Ron Heimark

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.