Steven N Quayle
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Explore the profile of Steven N Quayle including associated specialties, affiliations and a list of published articles.
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24
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1152
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Recent Articles
11.
Putcha P, Yu J, Rodriguez-Barrueco R, Saucedo-Cuevas L, Villagrasa P, Murga-Penas E, et al.
Breast Cancer Res
. 2015 Dec;
17(1):149.
PMID: 26643555
Introduction: Inflammatory breast cancer (IBC) is the most lethal form of breast cancers with a 5-year survival rate of only 40 %. Despite its lethality, IBC remains poorly understood which...
12.
Mishima Y, Santo L, Eda H, Cirstea D, Nemani N, Yee A, et al.
Br J Haematol
. 2015 Feb;
169(3):423-34.
PMID: 25709080
Proteasome inhibition induces the accumulation of aggregated misfolded/ubiquitinated proteins in the aggresome; conversely, histone deacetylase 6 (HDAC6) inhibition blocks aggresome formation. Although this rationale has been the basis of proteasome...
13.
Johnson D, Spitz G, Tharkar S, Quayle S, Shearstone J, Jones S, et al.
Oncotarget
. 2015 Jan;
6(7):4863-87.
PMID: 25605023
Gain-of-function mutations in the catalytic site of EZH2 (Enhancer of Zeste Homologue 2), is observed in about 22% of diffuse large B-cell lymphoma (DLBCL) cases. Here we show that selective...
14.
Dasmahapatra G, Patel H, Friedberg J, Quayle S, Jones S, Grant S
Mol Cancer Ther
. 2014 Sep;
13(12):2886-97.
PMID: 25239935
Interactions between the HDAC6 inhibitor ricolinostat (ACY1215) and the irreversible proteasome inhibitor carfilzomib were examined in non-Hodgkin lymphoma (NHL) models, including diffuse large B-cell lymphoma (DLBCL), mantle cell lymphoma (MCL),...
15.
Quayle S, Lee J, Cheung L, Ding L, Wiedemeyer R, Dewan R, et al.
PLoS One
. 2012 Nov;
7(11):e49466.
PMID: 23166678
The phosphoinositide 3-kinase (PI3K) pathway is targeted for frequent alteration in glioblastoma (GBM) and is one of the core GBM pathways defined by The Cancer Genome Atlas. Somatic mutations of...
16.
Quayle S, Chheda M, Shukla S, Wiedemeyer R, Tamayo P, Dewan R, et al.
Neuro Oncol
. 2012 Oct;
14(11):1325-31.
PMID: 23074196
Large-scale cancer genomics efforts are identifying hundreds of somatic genomic alterations in glioblastoma (GBM). Distinguishing between active driver and neutral passenger alterations requires functional assessment of each gene; therefore, integrating...
17.
Genovese G, Ergun A, Shukla S, Campos B, Hanna J, Ghosh P, et al.
Cancer Discov
. 2012 Jul;
2(8):736-49.
PMID: 22750848
Unlabelled: Leveraging The Cancer Genome Atlas (TCGA) multidimensional data in glioblastoma, we inferred the putative regulatory network between microRNA and mRNA using the Context Likelihood of Relatedness modeling algorithm. Interrogation...
18.
Dunn G, Rinne M, Wykosky J, Genovese G, Quayle S, Dunn I, et al.
Genes Dev
. 2012 Apr;
26(8):756-84.
PMID: 22508724
Glioblastoma is both the most common and lethal primary malignant brain tumor. Extensive multiplatform genomic characterization has provided a higher-resolution picture of the molecular alterations underlying this disease. These studies...
19.
Wiedemeyer W, Dunn I, Quayle S, Zhang J, Chheda M, Dunn G, et al.
Proc Natl Acad Sci U S A
. 2010 Jun;
107(25):11501-6.
PMID: 20534551
Glioblastoma multiforme (GBM) is a fatal primary brain tumor harboring myriad genetic and epigenetic alterations. The recent multidimensional analysis of the GBM genome has provided a more complete view of...
20.
Zheng H, Ying H, Wiedemeyer R, Yan H, Quayle S, Ivanova E, et al.
Cancer Cell
. 2010 May;
17(5):497-509.
PMID: 20478531
A hallmark feature of glioblastoma is its strong self-renewal potential and immature differentiation state, which contributes to its plasticity and therapeutic resistance. Here, integrated genomic and biological analyses identified PLAGL2...