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Brian  Ruffell

Brian Ruffell

Brian Ruffell
Assistant Professor

Contact

Office: SRB-2, SRB 22214
Phone: 813/745-8135
Email: Brian.Ruffell@moffitt.org

Education

PhD in Molecular Immunology 2002-2008 University of British Columbia
Postdoc, UC San Francisco 2008-2012
Postdoc, Oregon Health & Science University 2012-2013
Research Assistant Professor, Oregon Health & Science University 2013-2015
Assistant Member, Moffitt Cancer Center 2015-
Assistant Professor, Dept of Oncologic Sciences, USF 2015 -

Research

Effectively harnessing the power of the immune system is one of the most promising advances in cancer therapy. Immune-based therapies take advantage of the tumor killing capacity of cytotoxic T cells, an ability that is normally limited within tumors via multiple suppressive pathways. Supporting the activity of the cytotoxic T cells can provide long-term survival advantages, but despite recent successes, only a fraction of patients respond to immunotherapy, and efficacious treatment has so far been largely limited to select tumor types such as melanoma, kidney and lung. The identification of additional therapeutic targets is urgently needed to address these issues and expand upon the number of patients who will benefit from the relatively safe and effective treatment approach.

Dendritic cells are a rare population of immune cells that are responsible for controlling when, where and how the immune system responds to infection and insult, essentially acting as 'generals' of the immune system. We have recently found that dendritic cells are also critical in supporting cytotoxic T cell activity within breast tumors following chemotherapy, and expression of dendritic cell genes can predict response to chemotherapy as well as long-term survival. We therefore hypothesize that dendritic cells have an unappreciated role in providing 'logistical support' to cytotoxic T cells within tumors. By evaluating therapeutic targeting of putative activating and inhibitory pathways on dendritic cells we seek to enhance their capacity to support cytotoxic T activity within hormone-driven malignancies to improve response rates to both traditional and emerging therapeutics.

Graduate Students

Alycia