R
Robert S. Fulton
Researcher at Washington University in St. Louis
Publications - 254
Citations - 167513
Robert S. Fulton is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Genome & Gene. The author has an hindex of 109, co-authored 230 publications receiving 143530 citations. Previous affiliations of Robert S. Fulton include University of Washington & Brown University.
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Journal ArticleDOI
Clinical outcomes and differential effects of PI3K pathway mutation in obese versus non-obese patients with cervical cancer.
Perry W. Grigsby,Adnan Elhammali,Fiona Ruiz,Stephanie Markovina,Michael D. McLellan,Christopher A. Miller,Anupama Chundury,Ngoc Anh L. Ta,Ramachandran Rashmi,John D. Pfeifer,Robert S. Fulton,Todd DeWees,Julie K. Schwarz +12 more
TL;DR: It is shown that patients with obesity at the time of diagnosis of cervical cancer exhibit improved outcomes after radiation, and PI3K/AKT pathway mutations are common in obese patients, but are not associated with activation of AKT signaling.
Journal ArticleDOI
Immunosuppression and outcomes in adult patients with de novo acute myeloid leukemia with normal karyotypes.
Francesca Ferraro,Christopher A. Miller,Keegan A. Christensen,Nichole M. Helton,Margaret O’Laughlin,Catrina Fronick,Robert S. Fulton,Jessica Kohlschmidt,Ann-Kathrin Eisfeld,Clara D. Bloomfield,Sai Mukund Ramakrishnan,Ryan B. Day,Lukas D. Wartman,Geoffrey L. Uy,John S. Welch,Matthew J. Christopher,Sharon Heath,Jack Baty,Matthew J. Schuelke,Jacqueline E. Payton,David H. Spencer,Michael P. Rettig,Daniel C. Link,Matthew J. Walter,Peter Westervelt,John F. DiPersio,Timothy J. Ley +26 more
TL;DR: Using exome sequencing, RNA-sequencing, and functional immunologic studies, this article characterized 28 normal karyotype (NK)-AML patients with >5 y first remissions after chemotherapy (LFRs).
Journal ArticleDOI
The Role Of Early TP53 Mutations On The Evolution Of Therapy-Related AML
Giridharan Ramsingh,Andrew L. Young,Dong Shen,Christopher A. Miller,Tamara Lamprecht,Sharon Heath,Robert S. Fulton,Elaine R. Mardis,Li Ding,Peter Westervelt,John S. Welch,Matthew J. Walter,Timothy A. Graubert,John F. DiPersio,Timothy J. Ley,Todd E. Druley,Richard K. Wilson,Daniel C. Link +17 more
TL;DR: There is no evidence that chemotherapy induces genome-wide DNA damage in t-AML, and a model in which rare TP53 mutant-bearing HSC clones have a selective growth advantage in patients undergoing chemotherapy is proposed.
Posted ContentDOI
Mutation detection in thousands of acute myeloid leukemia cells using single cell RNA-sequencing
Allegra A. Petti,Stephen R. Williams,Christopher A. Miller,Ian T. Fiddes,Sridhar Nonavinkere Srivatsan,David Y. Chen,Catrina Fronick,Robert S. Fulton,Deanna M. Church,Timothy J. Ley +9 more
TL;DR: An approach that integrates enhanced whole genome sequencing with the 10x Genomics Chromium Single Cell 5’ Gene Expression workflow to directly link expressed mutations with transcriptional profiles at single cell resolution is developed and is broadly applicable for analysis of any sample that is phenotypically and genetically heterogeneous.
Journal ArticleDOI
Brief Report: The Role of Rare Protein-Coding Variants in Anti-Tumor Necrosis Factor Treatment Response in Rheumatoid Arthritis.
Jing Cui,Dorothée Diogo,Eli A. Stahl,Helena Canhão,Xavier Mariette,Jeff Greenberg,Yukinori Okada,Dimitrios A. Pappas,Robert S. Fulton,Paul P. Tak,Michael T. Nurmohamed,Annette Lee,David E. Larson,Fina A S Kurreeman,Tracie L. Deluca,Michelle O'Laughlin,Catrina Fronick,Lucinda Fulton,Elaine R. Mardis,Irene E. van der Horst-Bruinsma,Gertjan Wolbink,Peter K. Gregersen,Joel M. Kremer,J. Bart A. Crusius,Niek de Vries,Tom W J Huizinga,João Eurico Fonseca,Corinne Miceli-Richard,Elizabeth W. Karlson,Marieke J H Coenen,Anne Barton,Robert M. Plenge,Soumya Raychaudhuri +32 more
TL;DR: In this paper, the coding region of 750 genes in 1,094 rheumatoid arthritis patients of European ancestry treated with anti-TNF medications were sequenced, and the authors found that rare and low-frequency protein-coding variants in TNF signaling pathway genes or other genes do not contribute substantially to RA patients.