Natalia Ignatenko

Associate Professor, Cellular and Molecular Medicine

Leon Levy Cancer Center, 1939

1984, MS, Biophysics, Shevchenko Kiev State University, Kiev, Ukraine

1989, PhD, Oncology, Kavetsky Institute of Oncology Problems, Kiev, Academy of Science of the USSR

1989-1992 Postdoc, Cancer Biology, Kavetsky Institute of Oncology Problems, Kiev, Ukraine

1992-1996, Postdoc, University of Arizona Cancer Center, Tucson, Arizona, USA
1996-1999, Assistant Scientific Investigator, University of Arizona cancer center, Tucson, AZ

1999-2003, Assistant Professor (research track) Department of Radiation Oncology, University of Arizona Cancer Center, Tucson, Arizona

2003- 2008 Assistant Professor (research track), Department of Cell Biology and Anatomy, College of Medicine, University of Arizona, Tucson, Arizona

2009-present, Associate Professor (Research Scholar Track, career Track) , Department of Cellular and Molecular Medicine, College of Medicine, University of Arizona, Tucson, Arizona

Research Interest
For the past 20 years I have been involved in colorectal cancer (CRC) research with the focus on the molecular mechanisms of detection and prevention. My research activity include identification and validation of downstream effectors of Adenomatous Polyposis Coli (APC) tumor suppressor gene and K-ras protooncogene within polyamine and prostaglandin pathways and study the luminal and dietary risk factors of colonic inflammation and colorectal carcinogenesis. I also have an expertise in developing Genetically Engineered Mouse (GEM) models of gastrointestinal cancer for studying different steps of carcinogenesis. Current research in my laboratory is focused on regulation and pathophysiological functions of kallikrein-related peptidase 6 (KLK6) in cancer with the focus on cancer cells invasion and metastasis. KLK6 is a secreted serine protease with the specific function to cleave components of the extracellular matrix and activate latent growth factors involved in epithelial-to-mesenchymal transition (EMT) pathways. Our recent findings indicate that KLK6 expression in colon cancer cells is determined by the tumor subtype and the genetic mutations developed during the colon cancer progression. KLK6 protein will be useful for imaging purposes and an appropriate target for evaluation as a colon biomarker.
Offering Research Opportunities
Yes
Prerequisite Courses
None
Majors Considered
UBRP
Types of Opportunities
Description of Opportunity
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