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Richard K. Wilson
Researcher at Nationwide Children's Hospital
Publications - 501
Citations - 294778
Richard K. Wilson is an academic researcher from Nationwide Children's Hospital. The author has contributed to research in topics: Genome & Gene. The author has an hindex of 173, co-authored 463 publications receiving 260000 citations. Previous affiliations of Richard K. Wilson include University of Washington & St. Jude Children's Research Hospital.
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Journal ArticleDOI
Tumor Evolution in Two Patients with Basal-like Breast Cancer: A Retrospective Genomics Study of Multiple Metastases
Katherine A. Hoadley,Marni B. Siegel,Krishna L. Kanchi,Christopher A. Miller,Li Ding,Wei Zhao,Xiaping He,Joel S. Parker,Michael C. Wendl,Robert S. Fulton,Ryan Demeter,Richard K. Wilson,Lisa A. Carey,Charles M. Perou,Elaine R. Mardis +14 more
TL;DR: In these two patients, mutations and DNA copy number changes in the primary tumors appear to have had a biologic impact on metastatic potential, whereas mutations arising in the metastases were much more likely to be passengers.
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Key gp120 Glycans Pose Roadblocks to the Rapid Development of VRC01-Class Antibodies in an HIV-1-Infected Chinese Donor.
Leopold Kong,Leopold Kong,Leopold Kong,Bin Ju,Yajing Chen,Linling He,Li Ren,Jiandong Liu,Kunxue Hong,Bin Su,Zheng Wang,G. Ozorowski,G. Ozorowski,G. Ozorowski,Xiaolin Ji,Yuanzi Hua,Yuanzi Hua,Yuanzi Hua,Yanli Chen,Marc C. Deller,Yanling Hao,Yi Feng,Fernando Garces,Fernando Garces,Fernando Garces,Richard K. Wilson,Kaifan Dai,Sijy O'Dell,Krisha McKee,John R. Mascola,Andrew B. Ward,Andrew B. Ward,Andrew B. Ward,Richard T. Wyatt,Richard T. Wyatt,Yuxing Li,Ian A. Wilson,Jiang Zhu,Yiming Shao,Yiming Shao,Yiming Shao +40 more
TL;DR: Although the DRVIA7 lineage was unable to acquire broad neutralization, longitudinal analysis revealed a repertoire-encoded VRC 01 light-chain CDR3 signature and VRC01-like neutralizing heavy-chain precursors that rapidly matured within 2 years.
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Pangolin genomes and the evolution of mammalian scales and immunity
Siew Choo,Mike Rayko,Tze King Tan,Ranjeev Hari,Aleksey Komissarov,Wei Yee Wee,Andrey A. Yurchenko,Sergey Kliver,Gaik Tamazian,Agostinho Antunes,Richard K. Wilson,Wesley C. Warren,Klaus-Peter Koepfli,Patrick Minx,Ksenia Krasheninnikova,Antoinette Kotze,Desiré L. Dalton,Elaine Vermaak,Ian C. Paterson,Pavel Dobrynin,Frankie Thomas Sitam,Jeffrine J. Rovie-Ryan,Warren E. Johnson,Aini Mohamed Yusoff,Shu-Jin Luo,Kayal Vizi Karuppannan,Gang Fang,Deyou Zheng,Mark Gerstein,Leonard Lipovich,Stephen J. O'Brien,Guat Jah Wong +31 more
TL;DR: It is proposed that scale development was an innovation that provided protection against injuries or stress and reduced pangolin vulnerability to infection, and perhaps a new natural IFNE-deficient animal model for studying mammalian immunity.
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RB1 gene inactivation by chromothripsis in human retinoblastoma
Justina McEvoy,Panduka Nagahawatte,David Finkelstein,Jennifer Richards-Yutz,Marcus B. Valentine,Jing Ma,Charles G. Mullighan,Guangchun Song,Xiang Chen,Matthew W. Wilson,Rachel C. Brennan,Stanely Pounds,Jared Becksfort,Robert Huether,Charles Lu,Robert S. Fulton,Lucinda Fulton,Xin Hong,David J. Dooling,Kerri Ochoa,Elaine R. Mardis,Richard K. Wilson,John Easton,Jinghui Zhang,James R. Downing,Arupa Ganguly,Michael A. Dyer,Michael A. Dyer +27 more
TL;DR: This study identifed recurrent chromosomal, regional and focal genomic lesions in 94 primary retinoblastomas with their matched normal DNA using SNP 6.0 chips and identified 3 tumors with chromothripsis at the RB1 locus, the first report of chromothRIpsis as a mechanism for RB1 gene inactivation in cancer.
Journal ArticleDOI
Distinct patterns of mutations occurring in de novo AML versus AML arising in the setting of severe congenital neutropenia
Daniel C. Link,Ghada M Kunter,Yumi Kasai,Yu Zhao,Tracie L. Miner,Michael D. McLellan,Rhonda E. Ries,Deepak Kapur,Rakesh Nagarajan,David C. Dale,Audrey Anna Bolyard,Laurence A. Boxer,Karl Welte,Cornelia Zeidler,Jean Donadieu,Christine Bellanné-Chantelot,James W. Vardiman,James W. Vardiman,Michael A. Caligiuri,Clara D. Bloomfield,John F. DiPersio,Michael H. Tomasson,Timothy A. Graubert,Peter Westervelt,Mark A. Watson,William D. Shannon,Jack Baty,Elaine R. Mardis,Richard K. Wilson,Timothy J. Ley +29 more
TL;DR: Mutational profiling of 14 genes previously implicated in leukemogenesis using 14 MDS/leukemia samples from patients with SCN supports the hypothesis that mutations of CSF3R may provide the "activated tyrosine kinase signal" that is thought to be important for leukeMogenesis.