Academic Rank:
Professor, UBC
Distinguished Scientist, Michael Smith Genome Sciences Centre, BC Cancer Agency
Short Bio:
  • Distinguished Scientist, Genome Sciences Centre, BC Cancer Agency
  • President, Society of Basic Urologic Research
  • Chief Scientific Officer, ESSA Pharma Inc
  • Professor, Pathology and Laboratory Medicine, University of British Columbia (UBC)

Provincial Program Leader for Prostate Cancer Research

Dr. Sadar’s career in prostate cancer started at the BC Cancer Agency as a post-doctoral fellow in Dr. Nicholas Bruchovsky’s laboratory. Her research has focused upon discovering new treatments for advanced prostate cancer. Dr. Sadar recently developed an experimental drug that shrinks prostate cancer tumours in the lab and is the first drug in the world that targets the “engine” of the tumour that causes the cancer to grow.

Dr. Sadar is the author of over 50 peer-reviewed publications, has served on more than 30 scientific panels, and has been a recipient of several prestigious awards, including the Terry Fox Young Investigator Award, Simon Fraser University Alumni Award for Academic Excellence. She is the first non-American to receive the Society of Women in Urology/Society of Basic Urologic Research Award for Excellence in Urologic Research.

You can read Dr. Sadar’s blog posts here.

Academic background

  • PhD, Biochemistry, University of Bradford, UK / University of Göteborg, Sweden.  1995
  • BSc, Biochemistry, Simon Fraser University. 1988
Primary Research Area
Secondary Research Area
Genetics genomics proteomics and related approaches

Research Interest

  • Prostate cancer
  • Drug Development
  • Transcriptional regulation

The major focus of my research is to develop therapies that will delay or prevent tumour progression and emergence of hormone independence in prostate cancer. Current treatment for the onset of early stages of prostate cancer is the removal of male hormones, also called androgens, by either drug or surgical treatments. While initially effective in reducing cancer symptoms and PSA levels, this treatment is unable to completely and permanently eliminate all prostate cancer cells. After a predictable initial response to treatment, there is a relapse as the cancer progresses to a more aggressive androgen-independent stage. An early sign of progression to androgen independence, related to reduced survival, is the reappearance of elevated serum levels of PSA. The proteins that regulate the expression of the PSA gene have been shown to correlate well with the progression of prostate cancer, with both gene expression and the disease going from an androgen-dependent to an androgen-independent stage. One of these proteins is the one that actually recognizes and interacts directly with androgens and is called the androgen receptor. Thus the major objective of one area of my research program is to identify the molecular mechanisms that orchestrate the behaviour of proteins such as the androgen recptor during the progression of prostate cancer to androgen independence. To do this, I am presently characterising how these proteins affect the regulation of PSA gene expression both in the presence, and in the absence of androgen.

The results of our PSA gene expression experiments have resulted led to a hypothesis which suggests that the anomalous expression of the PSA gene may involve alternative regulatory pathways which act to either bypass the androgen receptor or result in its activation in the absence of androgen. Recently, I have shown that indeed the androgen receptor can be activated in the absence of androgen by interacting with other proteins in the cAMP-dependent protein kinase (PKA) pathway. These interactions may prove to be important in the progression of prostate cancer to androgen independence. Therefore, I am mapping the region of the androgen receptor that is required for androgen-independent activation and developing molecular recognition peptide sequences that interfere with these activating interactions. The goal is to utilize these peptides for therapeutic treatment for reversing or preventing advanced prostate cancer.

Recently, to identify the molecular events involved in the progression of prostate cancer, I developed a unique mouse model that allowed me to grow and recover homogenous populations of human prostate cancer cells. This model has allowed me to perform molecular analysis on cells harvested from animals during different stages of progression. These studies have already identified new molecular targets that are currently being evaluated for therapeutic potential.

The most common site of secondary prostate cancer malignancy is the bone. Unlike most other cancers which destroy bone when they metastasize to this tissue, prostate cancer cells actually cause new bone growth by the promotion of cells called osteoblasts. Therefore I am currently investigating interactions between prostate cancer cells and bone which results in the proliferation of both prostate cancer cells and bone osteoblasts. Inhibiting the interaction of these osteoblast-specific factors with metastatic prostate cancer cells may prevent or delay the progression of prostate cancer cells to androgen independence, alleviate the severe pain often associated with new bone formation and provide a better quality of life for those prostate cancer patients with bone metastases.