2016 Scientific Report

JEFFREY P. MACKEIGAN, PH.D.
Dr. MacKeigan received his Ph.D. in microbiology and immunology at
the University of North Carolina Lineberger Comprehensive Cancer
Center in 2002. Dr. MacKeigan joined VARI in 2006 as an Assistant
Professor and was promoted to Associate Professor in 2010.
STAFF
STEPHANIE CELANO, M.S.
LUCUS CHAN, PH.D.
KRISTIN DITTENHAFER-REED, PH.D.
NICOLE DOPPEL, B.S.
MATT KORTUS, M.S.
KATIE MARTIN, PH.D.
JOSH SCHIPPER, PH.D.
KELLIE SISSON, B.S.
STUDENTS
ADITI BAGCHI, M.D.
ANNALISE BOWEN
DANIELLE BURGENSKE, PH.D.
LELAND DUNWOODIE
NATE MERRILL, B.S.
NANDA KUMAR SASI, B.S.
ABIGAIL SOLITRO, B.S.
MEGAN VANBAREN
RESEARCH INTERESTS
The MacKeigan lab focuses on two hallmarks of cancer: the deregulation of cellular
energetics and resistance to cell death. These hallmarks are regulated by mTOR
signaling and contribute significantly to drug resistance in cancer. We seek a
systems-level understanding of the network that encompasses the cell metabolism and
autophagy signaling pathways. While our research focuses on human cancers, we also
apply our tumor biology expertise and pathway knowledge to study tuberous sclerosis
complex. Our laboratory uses cutting-edge tools and collaborates with multidisciplinary
experts for robust experimental design and comprehensive data analysis. All of our
research projects have one common goal: to identify novel therapeutic targets.
Autophagy and resistance to cell death
The process of autophagy functions to generate energy, clear damaged organelles,
and delay or prevent cell death during times of cellular stress. Chemotherapeutic
agents trigger autophagy, which allows cancer cells to adapt and withstand treatment.
Therefore, a better understanding of autophagy is crucial for developing new and
improved treatment strategies against cancer.
ADJUNCT FACULTY
BRIAN LANE, M.D., PH.D.
In partnership with Los Alamos National Laboratory, our lab has used predictive
computational modeling and cell-based measurements to accurately model the
autophagic process. We are pleased to report that we have received a collaborative
National Cancer Institute R01 award to validate and extend this model. The current
efforts to enhance our model will help us predict the therapeutic benefit of inhibiting
autophagy in cancer. We are also working with industry partners to determine the
effects of candidate drugs on autophagic flux, and we have identified novel genes
that are required for drug-induced autophagy. Lastly, our group conducts optimized
kinase and phosphatase assays for in vitro evaluation of compounds identified in silico.
Our research suggests that kinase inhibitors modulate autophagy and may be more
selective and effective than current lysosomotropic agents.
14 Van Andel Research Institute | Scientific Report