Nature Communications (Sep 2018)
Differentiation-state plasticity is a targetable resistance mechanism in basal-like breast cancer
- 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
Affiliations
- Tyler Risom
- Department of Molecular and Medical Genetics, Oregon Health & Science University
- Ellen M. Langer
- Department of Molecular and Medical Genetics, Oregon Health & Science University
- Margaret P. Chapman
- Department of Electrical Engineering and Computer Sciences, University of California at Berkeley
- Juha Rantala
- Misvik Biology
- Andrew J. Fields
- Department of Molecular and Medical Genetics, Oregon Health & Science University
- Christopher Boniface
- Department of Molecular and Medical Genetics, Oregon Health & Science University
- Mariano J. Alvarez
- DarwinHealth Inc.
- Nicholas D. Kendsersky
- Department of Molecular and Medical Genetics, Oregon Health & Science University
- Carl R. Pelz
- Department of Molecular and Medical Genetics, Oregon Health & Science University
- Katherine Johnson-Camacho
- Department of Molecular and Medical Genetics, Oregon Health & Science University
- Lacey E. Dobrolecki
- Lester and Sue Smith Breast Center, Baylor College of Medicine
- Koei Chin
- Center for Spatial Systems Biomedicine, Oregon Health & Science University
- Anil J. Aswani
- Department of Industrial Engineering and Operations Research, University of California at Berkeley
- Nicholas J. Wang
- Center for Spatial Systems Biomedicine, Oregon Health & Science University
- Andrea Califano
- DarwinHealth Inc.
- Michael T. Lewis
- Department of Biochemistry and Molecular Biology, Baylor College of Medicine
- Claire J. Tomlin
- Department of Electrical Engineering and Computer Sciences, University of California at Berkeley
- Paul T. Spellman
- Department of Molecular and Medical Genetics, Oregon Health & Science University
- Andrew Adey
- Department of Molecular and Medical Genetics, Oregon Health & Science University
- Joe W. Gray
- Center for Spatial Systems Biomedicine, Oregon Health & Science University
- Rosalie C. Sears
- Department of Molecular and Medical Genetics, Oregon Health & Science University
- DOI
- https://doi.org/10.1038/s41467-018-05729-w
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 17
Abstract
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.
