A. Hunter Shain
University of California, San Francisco
44 Papers
92 Citations
A. Hunter Shain is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Melanoma & Biology. The author has an hindex of 22, co-authored 35 publications. Previous affiliations of A. Hunter Shain include Stanford University & University of California, Berkeley.
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Papers
CNVkit: Genome-Wide Copy Number Detection and Visualization from Targeted DNA Sequencing
TL;DR: A method for copy number detection, implemented in the software package CNVkit, that uses both the targeted reads and the nonspecifically captured off-target reads to infer copy number evenly across the genome, successfully inferred copy number at equivalent to 100-kilobase resolution genome-wide from a platform targeting as few as 293 genes.
The Genetic Evolution of Melanoma from Precursor Lesions
A. Hunter Shain,Iwei Yeh,Ivanka Kovalyshyn,Aravindhan Sriharan,Eric Talevich,Alexander Gagnon,Reinhard Dummer,Jeffrey P. North,Laura B. Pincus,Beth S. Ruben,William Rickaby,Corrado D’Arrigo,Alistair Robson,Boris C. Bastian +13 more
TL;DR: The succession of genetic alterations during melanoma progression was defined, showing distinct evolutionary trajectories for different melanoma subtypes, and an intermediate category of melanocytic neoplasia was identified, characterized by the presence of more than one pathogenic genetic alteration and distinctive histopathological features.
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From melanocytes to melanomas
A. Hunter Shain,Boris C. Bastian +1 more
TL;DR: This Review delineates several of the more common progression trajectories that occur in the patient setting and proposes models for tumour evolution that integrate genetic, histopathological, clinical and biological insights from the melanoma literature.
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The spectrum of SWI/SNF mutations, ubiquitous in human cancers.
TL;DR: SWI/SNF mutations were widespread across diverse human cancers, with an excess of deleterious mutations, and an overall frequency approaching TP53 mutation, and provide a key resource to guide future investigations.
Exome sequencing of desmoplastic melanoma identifies recurrent NFKBIE promoter mutations and diverse activating mutations in the MAPK pathway.
A. Hunter Shain,Maria C. Garrido,Thomas Botton,Eric Talevich,Iwei Yeh,J. Zachary Sanborn,Jongsuk Chung,Nicholas J. Wang,Hojabr Kakavand,Graham J. Mann,John F. Thompson,John F. Thompson,Thomas Wiesner,Ritu Roy,Adam B. Olshen,Alexander Gagnon,Joe W. Gray,Nam Huh,Joe S Hur,Klaus J. Busam,Richard A. Scolyer,Richard A. Scolyer,Raymond J. Cho,Rajmohan Murali,Boris C. Bastian +24 more
TL;DR: High mutation burden ranked desmoplastic melanoma among the most highly mutated cancers, and genetic alterations known to activate the MAPK and PI3K signaling cascades were identified in 73% of samples, affecting NF1, CBL, ERBB2, MAP2k1, MAP3K1, BRAF, EGFR, PTPN11, MET, RAC1, SOS2, NRAS and PIK3CA.