Department of Urology

Colm Morrissey

Associate Professor, Research
Co-Director, GU Cancer Research Lab

Faculty: Research

Telephone: 206 543-1461

Email: cmorriss@uw.edu

Office Location: UW Health Sciences Building

Dr. Colm Morrissey is a researcher who specializes in prostate cancer with an emphasis on metastatic disease. He is co-Director of the GU Cancer Research Lab.

NIH Publications List

At the GU Cancer Research Lab, Dr. Morrissey is working in four focus areas:

  1. Identifying and testing new therapeutic targets for castrate-resistant prostate cancer (CRPC): Due to the highly collaborative nature of the prostate cancer group at the University of Washington, there is a considerable biorepository of primary and metastatic tissue for analysis and patient-derived prostate cancer xenograft (PDX) models for pre-clinical studies of therapeutic targets of interest. Our approach is to use tissue obtained from radical prostatectomies, our rapid autopsy program, and the PDX models to characterize the many faces of hormone sensitive and CRPC. Once we have identified molecular pathways and targets of interest, we utilize the LuCaP patient-derived xenograft (PDX) models developed at the University of Washington for pre-clinical studies on therapeutic targets of interest. Our studies have ranged from studying tumor evolution, to androgen receptor variants, angiogenesis, epithelial mesenchymal transition, and the hypermutated phenotype in CRPC. Our ultimate goal is the development of more effective therapies that substantially prolong survival for patients with CRPC.
  1. Androgen receptor negative CRPC: With the advent of new and more effective androgen deprivation therapy, androgen receptor negative CRPC has become more prevalent. Currently, there is no effective treatment for androgen receptor negative disease. Our efforts are directed towards understanding the survival pathways that are engaged in these androgen receptor negative CRPC tumors that replace the androgen receptor as the driver of survival and proliferation in CRPC. Defining the drivers of androgen receptor negative CRPC is critical for the development and testing of new therapeutic strategies.
  1. Bone response in CRPC metastases: From our prostate cancer rapid autopsy program, we have determined that prostate cancer metastasized to the bone in approximately 90% of patients who died from prostate cancer. Growth of tumor cells in the bone can lead to replacement of bone marrow, spinal cord compression, severe bone pain, cachexia and death. Rapid autopsy data from patients who have died of prostate cancer shows that the disease is predominantly osteoblastic with an osteolytic component. The focus of our research is to identify and target factors that promote the osteoblastic and osteolytic reaction in prostate cancer bone metastasis to alleviate the pain and suffering associated with bone metastases.
  1. Tumor cell dormancy: The long latency period that occurs in some patients between initial treatment and evidence of metastasis is attributed to tumor cell dormancy. These dormant disseminated tumor cells represent a nidus for disease recurrence and studying tumor cell dormancy. Studying these cells will significantly impact our ability to identify, understand, and target tumor cells in individuals with no evidence of disease that may recur at a later point in time.