Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer
Resistance to therapy can be driven by intratumoral heterogeneity. Here, the authors show that drug tolerant persistent cell populations emerge during treatment, and these emergent populations arise through epigenetically mediated cell state transitions rather than sub population selection.
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Nature Portfolio
2018
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oai:doaj.org-article:b334216fc1b74e778b875f012ede0e202021-12-02T16:50:06ZDifferentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer10.1038/s41467-018-05729-w2041-1723https://doaj.org/article/b334216fc1b74e778b875f012ede0e202018-09-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-05729-whttps://doaj.org/toc/2041-1723Resistance to therapy can be driven by intratumoral heterogeneity. Here, the authors show that drug tolerant persistent cell populations emerge during treatment, and these emergent populations arise through epigenetically mediated cell state transitions rather than sub population selection.Tyler RisomEllen M. LangerMargaret P. ChapmanJuha RantalaAndrew J. FieldsChristopher BonifaceMariano J. AlvarezNicholas D. KendserskyCarl R. PelzKatherine Johnson-CamachoLacey E. DobroleckiKoei ChinAnil J. AswaniNicholas J. WangAndrea CalifanoMichael T. LewisClaire J. TomlinPaul T. SpellmanAndrew AdeyJoe W. GrayRosalie C. SearsNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-17 (2018) |
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Science Q |
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Science Q Tyler Risom Ellen M. Langer Margaret P. Chapman Juha Rantala Andrew J. Fields Christopher Boniface Mariano J. Alvarez Nicholas D. Kendsersky Carl R. Pelz Katherine Johnson-Camacho Lacey E. Dobrolecki Koei Chin Anil J. Aswani Nicholas J. Wang Andrea Califano Michael T. Lewis Claire J. Tomlin Paul T. Spellman Andrew Adey Joe W. Gray Rosalie C. Sears Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer |
description |
Resistance to therapy can be driven by intratumoral heterogeneity. Here, the authors show that drug tolerant persistent cell populations emerge during treatment, and these emergent populations arise through epigenetically mediated cell state transitions rather than sub population selection. |
format |
article |
author |
Tyler Risom Ellen M. Langer Margaret P. Chapman Juha Rantala Andrew J. Fields Christopher Boniface Mariano J. Alvarez Nicholas D. Kendsersky Carl R. Pelz Katherine Johnson-Camacho Lacey E. Dobrolecki Koei Chin Anil J. Aswani Nicholas J. Wang Andrea Califano Michael T. Lewis Claire J. Tomlin Paul T. Spellman Andrew Adey Joe W. Gray Rosalie C. Sears |
author_facet |
Tyler Risom Ellen M. Langer Margaret P. Chapman Juha Rantala Andrew J. Fields Christopher Boniface Mariano J. Alvarez Nicholas D. Kendsersky Carl R. Pelz Katherine Johnson-Camacho Lacey E. Dobrolecki Koei Chin Anil J. Aswani Nicholas J. Wang Andrea Califano Michael T. Lewis Claire J. Tomlin Paul T. Spellman Andrew Adey Joe W. Gray Rosalie C. Sears |
author_sort |
Tyler Risom |
title |
Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer |
title_short |
Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer |
title_full |
Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer |
title_fullStr |
Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer |
title_full_unstemmed |
Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer |
title_sort |
differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer |
publisher |
Nature Portfolio |
publishDate |
2018 |
url |
https://doaj.org/article/b334216fc1b74e778b875f012ede0e20 |
work_keys_str_mv |
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_version_ |
1718383120109010944 |