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dc.contributor.author Boss, K
dc.contributor.author Bowie, Michelle
dc.contributor.author Choudhury, KR
dc.contributor.author Darr, D
dc.contributor.author Dewhirst, Mark Wesley
dc.contributor.author Fuller, Julie
dc.contributor.author Glass, Oliver Kent
dc.contributor.author Jones, LW
dc.contributor.author Liu, X
dc.contributor.author Locasale, Jason
dc.contributor.author Seewaldt, Victoria Louise
dc.contributor.author Usary, J
dc.contributor.author Williams, Christina
dc.contributor.author Zhang, Z
dc.date.accessioned 2017-12-07T16:42:15Z
dc.date.available 2017-12-07T16:42:15Z
dc.date.issued 2017-01-01
dc.identifier.uri http://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.relation.ispartof Oncotarget
dc.relation.isversionof 10.18632/oncotarget.21054
dc.title Differential response to exercise in claudin-low breast cancer
dc.type Journal article
pubs.begin-page 100989
pubs.end-page 101004
pubs.issue 60
pubs.organisational-group Basic Science Departments
pubs.organisational-group Biomedical Engineering
pubs.organisational-group Clinical Science Departments
pubs.organisational-group Duke
pubs.organisational-group Duke Cancer Institute
pubs.organisational-group Institutes and Centers
pubs.organisational-group Medicine
pubs.organisational-group Medicine, General Internal Medicine
pubs.organisational-group Pathology
pubs.organisational-group Pharmacology & Cancer Biology
pubs.organisational-group Pratt School of Engineering
pubs.organisational-group Radiation Oncology
pubs.organisational-group School of Medicine
pubs.organisational-group Temp group - logins allowed
pubs.publication-status Published
pubs.volume 8
dc.identifier.eissn 1949-2553


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