Ronald L Heimark, PhD

Associate Professor, Cellular and Molecular Medicine
Associate Professor, Pathology
Member of the Graduate Faculty
Professor, Cancer Biology - GIDP
Professor, Ophthalmology
Professor, Surgery

Ronald Heimark received his PhD in biochemistry from the University of California at Davis. Dr. Heimark was a Postdoctoral Fellow at the University of Washington in the Department of Biochemistry in Earl Davie's laboratory investigating the initiation of blood coagulation. These studies were expanded in a second fellowship in the cardiovascular biology laboratory of Stephen M. Schwartz in the Department of Pathology at the University of Washington. In 1990, Dr. Heimark was one of the scientific members that started the biotechnology company ICOS Corporation, which developed the product Cialis (tadalafil). In 1993, Dr. Heimark left the biotechnology world and returned to academics at the University of Arizona. He has served on numerous NIH Study Sections and has published more than 80 publications.

Research Interests

The Heimark laboratory is currently actively engaged in projects investigating mechanisms of cancer progression and metastasis in prostate and pancreatic cancer. It is unknown why prostate cancer patients progress in some patients and not others. My lab was the first group to propose that a late step in prostate cancer progression is the loss of differentiation in Epithelial Mesenchymal Transition. At the time the current theory was that loss of the epithelial cell-cell adhesion molecule, E-cadherin, through transcriptional repression and this led to detachment of cells from the primary tumor. Our results showed a switch in cadherin types with the loss of E- was accompanied by the gain of N- which is the main cadherin type in stroma. This cadherin switch was beneficial for invasive cells and N-cadherin engagement initiated prosurvival signaling. These studies have led to identifying transcription regulators of these adhesion molecules that could be useful biomarkers and distinguish aggressive prostate cancer from the indolent form of the disease. In addition we have used our knowledge of cellular RNA-RNA interactions to develop a multilocus genotypic assessment that will allow for improved stratification of cancer risk profiles. One of our current project has developed from a collaboration in which we have discovered and evaluated biofunctional SNPs affecting competitive endogenous RNA interaction networks important in prostate cancer. We have recently discovered that the SNP rs13136837(G/T), which resides in the flanking region of the stem cell miR-302/367 pri-miRNA sequence, and affects mature miRNA processing. Genotyping of this genetic variant in prostate cancer patients further suggests that it has potential to predict for risk of aggressive disease.†


  • BA: Western Washington State University, Biology and Chemistry, 1970, PhD: University of California Davis, Biochemistry, 1976
University of Washington, Biochemistry, 1976, University of Washington, Pathology, 1981