Ronald S. Pardini

Department: Biochemistry & Molecular Biology
Academic Unit:  CABNR
Title: Associate Director of the Nevada Agriculture Experimental Station
Professional degrees (Degree, year, Institution): Ph.D., 1965, University of Illinois

Contact Information

Mail Stop: 330
Phone: (775) 784-4107
Fax: (775) 784-1419
e-mail: ronp@cabnr.unr.edu

Research Area(s)

Cancer, Cell Biology, Nutrition

Research Interests

Previous work in the laboratory has explored how omega-3 polyunsaturated fatty acids (PUFAs) can be used to diminish tumor growth and enhance the response of tumors to common chemotherapeutic agents in in vitro cell culture and in vivo athymic mouse models.  Additionally, the laboratory has done investigations to determine the mechanisms by which growth inhibition and chemosensitivity are achieved.  The potential to use nutrition alone to enhance the effectiveness of existing anti-cancer agents, while not adding to the suffering of those afflicted with cancer, is the overreaching goal of the laboratory.

Among the active projects in the laboratory, is a study looking at combining omega-3 PUFA supplementation with radiation therapy.  Radiation therapy is used in more than half of all cancer treatments, and works by inducing genetic and oxidative damage specifically targeted to tumors.  Since many of the anti-cancer properties of omega-3 PUFAs are attributed to upregulation of pathways involved in oxidative stress, the laboratory is currently investigating how omega-3 PUFA supplementation might enhance response to radiation therapy.  Preliminary data from the laboratory finds a significant enhancement of tumor cells undergoing cell death in response to combination treatment with omega-3 PUFAs, specifically docosahexaenoic acid (DHA), and radiation.  Additionally, the laboratory has developed a novel in vitro approach to looking at the potential clinical impact of these findings by employing anchorage-independent growth assays, which involves growing tumor cells in a gelatinous substance called soft agar and looking at colony formation that is indicative of how well these cells would grow in vivo in a mouse or human.  The findings have shown a striking amount of synergism between DHA and radiation in suppressing soft agar colony formation, which warrants further investigation.  Finally, the laboratory has correlated these findings with levels of lipid peroxidation, a specific marker of oxidative stress.

Current Graduate Students

Michael Mouradian,
Kristina R. Rogers-Klette

Other lab members:

Keith D. Kikawa (Postdoctoral Fellow)
Lani Pardini (Animal Care Technician)
Jimi Francis (Visiting Scientist)
Shayne Ahwah
George Edogun
Karla Hernandez
Kelsey Heslington
Alejandro Ibarra
Eric Johnson
Jason Kelton,
Kristen McKinnon
Kristen Spencer
Rachael Tateo

Selected Publications

Yamagami T, Porada CD, Pardini RS, Zanjani ED, Almeida-Porada G 2009, “Docosahexaenoic acid induces dose-dependent cell death in an early undifferentiated subtype of acute myeloid leukemia cell line” Cancer Biology & Therapy, 8(4), 331-337

Link 1

 

T. Kato, N. Kolenic, and R. S. Pardini 2007, "Docosahexaenoic Acid (DHA), a Primary Tumor Suppressive Omega-3 Fatty Acid, Inhibits Growth of Colorectal Cancer Independent of p53 Mutational Status" Nutrition and Cancer, 58(2), 178–187  

Link 2

Ronald S. Pardini 2006, "Nutritional intervention with omega-3 fatty acids enhances tumor response to anti-neoplastic agents" Chemico-Biological Interactions 162 (2006) 89–105

Link 3

R. S. Pardini, D. Wilson, S. Schiff, S. A. Bajo, and R. Pierce 2005, "Nutritional Intervention With Omega-3 Fatty Acids in a Case of Malignant Fibrous Histiocytoma of the Lungs" Nutrition and Cancer, 52(2), 121–129  

Link 4

Kato, T., R. Hancock. M. Mohammadpour, B. McGregor, P. Manalo, S. Khaiboullina, M.R. Hall, L. Pardini and R.S. Pardini 2002, "Influence of Omega-3 fatty acids on the growth of human colon carcinoma in nude mice" Cancer Letters 187, 169-177.  

Link 5