Stephanie G Willis
Overview
Explore the profile of Stephanie G Willis including associated specialties, affiliations and a list of published articles.
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Articles
12
Citations
673
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0
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Recent Articles
1.
Chang B, Willis S, Stork L, Hunger S, Carroll W, Camitta B, et al.
Br J Haematol
. 2012 Feb;
157(4):507-10.
PMID: 22299775
No abstract available.
2.
McWeeney S, Pemberton L, Loriaux M, Vartanian K, Willis S, Yochum G, et al.
Blood
. 2009 Oct;
115(2):315-25.
PMID: 19837975
In chronic-phase chronic myeloid leukemia (CML) patients, the lack of a major cytogenetic response (< 36% Ph(+) metaphases) to imatinib within 12 months indicates failure and mandates a change of...
3.
Press R, Willis S, Laudadio J, Mauro M, Deininger M
Blood
. 2009 Jul;
114(13):2598-605.
PMID: 19625707
In imatinib-treated chronic myeloid leukemia (CML), secondary drug resistance is often caused by mutations in the BCR-ABL kinase domain (KD). As alternative therapies are available for imatinib resistance, early identification...
4.
Tyner J, Deininger M, Loriaux M, Chang B, Gotlib J, Willis S, et al.
Proc Natl Acad Sci U S A
. 2009 May;
106(21):8695-700.
PMID: 19433805
Targeted therapy has vastly improved outcomes in certain types of cancer. Extension of this paradigm across a broad spectrum of malignancies will require an efficient method to determine the molecular...
5.
Tyner J, Erickson H, Deininger M, Willis S, Eide C, Levine R, et al.
Blood
. 2008 Dec;
113(8):1749-55.
PMID: 19075190
Transforming mutations in NRAS and KRAS are thought to play a causative role in the development of numerous cancers, including myeloid malignancies. Although mutations at amino acids 12, 13, or...
6.
Agarwal A, Bumm T, Corbin A, OHare T, Loriaux M, VanDyke J, et al.
Blood
. 2008 Jun;
112(5):1960-70.
PMID: 18559973
BCR-ABL is proposed to impair cell-cycle control by disabling p27, a tumor suppressor that inhibits cyclin-dependent kinases. We show that in cell lines p27 expression is inversely correlated with expression...
7.
Tyner J, Walters D, Willis S, Luttropp M, Oost J, Loriaux M, et al.
Blood
. 2007 Nov;
111(4):2238-45.
PMID: 18025156
Despite vast improvements in our understanding of cancer genetics, a large percentage of cancer cases present without knowledge of the causative genetic events. Tyrosine kinases are frequently implicated in the...
8.
Press R, Galderisi C, Yang R, Rempfer C, Willis S, Mauro M, et al.
Clin Cancer Res
. 2007 Oct;
13(20):6136-43.
PMID: 17947479
Purpose: Imatinib induces a complete cytogenetic response (CCR) in most chronic myeloid leukemia patients in chronic phase. Although CCR is usually durable, a minority of patients relapse. Biomarkers capable of...
9.
Bradeen H, Eide C, OHare T, Johnson K, Willis S, Lee F, et al.
Blood
. 2006 Jun;
108(7):2332-8.
PMID: 16772610
BMS-354825 (dasatinib) and AMN107 (nilotinib) are potent alternate Abl inhibitors with activity against many imatinib mesylate-resistant BCR-ABL kinase domain (KD) mutants, except T315I. We used N-ethyl-N-nitrosourea (ENU)-exposed Ba/F3-p210(BCR-ABL) cells to...
10.
Lange T, Park B, Willis S, Deininger M
Cell Cycle
. 2005 Dec;
4(12):1761-6.
PMID: 16319529
Patients with chronic myeloid leukemia (CML) treated with imatinib in early chronic phase tend to have durable remissions, but there is a high rate of relapse in patients with advanced...