Sean D McGrath
Overview
Explore the profile of Sean D McGrath including associated specialties, affiliations and a list of published articles.
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24
Citations
7231
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Recent Articles
1.
Miller A, Wijeratne S, McGrath S, Schieffer K, Miller K, Lee K, et al.
J Mol Diagn
. 2022 Oct;
24(12):1292-1306.
PMID: 36191838
Genomic profiling using short-read sequencing has utility in detecting disease-associated variation in both DNA and RNA. However, given the frequent occurrence of structural variation in cancer, molecular profiling using long-read...
2.
LaHaye S, Fitch J, Voytovich K, Herman A, Kelly B, Lammi G, et al.
BMC Genomics
. 2021 Dec;
22(1):872.
PMID: 34863095
Background: Pediatric cancers typically have a distinct genomic landscape when compared to adult cancers and frequently carry somatic gene fusion events that alter gene expression and drive tumorigenesis. Sensitive and...
3.
Melas M, Kautto E, Franklin S, Mori M, McBride K, Mosher T, et al.
Hum Mutat
. 2021 Dec;
43(2):189-199.
PMID: 34859533
Synpolydactyly 1, also called syndactyly type II (SDTY2), is a genetic limb malformation characterized by polydactyly with syndactyly involving the webbing of the third and fourth fingers, and the fourth...
4.
Koo S, LaHaye S, Kovari B, Schieffer K, Ranalli M, Aldrink J, et al.
Genes Chromosomes Cancer
. 2021 May;
60(9):640-646.
PMID: 34041825
Gastroblastomas are rare tumors with a biphasic epithelioid/spindle cell morphology that typically present in early adulthood and have recurrent MALAT1-GLI1 fusions. We describe an adolescent patient with Wiskott-Aldrich syndrome who...
5.
Gupta A, Belsky J, Schieffer K, Leraas K, Varga E, McGrath S, et al.
Cold Spring Harb Mol Case Stud
. 2020 Oct;
6(5).
PMID: 33028644
Infantile fibrosarcoma (IFS) is nearly universally driven by gene fusions involving the NTRK family. fusions account for ∼85% of alterations; the remainder are attributed to NTRK-variant fusions. Rarely, other genomic...
6.
Audano P, Sulovari A, Graves-Lindsay T, Cantsilieris S, Sorensen M, Welch A, et al.
Cell
. 2019 Jan;
176(3):663-675.e19.
PMID: 30661756
In order to provide a comprehensive resource for human structural variants (SVs), we generated long-read sequence data and analyzed SVs for fifteen human genomes. We sequence resolved 99,604 insertions, deletions,...
7.
Zhang J, Griffith M, Miller C, Griffith O, Spencer D, Walker J, et al.
Exp Hematol
. 2017 Aug;
55:19-33.
PMID: 28760689
To detect diverse and novel RNA species comprehensively, we compared deep small RNA and RNA sequencing (RNA-seq) methods applied to a primary acute myeloid leukemia (AML) sample. We were able...
8.
Griffith M, Miller C, Griffith O, Krysiak K, Skidmore Z, Ramu A, et al.
Cell Syst
. 2015 Dec;
1(3):210-223.
PMID: 26645048
Tumors are typically sequenced to depths of 75-100× (exome) or 30-50× (whole genome). We demonstrate that current sequencing paradigms are inadequate for tumors that are impure, aneuploid or clonally heterogeneous....
9.
Welch J, Ley T, Link D, Miller C, Larson D, Koboldt D, et al.
Cell
. 2012 Jul;
150(2):264-78.
PMID: 22817890
Most mutations in cancer genomes are thought to be acquired after the initiating event, which may cause genomic instability and drive clonal evolution. However, for acute myeloid leukemia (AML), normal...
10.
Ding L, Ley T, Larson D, Miller C, Koboldt D, Welch J, et al.
Nature
. 2012 Jan;
481(7382):506-10.
PMID: 22237025
Most patients with acute myeloid leukaemia (AML) die from progressive disease after relapse, which is associated with clonal evolution at the cytogenetic level. To determine the mutational spectrum associated with...