Authors

Bradley Garman, University of Pennsylvania
Ioannis N. Anastopoulos, University of Pennsylvania
Clemens Krepler, The Wistar Institute
Patricia Brafford, The Wistar Institute
Katrin Sproesser, The Wistar Institute
Yuchao Jiang, University of Pennsylvania
Bradley Wubbenhorst, University of Pennsylvania
Ravi Amaravadi, University of Pennsylvania
Joseph Bennett, Christiana Care Health System
Marilda Beqiri, The Wistar Institute
David Elder, University of Pennsylvania
Keith T. Flaherty, Massachusetts General Hospital
Dennie T. Frederick, Massachusetts General Hospital
Tara C. Gangadhar, University of Pennsylvania
Michael Guarino, Christiana Care Health System
David Hoon, Providence Saint John's Health Center
Giorgos Karakousis, University of Pennsylvania
Qin Liu, The Wistar Institute
Nandita Mitra, University of Pennsylvania
Nicholas J. Petrelli, Christiana Care Health System
Lynn Schuchter, University of Pennsylvania,
Batool Shannan, The Wistar Institute
Carol L. Shields, Thomas Jefferson UniversityFollow
Jennifer Wargo, University of Texas MD Anderson Cancer Center
Brandon Wenz, University of Pennsylvania,
Melissa A. Wilson, NYU School of Medicine, NYU Langone Medical Center
Min Xiao, The Wistar Institute
Wei Xu, University of Pennsylvania
Xaiowei Xu, University of Pennsylvania
Xiangfan Yin, The Wistar Institute
Nancy R. Zhang, University of Pennsylvania,
Michael A. Davies, University of Texas MD Anderson Cancer Center
Meenhard Herlyn, The Wistar Institute
Katherine L. Nathanson, University of Pennsylvania,

Document Type

Article

Publication Date

11-14-2017

Comments

This article has been peer reviewed. It is the author’s final published version in Cell Reports

Volume 21, Issue 7, November 2017, Pages 1936-1952

The published version is available at DOI: 10.1016/j.celrep.2017.10.052. Copyright © Garman et al.

Abstract

Tumor-sequencing studies have revealed the widespread genetic diversity of melanoma. Sequencing of 108 genes previously implicated in melanomagenesis was performed on 462 patient-derived xenografts (PDXs), cell lines, and tumors to identify mutational and copy number aberrations. Samples came from 371 unique individuals: 263 were naive to treatment, and 108 were previously treated with targeted therapy (34), immunotherapy (54), or both (20). Models of all previously reported major melanoma subtypes (BRAF, NRAS, NF1, KIT, and WT/WT/WT) were identified. Multiple minor melanoma subtypes were also recapitulated, including melanomas with multiple activating mutations in the MAPK-signaling pathway and chromatin-remodeling gene mutations. These well-characterized melanoma PDXs and cell lines can be used not only as reagents for a large array of biological studies but also as pre-clinical models to facilitate drug development.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

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