Document Detail


Effect of aerobic exercise on tumor physiology in an animal model of human breast cancer.
MedLine Citation:
PMID:  19959769     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recent epidemiologic studies report that regular exercise may be associated with substantial reductions in cancer-specific and all-cause mortality following a breast cancer diagnosis. The mechanisms underlying this relationship have not been identified. We investigated the effects of long-term voluntary wheel running on growth and progression using an animal model of human breast cancer. We also examined effects on the central features of tumor physiology, including markers of tumor blood perfusion/vascularization, hypoxia, angiogenesis, and metabolism. Athymic female mice fed a high-fat diet were orthotopically (direct into the mammary fat pad) implanted with human breast cancer cells (MDA-MB-231 at 1 x 10(6)) into the right dorsal mammary fat pad and randomly assigned (1:1) to voluntary wheel running (n = 25) or a nonintervention (sedentary) control group (n = 25). Tumor volume was measured every three days using digital calipers. All experimental animals were killed when tumor volume reached > or = 1,500 mm(3). Kaplan-Meier (KM) analysis indicated that tumor growth (survival) was comparable between the experimental groups (exercise 44 days vs. control 48 days; KM proportional hazard ratio = 1.41, 95% confidence interval, 0.77-2.58, P = 0.14). However, tumors from exercising animals had significantly improved blood perfusion/vascularization relative to the sedentary control group (P < 0.05). Histological analyses indicated that intratumoral hypoxia levels (as assessed by hypoxia-inducible factor 1) were significantly higher in the exercise group relative to sedentary control (P < 0.05). Aerobic exercise can significantly increase intratumoral vascularization, leading to "normalization" of the tissue microenvironment in human breast tumors. Such findings may have important implications for inhibiting tumor metastasis and improving the efficacy of conventional cancer therapies.
Authors:
Lee W Jones; Benjamin L Viglianti; Jessica A Tashjian; Sejal M Kothadia; Stephen T Keir; Stephen J Freedland; Michael Q Potter; Eui Jung Moon; Thies Schroeder; James E Herndon; Mark W Dewhirst
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-12-03
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  108     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-01     Completed Date:  2010-04-23     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  343-8     Citation Subset:  IM    
Affiliation:
Duke Univ. Medical Center, Durham, NC 27710, USA. lee.w.jones@duke.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / physiopathology
Blotting, Western
Body Weight / physiology
Breast Neoplasms / blood supply,  metabolism,  pathology*
Cell Line, Tumor
Disease Progression
Energy Metabolism / physiology
Female
Humans
Immunohistochemistry
Kaplan-Meier Estimate
Mice
Mice, Nude
Necrosis
Neoplasm Transplantation
Neoplasms, Experimental / pathology
Neovascularization, Pathologic / pathology
Physical Conditioning, Animal / physiology*
Regional Blood Flow / physiology
Survival Analysis
Tumor Markers, Biological / metabolism
Grant Support
ID/Acronym/Agency:
CA 40355/CA/NCI NIH HHS; R01 CA040355/CA/NCI NIH HHS; R01 CA040355-25/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Tumor Markers, Biological
Comments/Corrections
Erratum In:
J Appl Physiol. 2010 Apr;108(4):1021

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


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