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Ethan S. Barnett on Muck Rack

Ethan S. Barnett

As seen in: Nature, Cell Press, European Urology
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Articles

Germline homologous recombination deficiency influences TP53 -mutant clonal hematopoiesis fitness during platinum and PARP inhibitor treatment

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By Jeremy T. Baeten, Irenaeus C. C. Chan, Lea A. Moukarzel, Giulia Petrone, Jie Liu, Duc Thanh Tran, Imene Tabet, Sumedha Agashe, Amber Carter, Minal Patel, Konrad H. Stopsack, Philip W. Kantoff, Weiyin Zhou, J. Scott Beeler, Griffen Mustion, Paul Pharoah, James Brenton, Kenneth Offit, Ethan S. Barnett, Bob Li, Wassim Abida, Alison M. Schram, Britta Weigelt, David M. Mutch, Alessandro Vindigni, Mary Mullen, Carlos Cruchaga, Howard I. Scher, Ross Levine, Elli Papaemmanuil, Mitchell J Machiela, Karen A Cadoo, Daniel Link, Kelly Bolton, Jacob Tabs, Elaheh Nasrollahzadeh, Ankush Vasireddy, Armel L. Batchi-Bouyou
| Nature Verified
Abstract Poly(ADP-ribose) polymerase inhibitors (PARPi) are commonly used in tumors with homologous recombination deficiency (HRD) but are associated with an increased risk of therapy-related myeloid neoplasms (tMN). Clonal hematopoiesis (CH) driven by DNA damage response (DDR) mutations is the origin of most tMN. Here, to better understand the causes of tMN following PARPi therapy, we studied the relationship between PARPi use and CH.
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Analysis of BRCA2 Copy Number Loss and Genomic Instability in Circulating Tumor Cells from Patients with Metastatic Castration-resistant Prostate Cancer

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By Ethan S. Barnett, Nikolaus Schultz, Konrad H. Stopsack, Ernest T Lam
| European Urology Verified
BRCA2 alterations predict for a response to poly-ADP-ribose polymerase inhibition in metastatic castration-resistant prostate cancer (mCRPC). However, detection is hindered by insufficient tumor tissue and low sensitivity of cell-free DNA for detecting copy number loss. To evaluate the BRCA2 loss detection using single-cell, shallow whole-genome sequencing (sWGS) of circulating tumor cells (CTCs) in patients with mCRPC.
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Optimizing the future: how mathematical models inform treatment schedules for cancer

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By Deepti Mathur, Ethan S. Barnett, Howard I. Scher, João Xavier
| Cell Press Verified
Highlights For decades, mathematical models have influenced how we schedule chemotherapeutics: the most notable example stems from the Norton–Simon hypothesis which led to the advent of dose-dense scheduling to improve disease-free and overall survival. Newer mathematical models have leveraged game theory and ecological principles to propose adaptive therapy scheduling, with the aim of stabilizing a patient's disease and preventing the growth of surviving resistant cell populations.
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