Schmit, Travis - Date Last Updated: 09/30/2009

Travis Schmit - Email
PhD Candidate - Started 2005
Stoughton, WI
Lab of Nihal Ahmad, PhD

Undergraduate Work
University of Wisconsin-Madison
Bachelors of Science, Genetics (2005)

Memberships
Associate Member of American Association for Cancer Research

Interests/Hobbies
Photography, football, baseball, hunting, fishing, in other words, anything outdoors, and playing with my 2-year old son Mason.

Research as of May 2006
The focus of my research is to explore the involvement of the Polo-like kinases (Plks), a conserved serine/threonine family of kinases critical for mitosis regulation, in the development of cancer. Many environmental stresses (such as shifts in temperature, osmolarity, radiation and chemicals) may lead to problems with actin cytoskeleton and cytokinesis, and Plks have been shown to be critical regulators of these processes. Further, a major hallmark of cancer is the dysregulation of key cell cycle components arising from mutations produced by environmentally induced oxidative stress and the resulting DNA damage. These include tumor suppressor genes that, when mutated, are unable to control cell cycle checkpoints and allow the cell to proliferate unchecked, or oncogenes which become constitutively active and promote cellular growth. The Plk family of mitotic kinases contains both members that can act in an oncogenic manner and members that act as tumor suppressors.

I am studying the role of Plk1 and Plk3 in cancer development. Plk1, the most widely studied member of this kinase family, promotes Cdk1/CyclinB1 activity which is the main driving force into and through mitosis. Conversely, Plk3 acts in an inhibitory manner in the presence of DNA damage opposing the activity of Plk1 and halting cell cycle progression until repair is performed or the cell undergoes apoptosis. Thus, my focus is to determine the role of the Plks in cancer development and to establish if their dysregulation has a cause-and-effect association with disease progression. The outcome of this work may lead to development of novel strategies for the management of cancer.

Publications

Schmit TL, Zhong W, Setaluri V, Spiegelman VS, Ahmad N. Targeted Depletion of Polo-Like Kinase (Plk) 1 Through Lentiviral shRNA or a Small-Molecule Inhibitor Causes Mitotic Catastrophe and Induction of Apoptosis in Human Melanoma Cells. J
Invest Dermatol 2009 (Epub ahead of print)
Schmit TL, Zhong W, Nihal M, Ahmad - Polo-like kinase 1 (Plk1) in non-melanoma skin cancers. N. Cell Cycle 8:17, 2697-2702. 2009
Schmit TL, Ahmad N. Regulation of mitosis via mitotic kinases: new opportunities for cancer management. Mol Cancer Ther 2007;6(7):1920–31.

Abstracts/Posters

Travis L. Schmit, Nihal Ahmad. Inhibition of polo-like kinase 1 activity causes G2/M phase cell cycle arrest and induction of apoptosis in human melanoma cells. International Investigative Dermatology 2008; May 14-17; Kyoto, Japan; Abstract 1325.
Travis L. Schmit, Nihal Ahmad. Inhibition of polo-like kinase 1 activity by a small molecule inhibitor GW842682X causes a G2/M phase cell cycle arrest and induction of apoptosis in human melanoma cells. Proc. Amer. Assoc. Can. Res.; 2008, Apr 12-16; San Diego, CA. Abstract 5662.
Travis L. Schmit, Minakshi Nihal, Nihal Ahmad. Polo-like kinase 1 is overexpressed in skin cancer cells and human skin cancers: A novel target for intervention. J. Invest. Dermatol. 2007; 127(S1): S28 Abstract 167.
Travis L. Schmit, Minakshi Nihal, Nihal Ahmad. Polo-like kinase 1: a new target for the management of skin cancers. Proc. Amer. Assoc. Can. Res.; 2007 Apr 14-18; Los Angeles, CA. Abstract 5410.

Travis Schmit

Photo Credit: Chris Frazee, Media Solutions

Date Last Updated: 09/30/2009 webteam@med.wisc.edu