Dr. Cheryl Helgason, PhD
Senior Scientist
chelgaso@bccrc.ca
Tel: 604-675-8011
Fax: 604-675-8019
675 West 10th Avenue, Vancouver, V5Z 1L3
Research Role:
Education:
Research Interests:
Despite intensive research to identify tumor associated antigens and to devise novel strategies to enhance anti-tumor immune responses, clinical trials using immunotherapy have generally yielded disappointing results. There is a wealth of data to support the concept of tumor immunosurveillance that encompasses a preliminary elimination of the majority of the tumor cells, followed by an equilibrium phase in which the remaining cells acquire additional genetic alterations that ultimately lead to their escape from immune destruction. The basic premise of this model is that pressures from the innate and adaptive immune systems force the tumor cells to alter their properties or face elimination. Understanding the mechanisms by which tumors interact with the immune system and evade immune destruction will facilitate the development of more effective immunotherapeutic strategies for cancer treatment and ultimately perhaps cancer prevention. To this end, my laboratory has two current research interests.
The cancer stem cell theory states that a small population of stem cells is responsible for the growth and progression of cancer. The hypothesis driving our work is that prostate cancer tumor-initiating cells (PCaTICs) can be partially defined by their expression of immune regulatory molecules that facilitate tumor initiation by subversion of immune surveillance. Moreover, PCaTICs possess the innate ability to alter their genotype and/or phenotype, regardless of external pressures (although perhaps accelerated by them), thus allowing them to effectively communicate with cells of the immune system to facilitate their invasive and metastatic properties. The goal of this research project is to more clearly define the phenotypic and functional properties of PCaTICs present in non-metastatic and metastatic prostate cancer. Once we have succeeded in more clearly characterizing this critical cell population, further efforts will be directed toward understanding the molecular mechanisms that facilitate the escape from immune surveillance and progression to metastasis.
There is increasing evidence that the dynamic interaction between the stromal microenvironment and epithelial tumor cells plays a critical role in the progression of prostate cancer from localized disease through invasion to metastasis. The tumor microenvironment is composed of a variety of cell types including endothelial cells, pericytes, fibroblasts, inflammatory cells, leucocytes and elements of the extracellular matrix. Tumor-associated fibroblasts have been shown to alter the phenotype of malignant epithelial cells in vitro and to direct tumor progression of prostate epithelium. Tumor-associated macrophages (TAMs) have also been identified as playing a role in tumor progression. However, the precise function of TAMs and other cells of the tumor microenvironment in cancer progression, and specifically metastasis, have yet to be fully elucidated. Thus, understanding the phenotypic and molecular changes in the stroma that lead to or contribute to the metastatic phenotype is likely to facilitate the design of novel therapeutic strategies that target both the stromal and malignant epithelial compartments. To this end, we are working to characterize the cell populations present in the non-metastatic and metastatic prostate tumor stromal microenvironment and to elucidate the molecular mechanisms by which the stroma facilitates progression from localized disease to metastasis.
Academic Trainees:
Current:
Yan Tin Chiang, Ph.D, UBC
Alumni:
Mike Beach, M.Sc. 2007-2009
Amy Tien, Ph.D. 2002-2007
Lien Hsu, M.Sc. 2004-2006
Ida Zhang, M.Sc. 2002-2005
