Human pluripotent stem cells recurrently acquire and expand dominant negative P53 mutations

Florian T. Merkle, Sulagna Ghosh, Nolan Kamitaki, Jana Mitchell, Yishai Avior, Curtis Mello, Seva Kashin, Shila Mekhoubad, Dusko Ilic, Maura Charlton, Genevieve Saphier, Robert E. Handsaker, Giulio Genovese, Shiran Bar, Nissim Benvenisty, Steven A. McCarroll () and Kevin Eggan ()
Additional contact information
Florian T. Merkle: Harvard University
Sulagna Ghosh: Harvard University
Nolan Kamitaki: Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard
Jana Mitchell: Harvard University
Yishai Avior: The Azrieli Center for Stem Cells and Genetic Research, Institute of Life Sciences, Hebrew University of Jerusalem
Curtis Mello: Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard
Seva Kashin: Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard
Shila Mekhoubad: Harvard University
Dusko Ilic: Stem Cell Laboratories, Guy’s Assisted Conception Unit, Faculty of Life Sciences and Medicine, King’s College London
Maura Charlton: Harvard University
Genevieve Saphier: Harvard University
Robert E. Handsaker: Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard
Giulio Genovese: Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard
Shiran Bar: The Azrieli Center for Stem Cells and Genetic Research, Institute of Life Sciences, Hebrew University of Jerusalem
Nissim Benvenisty: The Azrieli Center for Stem Cells and Genetic Research, Institute of Life Sciences, Hebrew University of Jerusalem
Steven A. McCarroll: Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard
Kevin Eggan: Harvard University

Nature, 2017, vol. 545, issue 7653, 229-233

Abstract: The authors surveyed whole-exome and RNA-sequencing data from 252 unique pluripotent stem cell lines, some of which are in the pipeline for clinical use, and found that approximately 5% of cell lines had acquired mutations in the TP53 gene that allow mutant cells to rapidly outcompete non-mutant cells, but do not prevent differentiation.

Date: 2017
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DOI: 10.1038/nature22312

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