Sheila A. Stewart, PhD
Gerty Cori Professor and Vice Chair, Department of Cell Biology & Physiology
Professor, Department of Medicine
The Stewart lab's research focuses on understanding how age-related changes in noncancerous cells (referred to as stroma) participate in cancer development.
Dr. Sheila Stewart’s research focuses on understanding how age-related changes in noncancerous cells (referred to as stroma) participate in cancer development. While it is clear that mutations in an incipient tumor cell are important for cancer development, it has become evident that changes in the surrounding stroma are also critical to the process. Indeed, old stromal cells can promote tumor cell growth. Dr. Stewart’s group is delving further into how old cells modulate the immune response and impact dormant tumor cells and thus promote cancer with the intent of identifying possible therapeutic targets.
- BS: University of Minnesota, 1990, Microbiology
- PhD: University of California-Los Angeles, 1996, Microbiology & Immunology
- Postdoc: University of California-Los Angeles, 1996-1998, Microbiology & Immunology
- Postdoc: The Whitehead Institute/MIT, 1998-2003, Cell Biology
Graduate & Fellowship Program Affiliations
BJC Institute of Health (MS: 8228-0004-07)
Senescence | Cancer | Immunotherapy | Therapy-induced Comorbidities | Age-related Cancer Drivers
Age remains the largest risk factor for the development of cancer, begging the question, what about aging drives the rapid increase in cancer we see in the 5th to 6th decade of life? While the answer is complicated, the Stewart laboratory focuses on how age-related changes in the tumor microenvironment contribute to tumor progression. This work includes delving into the mechanisms that drive senescence and secretion of pro-tumorigenic senescence associated secretory phenotype (SASP) factors. In addition, given senescent stromal cells recapitulate the phenotypes of cancer associated fibroblasts (CAFs), the laboratory also studies these important cells in both the primary and metastatic setting.