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.

Bibliographic Details
Main Authors: 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
Format: Article
Language:English
Published: Nature Publishing Group 2018-09-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-018-05729-w
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spelling doaj-b334216fc1b74e778b875f012ede0e202021-05-11T09:37:48ZengNature Publishing GroupNature Communications2041-17232018-09-019111710.1038/s41467-018-05729-wDifferentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancerTyler Risom0Ellen M. Langer1Margaret P. Chapman2Juha Rantala3Andrew J. Fields4Christopher Boniface5Mariano J. Alvarez6Nicholas D. Kendsersky7Carl R. Pelz8Katherine Johnson-Camacho9Lacey E. Dobrolecki10Koei Chin11Anil J. Aswani12Nicholas J. Wang13Andrea Califano14Michael T. Lewis15Claire J. Tomlin16Paul T. Spellman17Andrew Adey18Joe W. Gray19Rosalie C. Sears20Department of Molecular and Medical Genetics, Oregon Health & Science UniversityDepartment of Molecular and Medical Genetics, Oregon Health & Science UniversityDepartment of Electrical Engineering and Computer Sciences, University of California at BerkeleyMisvik BiologyDepartment of Molecular and Medical Genetics, Oregon Health & Science UniversityDepartment of Molecular and Medical Genetics, Oregon Health & Science UniversityDarwinHealth Inc.Department of Molecular and Medical Genetics, Oregon Health & Science UniversityDepartment of Molecular and Medical Genetics, Oregon Health & Science UniversityDepartment of Molecular and Medical Genetics, Oregon Health & Science UniversityLester and Sue Smith Breast Center, Baylor College of MedicineCenter for Spatial Systems Biomedicine, Oregon Health & Science UniversityDepartment of Industrial Engineering and Operations Research, University of California at BerkeleyCenter for Spatial Systems Biomedicine, Oregon Health & Science UniversityDarwinHealth Inc.Department of Biochemistry and Molecular Biology, Baylor College of MedicineDepartment of Electrical Engineering and Computer Sciences, University of California at BerkeleyDepartment of Molecular and Medical Genetics, Oregon Health & Science UniversityDepartment of Molecular and Medical Genetics, Oregon Health & Science UniversityCenter for Spatial Systems Biomedicine, Oregon Health & Science UniversityDepartment of Molecular and Medical Genetics, Oregon Health & Science UniversityResistance 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.https://doi.org/10.1038/s41467-018-05729-w
collection DOAJ
language English
format Article
sources DOAJ
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
spellingShingle 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
Nature Communications
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 Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2018-09-01
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.
url https://doi.org/10.1038/s41467-018-05729-w
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