Interdisciplinary Life Science - PULSe Great research is a matter of choice

Michael Wendt

Michael Wendt Profile Picture

Assistant Professor
Ph.D., Medical College of Wisconsin (2007)


Contact Info:

mwendt@purdue.edu

(765) 494-0860


Training Group(s):
Immunology and Infectious Diseases
Molecular Signaling and Cancer Biology


Current Research Interests:

Research in the Wendt lab focuses on pharmacological targeting of molecular players involved in the metastatic outgrowth of breast cancer. Systemic dissemination is an extremely early event in breast cancer progression, therefore we primarily focus on developing strategies that are specifically designed to target secondary tumors. We take two major approaches to this challenge: 1.Through metastatic progression breast cancer cells under epithelial-mesenchymal transition (EMT) and reverse process of mesenchymal-epithelial transition (MET). An overriding hypothesis in the lab is that through the processes of EMT:MET the secondary epithelial state that characterizes the metastatic tumor is fundamentally unique from the epithelial status of the primary tumors. We believe these differences hold the keys to developing therapeutics capable to pharmacologically treating metastatic lesions. 2.Subsequent to dissemination, a large fraction of tumor cells enter into an asymptomatic state of dormancy. The ability of normal organs to resist tumor secondary tumor formation is the body’s last defense against metastatic disease progression. The environmental factors (drugs, alcohol, diet, etc…) capable of “awaking” disseminated cells are poorly characterized. Understanding these factors is required if we hope to design therapeutics capable of maintaining systemic tumor dormancy.



Selected Publications:

Brown WS, Tan L, Smith A, Gray NS, Wendt MK. Covalent targeting of fibroblast growth factor receptor inhibits metastatic breast cancer. Molecular Cancer Therapeutics. 2016

Brown WS, Akhand SS, Wendt MK. FGFR signaling maintains a drug persistent state following induction of epithelial-mesenchymal transition. Oncotarget. 2016

Bartolowits MD, Brown W, Ali R, Pedley AM, Chen Q, Harvey KE, Wendt MK, Davisson VJ. Selective inhibition of STAT3 phosphorylation using a nuclear-targeted kinase inhibitor. ACS Chem Biol. 2017

Wilmanski T, Zhou X, Zheng W, Shinde A, Donkin SS, Wendt MK, Burgess JR, Teegarden D. Inhibition of Pyruvate Carboxylase by 1,alpha,25-Dihydroxyvitamin D Promotes Oxidative Stress in Early Breast Cancer Progression. Cancer Letters. 2017

Hardy S, Shinde A, Wang WH, Wendt MK, Geahlen R. Regulation of epithelial-mesenchymal transition and metastasis by TGF-, P-bodies, and autophagy. Oncotarget. 2017

Shinde A, Wilmanski T, Chen H, Teegarden D, Wendt MK. Pyruvate carboxylase supports the pulmonary tropism of metastatic breast cancer. Breast Cancer Research, 2018.

Reviews:

Ali RA, Akhand SS, Wendt MK. Targeting FGFR for the treatment of breast cancer. Resistance to Targeted Therapies in Breast cancer. 2017

Ali RA, Wendt MK. The paradoxical functions of EGFR during breast cancer progression. Signal transduction and targeted therapy. 2017.

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