Shaun D Fouse
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Explore the profile of Shaun D Fouse including associated specialties, affiliations and a list of published articles.
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19
Citations
3445
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Recent Articles
1.
Vainio L, Szabo Z, Lin R, Ulvila J, Yrjola R, Alakoski T, et al.
JACC Basic Transl Sci
. 2019 Mar;
4(1):83-94.
PMID: 30847422
Myocardial infarction (MI)-induced cardiac fibrosis attenuates cardiac contractile function, and predisposes to arrhythmias and sudden cardiac death. Expression of connective tissue growth factor (CTGF) is elevated in affected organs in...
2.
Bell R, Rube H, Kreig A, Mancini A, Fouse S, Nagarajan R, et al.
Science
. 2015 May;
348(6238):1036-9.
PMID: 25977370
Reactivation of telomerase reverse transcriptase (TERT) expression enables cells to overcome replicative senescence and escape apoptosis, which are fundamental steps in the initiation of human cancer. Multiple cancer types, including...
3.
van Thuijl H, Mazor T, Johnson B, Fouse S, Aihara K, Hong C, et al.
Acta Neuropathol
. 2015 Mar;
129(4):597-607.
PMID: 25724300
Temozolomide (TMZ) increases the overall survival of patients with glioblastoma (GBM), but its role in the clinical management of diffuse low-grade gliomas (LGG) is still being defined. DNA hypermethylation of...
4.
Nagarajan R, Zhang B, Bell R, Johnson B, Olshen A, Sundaram V, et al.
Genome Res
. 2014 Apr;
24(5):761-74.
PMID: 24709822
Aberrant DNA hypomethylation may play an important role in the growth rate of glioblastoma (GBM), but the functional impact on transcription remains poorly understood. We assayed the GBM methylome with...
5.
Johnson B, Mazor T, Hong C, Barnes M, Aihara K, McLean C, et al.
Science
. 2013 Dec;
343(6167):189-193.
PMID: 24336570
Tumor recurrence is a leading cause of cancer mortality. Therapies for recurrent disease may fail, at least in part, because the genomic alterations driving the growth of recurrences are distinct...
6.
Fouse S, Nakamura J, James C, Chang S, Costello J
Neuro Oncol
. 2013 Dec;
16(3):361-71.
PMID: 24311636
Background: Glioblastoma multiforme (GBM) contains a population of cells that exhibit stem cell phenotypes. These cancer stem cells (CSCs) may be a source of therapeutic resistance, although support for this...
7.
Sun M, Kim J, Oh M, Safaee M, Kaur G, Clark A, et al.
Neuro Oncol
. 2013 Jul;
15(11):1518-31.
PMID: 23887941
Background: Mechanisms of glioma invasion remain to be fully elucidated. Glioma cells within glioblastoma multiforme (GBM) range from well-differentiated tumor cells to less-differentiated brain tumor-initiating cells (BTICs). The β2-subunit of...
8.
Fouse S, Costello J
Cancer Cell
. 2013 Jun;
23(6):711-3.
PMID: 23763996
Activated STAT3 and increased expression of the histone methyltransferase EZH2 are independently associated with the most malignant subset of gliomas. In this issue of Cancer Cell, Kim and colleagues discover...
9.
Nagarajan R, Fouse S, Bell R, Costello J
Adv Exp Med Biol
. 2012 Sep;
754:313-38.
PMID: 22956508
Accurate detection of epimutations in tumor cells is crucial for -understanding the molecular pathogenesis of cancer. Alterations in DNA methylation in cancer are functionally important and clinically relevant, but even...
10.
Lu K, Chang J, Parachoniak C, Pandika M, Aghi M, Meyronet D, et al.
Cancer Cell
. 2012 Jul;
22(1):21-35.
PMID: 22789536
Inhibition of VEGF signaling leads to a proinvasive phenotype in mouse models of glioblastoma multiforme (GBM) and in a subset of GBM patients treated with bevacizumab. Here, we demonstrate that...