Eric P Stoffregen
Overview
Explore the profile of Eric P Stoffregen including associated specialties, affiliations and a list of published articles.
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Articles
17
Citations
1020
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0
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Recent Articles
1.
Ruchert J, Brady M, McMahan S, Lacey K, Latta L, Sekelsky J, et al.
Genetics
. 2021 Dec;
220(1).
PMID: 34849849
The absence of functional BLM DNA helicase, a member of the RecQ family of helicases, is responsible for the rare human disorder Bloom Syndrome, which results in developmental abnormalities, DNA...
2.
LaFave M, Andersen S, Stoffregen E, Holsclaw J, Kohl K, Overton L, et al.
Genetics
. 2013 Nov;
196(1):107-18.
PMID: 24172129
The Bloom syndrome helicase, BLM, has numerous functions that prevent mitotic crossovers. We used unique features of Drosophila melanogaster to investigate origins and properties of mitotic crossovers that occur when...
3.
Donley N, Stoffregen E, Smith L, Montagna C, Thayer M
PLoS Genet
. 2013 Apr;
9(4):e1003423.
PMID: 23593023
Mammalian chromosomes initiate DNA replication at multiple sites along their length during each S phase following a temporal replication program. The majority of genes on homologous chromosomes replicate synchronously. However,...
4.
Stoffregen E, Donley N, Stauffer D, Smith L, Thayer M
Hum Mol Genet
. 2011 Apr;
20(12):2366-78.
PMID: 21459774
Mammalian DNA replication initiates at multiple sites along chromosomes at different times, following a temporal replication program. Homologous alleles typically replicate synchronously; however, mono-allelically expressed genes such as imprinted genes,...
5.
Loriaux M, Levine R, Tyner J, Frohling S, Scholl C, Stoffregen E, et al.
Blood
. 2008 Feb;
111(9):4788-96.
PMID: 18252861
To determine whether aberrantly activated tyrosine kinases other than FLT3 and c-KIT contribute to acute myeloid leukemia (AML) pathogenesis, we used high-throughput (HT) DNA sequence ana-lysis to screen exons encoding...
6.
Griswold I, Macpartlin M, Bumm T, Goss V, OHare T, Lee K, et al.
Mol Cell Biol
. 2006 Aug;
26(16):6082-93.
PMID: 16880519
Kinase domain (KD) mutations of Bcr-Abl interfering with imatinib binding are the major mechanism of acquired imatinib resistance in patients with Philadelphia chromosome-positive leukemia. Mutations of the ATP binding loop...
7.
Walters D, Mercher T, Gu T, OHare T, Tyner J, Loriaux M, et al.
Cancer Cell
. 2006 Jul;
10(1):65-75.
PMID: 16843266
Tyrosine kinases are aberrantly activated in numerous malignancies, including acute myeloid leukemia (AML). To identify tyrosine kinases activated in AML, we developed a screening strategy that rapidly identifies tyrosine-phosphorylated proteins...
8.
Walters D, Goss V, Stoffregen E, Gu T, Lee K, Nardone J, et al.
Leuk Res
. 2006 Feb;
30(9):1097-104.
PMID: 16464493
STAT5 is constitutively phosphorylated in leukemic cells in approximately 70% of acute myeloid leukemia (AML) patients. To identify kinase candidates potentially responsible for STAT5 phosphorylation, we used liquid chromatography-tandem mass...
9.
OHare T, Walters D, Stoffregen E, Sherbenou D, Heinrich M, Deininger M, et al.
Clin Cancer Res
. 2005 Oct;
11(19 Pt 1):6987-93.
PMID: 16203792
Purpose: Chronic myeloid leukemia (CML) is effectively treated with imatinib. However, reactivation of Bcr-Abl via kinase domain mutations that reduce sensitivity to imatinib can cause relapse. As combination therapy is...
10.
OHare T, Walters D, Stoffregen E, Jia T, Manley P, Mestan J, et al.
Cancer Res
. 2005 Jun;
65(11):4500-5.
PMID: 15930265
Imatinib, a Bcr-Abl tyrosine kinase inhibitor, is a highly effective therapy for patients with chronic myelogenous leukemia (CML). Despite durable responses in most chronic phase patients, relapses have been observed...