authors:
Maria Soledad Sosa; Paloma Bragado; Jayanta Debnath; Julio A Aguirre-Ghiso
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review    
Journal Detail:
Title:  Advances in experimental medicine and biology     Volume:  734     ISSN:  0065-2598     ISO Abbreviation:  Adv. Exp. Med. Biol.     Publication Date:  2013  
Date Detail:
Created Date:  2012-11-12     Completed Date:  2013-04-04     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  0121103     Medline TA:  Adv Exp Med Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  73-89     Citation Subset:  IM    
Affiliation:
Department of Medicine and Otolaryngology, Mount Sinai School of Medicine, New York, NY, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antineoplastic Agents / pharmacology
Autophagy*
Cell Cycle Checkpoints
Cell Hypoxia
Cell Movement
Cell Survival
Endoplasmic Reticulum Stress
Epigenesis, Genetic
Gene Expression Regulation, Neoplastic*
Humans
MAP Kinase Signaling System
Neoplasm Proteins / genetics,  metabolism
Neoplasms / drug therapy,  genetics,  metabolism,  pathology*
Tumor Microenvironment*
Grant Support
ID/Acronym/Agency:
CA109182/CA/NCI NIH HHS; CA126792-S1/CA/NCI NIH HHS; CA163131/CA/NCI NIH HHS; ES017146/ES/NIEHS NIH HHS; R01 CA109182/CA/NCI NIH HHS; R01 CA126792/CA/NCI NIH HHS; R01 CA126792/CA/NCI NIH HHS; U54 CA163131/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/Neoplasm Proteins
Comments/Corrections

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


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