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dc.contributor.authorGlass, Oliver Kent
dc.contributor.authorBowie, Michelle
dc.contributor.authorFuller, Julie
dc.contributor.authorDarr, D
dc.contributor.authorUsary, J
dc.contributor.authorBoss, K
dc.contributor.authorChoudhury, KR
dc.contributor.authorLiu, X
dc.contributor.authorZhang, Z
dc.contributor.authorLocasale, JW
dc.contributor.authorWilliams, C
dc.contributor.authorDewhirst, MW
dc.contributor.authorJones, LW
dc.contributor.authorSeewaldt, V
dc.date.accessioned2017-12-07T16:42:15Z
dc.date.available2017-12-07T16:42:15Z
dc.date.issued2017-01-01
dc.identifier.citationOncotarget, 2017, 8 (60), pp. 100989 - 101004
dc.identifier.urihttp://hdl.handle.net/10161/15836
dc.description.abstract© Glass et al. Exposure to exercise following a breast cancer diagnosis is associated with reductions in the risk of recurrence. However, it is not known whether breast cancers within the same molecular-intrinsic subtype respond differently to exercise. Syngeneic mouse models of claudin-low breast cancer (i.e., EO771, 4TO7, and C3(1)SV40Tagp16- luc) were allocated to a uniform endurance exercise treatment dose (forced treadmill exercise) or sham-exercise (stationary treadmill). Compared to shamcontrols, endurance exercise treatment differentially affected tumor growth rate: 1- slowed (EO771), 2- accelerated (C3(1)SV40Tag-p16-luc), or 3- was not affected (4TO7). Differential sensitivity of the three tumor lines to exercise was paralleled by effects on intratumoral Ki-67, Hif1-a, and metabolic programming. Inhibition of Hif1-α synthesis by the cardiac glycoside, digoxin, completely abrogated exerciseaccelerated tumor growth in C3(1)SV40Tag-p16-luc. These results suggest that intratumoral Hif1-α expression is an important determinant of claudin-low breast cancer adaptation to exercise treatment.
dc.format.extent100989 - 101004
dc.relation.ispartofOncotarget
dc.relation.isversionof10.18632/oncotarget.21054
dc.titleDifferential response to exercise in claudin-low breast cancer
dc.typeJournal Article
pubs.issue60
pubs.organisational-group/Duke
pubs.organisational-group/Duke/Pratt School of Engineering
pubs.organisational-group/Duke/Pratt School of Engineering/Biomedical Engineering
pubs.organisational-group/Duke/School of Medicine
pubs.organisational-group/Duke/School of Medicine/Basic Science Departments
pubs.organisational-group/Duke/School of Medicine/Basic Science Departments/Pharmacology & Cancer Biology
pubs.organisational-group/Duke/School of Medicine/Clinical Science Departments
pubs.organisational-group/Duke/School of Medicine/Clinical Science Departments/Medicine
pubs.organisational-group/Duke/School of Medicine/Clinical Science Departments/Medicine/Medicine, General Internal Medicine
pubs.organisational-group/Duke/School of Medicine/Clinical Science Departments/Pathology
pubs.organisational-group/Duke/School of Medicine/Clinical Science Departments/Radiation Oncology
pubs.organisational-group/Duke/School of Medicine/Institutes and Centers
pubs.organisational-group/Duke/School of Medicine/Institutes and Centers/Duke Cancer Institute
pubs.organisational-group/Duke/Temp group - logins allowed
pubs.publication-statusPublished
pubs.volume8
dc.identifier.eissn1949-2553


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