Department of Urology

Eva Corey

Professor, Research
Co-Director, GU Cancer Research Lab

Faculty: Research

Telephone: 206-543-1461

Email: ecorey@uw.edu

Office Location: HSB Room I-340

Dr. Eva Corey’s major research objective is to investigate the molecular events associated with the progression of prostate cancer and prostate cancer metastasis to bone. As part of this research Dr. Corey has also been involved in the establishment and characterization of novel prostate cancer models and has used these models to investigate biology of prostate cancer as well as evaluate the efficacy of novel pipeline agents as potential treatment for this disease. She is co-Director of the GU Cancer Research Lab.

Dr. Corey received her RNDr. (M.S.) in 1989 from Charles University, Prague, Czechoslovakia, and her PhD in Organic Chemistry with specialization in Peptide Chemistry from the Czechoslovak Academy of Sciences, Prague, Czechoslovakia. She did postdoctoral studies in London at the University of London, School of Pharmacy, on synthesis of fragments of HIV p24; at the University of Colorado with Professor John M. Stewart in Denver, CO, on synthesis, purification, and characterization of an artificial enzyme; and at the University of Washington, Seattle, WA, where she concentrated on various aspects of prostate cancer.

NIH Publications List

Research areas: Dr. Corey’s research program focuses on investigation of advanced prostate cancer:

  1. The progress in understanding of advanced prostate cancer at least partially related to paucity of preclinical models that mimic the spectrum of phenotypic properties of human tumors. With few exceptions, preclinical efficacy studies have employed tumor cell lines that were passaged extensively in vitro prior to engraftment into mice. Such models typically fail to reproduce the complexity and architecture of the original tumors and are in many cases poorly predictive of clinical outcome. The need for testing using more relevant tumor models has shifted attention to the use of patient-derived xenografts (PDX) in preclinical setting to generate clinically relevant results. PDX models are generated by direct transfer and subsequent passage of patient tumors in immunocompromised mice in the absence of in vitro PDXs, compared to conventional cell line-derived xenografts can better reproduce the intratumoral heterogeneity, histology, drug sensitivity and other phenotypic features of the patient’s tumor. However, it is well-accepted that prostate cancer PDXs are very difficult to establish, with only ~ 10% establishment rate. We have succeeded to generate over 40 advanced prostate cancer PDX. These PDXs, the LuCaP PDX series, represent well the characteristics of advanced prostate cancer observed in patients and have been used for multiple important investigations into biology of prostate cancer.
  2. Androgen receptor signaling in prostate cancer. Prostate cancer progresses from androgen-dependent tumors that respond favorably to androgen deprivation (ADT) therapies to recurrent, metastatic, castration-resistant tumors. A common assumption at present is that the persistence of androgen receptor (AR) signaling accounts for the failure of ADT. Therefore mechanisms of responses and resistance to endocrine therapies are of intensive focus of investigations.
  3. Evaluation of new treatment modalities in preclinical settings. Castration-resistant prostate cancer is an aggressive disease and despite a growing number of treatment options it remains incurable and leads to death. The heterogeneous nature of CRPC indicates the importance of tailoring the therapy specifically for each patient’s disease. Furthermore, progression of the tumors through intrinsic or acquired resistance in essentially all cases adds new treatment challenges to our effort to attenuate this disease progression. It is clear that development of new effective agents and their evaluation as monotherapy or in combination with the existing treatments are urgently needed. We have use the LuCaP PDXs to evaluate efficacy of the new pipeline agents.