Rick Press

Tumorigenic signaling pathways of myb oncoprotein;

Prevalent genetic alterations in common diseases.

Research interests: Rick Press, MD, PhD

My basic science research lab studies the molecular mechanisms of tumorigenesis as transduced by the myb oncoprotein. Myb is a proto-oncogene that is involved in a variety of human and animal tumors (hematopoeitic and mesenchymal cells) and that elicits its tumorigenic signals by acting as a DNA-binding transcriptional transactivator. The target genes and partner proteins involved in myb dependent signaling pathways are an active focus of our research. In particular, we use state-of-the-art cell and molecular biological methods to examine the in vivo and in vitro target cells for myb-induced tumorigenesis and the target genes and effector proteins mediating this transfomation. Our long-term goal is to discover and characterize the molecular mechanisms by which myb signals its responsive target cell to cause perturbations in growth and differentiation that ultimately contribute to tumorigenesis. Site-directed alterations in this myb-induced signaling cascade will be manipulated in an attempt to prevent or revert the tumorigenic process and as potential target- and gene-specific cancer therapies.

In addition to my basic research, my lab also maintains a translational clinical research program on common genetic alterations that predispose to common human diseases such as vascular disease (venous and arterial thrombosis), cancer, and iron overload. In particular, we are studying very common genetic alterations in hemostasis genes (coagulation factors and co-factors), atherosclerosis-inducing genes, and genes regulating oxidative stress, and we are correlating these common predisposing genotypes to very prevalent disease-causing phenotypes using disease-specific human specimens. Our long-term goal is to characterize the complex genetic alterations that, in synchronomy, contribute to the common human diseases that represent the major killers of Western civilization : heart disease and cancer. In the coming genomics era, this information will be used to 1) define at-risk conditions to permit early disease-sparing preventional interventions; 2) define potential molecular targets for disease-specific therapy.

Recent References:

Parks SB, Popovich BW, & Press RD. Real-Time PCR with Fluorescent Hybridization Probes for the Detection of Prevalent Mutations Causing Common Thrombophilic and Iron Overload Phenotypes. Am J Clin Path 115: 439-47, 2001.

Gomez PS, Parks S, Ries R, Tran TC, Gomez PF, & Press RD. Polymorphism in intron 4 of HFE does not compromise haemochromatosis mutation results. Nature Genetics 23: 271-2, 1999.

Press RD, Wisner, TW, and Ewert DL. Induction of B cell lymphomas by overexpression of a myb oncogene truncated at either terminus. Oncogene 11:525-535, 1995.

 To contact Dr. Press directly: pressr@ohsu.edu