M
Michael W. Lee
Researcher at University of Texas at Austin
Publications - 36
Citations - 1014
Michael W. Lee is an academic researcher from University of Texas at Austin. The author has contributed to research in topics: Cancer & Apoptosis. The author has an hindex of 12, co-authored 32 publications receiving 830 citations. Previous affiliations of Michael W. Lee include University of Central Florida & University of South Florida.
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Journal ArticleDOI
The Use of Therapeutic Peptides to Target and to Kill Cancer Cells
TL;DR: Current research focuses on developing peptides that can (1) serve as tumor targeting moieties and (2) permeabilize membranes with cytotoxic consequences, and a survey of recent findings reveals significant trends.
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Inactivation of Wnt inhibitory factor-1 (WIF1) expression by epigenetic silencing is a common event in breast cancer
Lingbao Ai,Qian Tao,Sheng Zhong,C. Robert Fields,Wan Ju Kim,Michael W. Lee,Yan Cui,Kevin D. Brown,Keith D. Robertson +8 more
TL;DR: The findings establish the WIF1 gene as a target for epigenetic silencing in breast cancer and provide a mechanistic link between the dysregulation of Wnt signaling and breast tumorigenesis.
Journal Article
Epothilone B analogue (BMS-247550)-mediated cytotoxicity through induction of Bax conformational change in human breast cancer cells.
Hirohito Yamaguchi,Shanthi R. Paranawithana,Michael W. Lee,Ziwei Huang,Kapil N. Bhalla,Hong Gang Wang +5 more
TL;DR: It is demonstrated that EpoB induces apoptosis through a Bcl-2-suppressible pathway that controls a conformational change of the proapoptotic Bax protein.
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Valproic acid as an adjunctive therapeutic agent for the treatment of breast cancer
TL;DR: This review discusses the underlying molecular rationale for using HDAC inhibitors for the treatment of breast cancer, and focuses on the FDA approved HDAC inhibitor valproic acid (VPA), which has been shown to alter proliferation, survival, cell migration, and hormone receptor expression of Breast cancer cells in both the pre-clinical and clinical settings.
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Arsenic trioxide (As2O3) induces apoptosis through activation of Bax in hematopoietic cells
Yanhua Zheng,Hirohito Yamaguchi,Changhai Tian,Michael W. Lee,Hong Tang,Hong Gang Wang,Quan Chen +6 more
TL;DR: The data suggest that As2O3 might exert the cell killing in part by inducing Bax activation through a Bcl-2-suppressible pathway in hematopoietic cells that is caspase independent and intracellular ROS regulated.