Academic Rank:
Professor, UBC
Distinguished Scientist, Michael Smith Genome Sciences Centre, BC Cancer Agency
Short Bio:

Dr. Sadar’s research accomplishments and experience over 24 years is essentially entirely focused on the development of therapeutics for prostate cancer. In 1999, Dr. Sadar discovered a novel drug target for prostate cancer. She then partnered with a chemist, Dr. Andersen, to screen drugs against this target, and discovered a clinical candidate of this drug.

Dr. Sadar co-Founded a biotech company in 2009, called ESSA Pharma Inc, to develop the drug for testing in clinical trials. This was successful and First-in-human clinical trials proceeded at 4 sites in USA and 1 site in Canada Clinical/ Identifier: NCT02606123. Only one in a thousand drugs that show promise in laboratory studies and animal models ever reaches human testing. Dr. Sadar’s drug is the first drug in clinical trials that binds to an intrinsically disordered protein region and a first in class drug to the N-terminus of the androgen receptor. The work is precedent in the entire field of steroid hormone receptors, with no other small molecule inhibitor reported to bind to the N-terminus of any other steroid hormone receptor (Andersen et al Cancer Cell 2010; Myung et al JCI 2013). Validation of the novelty of her drug was provided by the USAN council and her drug was given a new stem class “-aniten” and the generic name “ralaniten”. In 2016, Dr. Sadar developed the first imaging agent to detect androgen receptor and its active splice variants in prostate cancer (Imamura et al JCI Insight. 2016).

Dr. Sadar has served in numerous leadership roles internationally and was the Y2017 Chair of the USA Army’s Department of Defence’s Programmatic Panel for their Prostate Cancer Research Program. She is the first Canadian to serve in this position. She was the President of the Society of Basic Urologic Research (USA) and a board member of education, research, and scientific advisory committees and boards for American and Canadian non-profit societies. Dr. Sadar was appointed to the Board of Trustees for Canada’s National Museum of Science and Technology by the Minister of Heritage in Oct 2017. Dr. Sadar has served on over 50 grant panels including 5 years on the NIH study session for Drug Discovery & Molecular Pharmacology. Her research has gained considerable media attention over the years with many interviews on radio, newspapers, television, and on the internet. Her contributions and research has also received awards such as an Honorary Doctorate (Doctor of Letters, honoris causa), USA SWIU/SBUR Award for Excellence in Urologic Research, Simon Fraser University’s Outstanding Alumni Award for Academic Achievements, the Terry Fox Young Investigator Award, and award for Excellence in Research and Discovery from UBC Department of Pathology and Laboratory Medicine. Dr. Sadar has trained 42 students and 21 fellows of which many have gone onto successful medical or scientific careers.

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.