Our focus is on translational nanomedicine, which encompasses the synthesis of biomaterials, formulation design and development, and evaluation of different biocompatible nanoparticle-based platform technologies for targeted drug/gene delivery and imaging agents.
Our basic research involves how best to design unique nanostructures for efficient, targeted drug/gene delivery systems. We strive to understand the biophysics and biomechanics of the interactions between nanoparticles and cell membrane lipids and the role of this critical interaction in cellular uptake and intracellular trafficking of nanoparticles, as well as their biodistribution in vivo.
In our current research projects, we aim to (a) understand the role of epigenetic changes in tumor drug resistance and metastasis and create nanotherapeutics to treat both primary and metastatic tumors; (b) explore effective therapies for stroke, particularly methods of preventing reperfusion injury and facilitating neurological repair mechanisms; (c) develop novel treatments for blast-associated traumatic brain injury and regenerative therapies for spinal cord injury; and (d) develop a non-stent approach to inhibit arterial restenosis following balloon angioplasty.
Dr. Labhasetwar leads the Cancer NanoMedicine program, a joint undertaking of the Department of Biomedical Engineering and Cleveland Clinic's Taussig Cancer Institute.
In other words ...
Our research focus is to explore the use of nanotechnology (such as tiny "nanoparticles" that can find their way into specific cells or tissues) to detect and treat various diseases, particularly cancer, stroke and cardiovascular conditions. To fight cancer, we are developing therapy to treat both original tumors and ones that have spread elsewhere.
Sharma B, et al. Selective biophysical interactions of surface modified nanoparticles with cancer cell lipids improve tumor targeting and gene therapy. Cancer Lett 2013;334:228-36.
Vijayaraghavalu S, Labhasetwar V. Efficacy of decitabine-loaded nanogels in overcoming cancer drug resistance is mediated via sustained DNA methyltransferase 1 (DNMT1) depletion. Cancer Lett 2013;331:122-9.
Lu S, Labhasetwar V. Drug resistant breast cancer cell line displays cancer stem cell phenotype and responds sensitively to epigenetic drug SAHA. Drug Deliv Transl Res 2013;3:183-194.
Vijayaraghavalu S, et al. Highly synergistic effect of sequential treatment with epigenetic and anticancer drugs to overcome drug resistance in breast cancer cells is mediated via activation of p21 gene expression leading to G2/M cycle arrest. Mol Pharmaceutics 2013;10:337-52.
Prabha S, et al. Inhibition of tumor angiogenesis and growth by nanoparticle-mediated p53 gene therapy in mice. Cancer Gene Ther 2012;19:530-7.