Rare cell variability and drug-induced reprogramming as a mode of cancer drug resistance

Sydney M. Shaffer, Margaret C. Dunagin, Stefan R. Torborg, Eduardo A. Torre, Benjamin Emert, Clemens Krepler, Marilda Beqiri, Katrin Sproesser, Patricia A. Brafford, Min Xiao, Elliott Eggan, Ioannis N. Anastopoulos, Cesar A. Vargas-Garcia, Abhyudai Singh, Katherine L. Nathanson, Meenhard Herlyn and Arjun Raj ()
Additional contact information
Sydney M. Shaffer: University of Pennsylvania
Margaret C. Dunagin: University of Pennsylvania
Stefan R. Torborg: University of Pennsylvania
Eduardo A. Torre: University of Pennsylvania
Benjamin Emert: Perelman School of Medicine, University of Pennsylvania
Clemens Krepler: The Wistar Institute, Molecular and Cellular Oncogenesis Program, Melanoma Research Center
Marilda Beqiri: The Wistar Institute, Molecular and Cellular Oncogenesis Program, Melanoma Research Center
Katrin Sproesser: The Wistar Institute, Molecular and Cellular Oncogenesis Program, Melanoma Research Center
Patricia A. Brafford: The Wistar Institute, Molecular and Cellular Oncogenesis Program, Melanoma Research Center
Min Xiao: The Wistar Institute, Molecular and Cellular Oncogenesis Program, Melanoma Research Center
Elliott Eggan: Perelman School of Medicine, University of Pennsylvania
Ioannis N. Anastopoulos: Perelman School of Medicine, University of Pennsylvania
Cesar A. Vargas-Garcia: Electrical and Computer Engineering, University of Delaware
Abhyudai Singh: Electrical and Computer Engineering, University of Delaware
Katherine L. Nathanson: Perelman School of Medicine, University of Pennsylvania
Meenhard Herlyn: The Wistar Institute, Molecular and Cellular Oncogenesis Program, Melanoma Research Center
Arjun Raj: University of Pennsylvania

Nature, 2017, vol. 546, issue 7658, 431-435

Abstract: Through drug exposure, a rare, transient transcriptional program characterized by high levels of expression of known resistance drivers can get ‘burned in’, leading to the selection of cells endowed with a transcriptional drug resistance and thus more chemoresistant cancers.

Date: 2017
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DOI: 10.1038/nature22794

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