Grant: CIHR Fellowship

Rationale: Although ovarian cancer is highly responsive using current treatment with surgery and chemotherapy, a high proportion of these women will have their cancer return. There are multiple factors that can be used to predict if this. Intriguingly, this includes the presence of tumor-reactive T-cells. In fact, two specific types of T-cells seem to account for this effect, CD8+ T cells and regulatory T cells (cells that attenuate the immune response). While early studies reported that FoxP3+ T cells (a transcription factor associated with regulatory T cells) attenuate the tumor-reactive CD8+ T cells, more recent studies in ovarian cancer show the opposite. This may be due to an alternate type of FoxP3+ T cell that acts to stimulate an immune response. Scientific Question (hypothesis): We hypothesize that FoxP3+ cells are acting to stimulate the CD8+ cells in ovarian cancer and provide a stronger anti-tumor response. Scientific Plan (Aims): Viable cells from 30 cases of ovarian cancer have been collected that include CD8+ cases with (n=15) and without (n=15) FoxP3+ T cells. To compare CD8+ and FoxP3+ T cell function in these two groups, we will measure cell surface markers and expressed molecules by flow cytometry. In addition, we will test these results in a mouse model that mimics human ovarian cancer by depleting or enriching FoxP3+ T cells. Relevance: By determining which cell types and functions promote a favourable outcome in ovarian cancer we can tip the balance toward a more robust and effective immune response in ovarian cancer patients.