Sharmila Shankar, PhD

Associate Professor of Pathology and Laboratory Medicine, Division of Cancer and Developmental Biology, KU Cancer Center Member, Division of Drug Development
PhD: 1999, University of Mumbai, India
Post doctoral: University of Maryland and National Institutes of Health

Publications: Click here

Laboratory:4020B Wah Hall East
Phone: (913) 945-7045 

Ph.D. students are welcome and Postdoctoral positions are available; contact me for more information.

Research Interests:

• Drug Development
• Cell Signaling Pathways in cancer progression, metastasis and angiogenesis
• Chemotherapeutic and Chemopreventive Strategies for cancer treatment
• Cancer stem cells
• Micro RNA
• Epigenetic regulation of cancer-related genes

Cancer is the most complex medical challenge facing our society. It is a biological process that has many manifestations and impacts. A multitude of factors drive uncontrolled cell growth. The focus of my research is on elucidating the pathogenesis of cancer, with the ultimate goal of developing new and improved methods for risk assessment, early detection, and prevention and therapy of cancer.

The primary research interest is in signal transduction, especially in the context of cancer chemotherapy. A major research effort is to investigate how transduction pathways regulate cell survival and cell death and to exploit intracellular signaling systems to benefit cancer therapy. We here are especially interested in the Notch signaling pathway and its role in cancer progression in breast, prostate and pancreatic cancer. We continue the molecular dissection of the intracellular events that lead to programmed cell death, or apoptosis through the death receptor pathway by developing death receptor agonist. We are developing strategies to reduce/inhibit breast and prostate cancer progression and are trying to understand the multi‑faceted mechanisms leading to angiogenesis and cancer metastases. The ultimate goal of cancer chemotherapy is selective eradication of malignant cells. Currently used anticancer agents are of limited value due to their toxicity to normal tissue and development of resistance by malignant tissue to these anti neoplastic agents. In this pursuit we are also investigating the biochemical and molecular mechanism of several dietary and synthetic agents to evaluate the cancer chemopreventive potential of curcumin and sulforaphane and diallyl trisulphide in the growth inhibition, apoptosis and angiogenesis.

Another area of our research is to elucidate the molecular mechanisms of tissue‑specific and cell type‑specific gene expression in cancer stem cells. Cancer evolves with genetic loss of function of tumor suppressor genes and over activity of oncogenes. Meanwhile, cancer progression also involves profound epigenetic deregulation of tumor suppressor genes, and chromatin alterations that affect genomic stability and gene expression. We are interested in understanding the biology of cancer with a focus on epigenetic regulation of tumor suppressor genes and oncogenes in development and tumorigenesis, and to develop mouse models for studying cancer epigenetics and testing strategies for cancer prevention and therapy. Our goal is to determine the molecular mechanisms that are involved in the formation of genetic changes and epigenetic changes in human cancer-relevant genes. We try to understand how these genetic and epigenetic changes that initially occur in the genome of normal cells eventually lead to malignancy.