Alain Charest,
Associate Professor,
Beth Israel Deaconess Medical Center, Cancer Research Institute, Department of Medicine, Harvard Medical School
Alain Charest, M.Sc., Ph.D. is a member of the Cancer Research Institute at Beth Israel Deaconess Medical Center and an Associate Professor in the Department of Medicine at Harvard Medical School, Boston, MA. Dr. Charest received his post-graduate degrees at McGill University, Montreal, Canada and pursued post-doctoral studies at MIT. The focus of the Charest laboratory is on leveraging clinically relevant genetically engineered mouse models of primary malignant brain cancer to study central aspects of gliomagenesis and molecular responses to therapeutic interventions. Recent work from the Charest lab involves studies on mechanisms of checkpoint blockade immunotherapy in EGFR-driven models of Glioblastoma Multiforme.
Insights into Immune Checkpoint Blockade Biology in EGFR-Driven Mouse Models of Glioblastoma
Wednesday, 2 November 2016 at 09:30
Add to Calendar ▼2016-11-02 09:30:002016-11-02 10:30:00Europe/LondonInsights into Immune Checkpoint Blockade Biology in EGFR-Driven Mouse Models of GlioblastomaCancer Immunotherapy and Biofluid Biopsies 2016 in Boston, USABoston, USASELECTBIOenquiries@selectbiosciences.com
Glioblastoma Multiforme (GBM) is a lethal disease with a median survival of approximately 15 months and a 5-year relative survival rate of 3%, despite an aggressive standard of care treatment regimen consisting of fractionated radiation and the chemotherapeutic agent Temozolomide (TMZ). This abysmal lack of response makes it clear that alternative therapeutic approaches must be explored. Phenomenal advances have been made in characterizing the molecular features of GBM through the cataloging of genomic data obtained through the efforts of The Cancer Genome Atlas. Despite these tumor-cell centric advancements, much less is known about how the tumor microenvironment plays a role in the maintenance, evolution, and response to therapies for GBMs. The adaptive immune system is endowed with intrinsic anti-tumor activity. However, many malignant tumors, including GBM, are associated with significant systemic and micro-environmental immunosuppression. Often, tumors escape immune surveillance by over-expressing a class of proteins known as immune checkpoints, resulting in uncontrolled growth of the tumors. Antibody-mediated inhibition of two immune checkpoint cell surface proteins (programmed death-1 [PD-1] and cytotoxic T-lymphocyte antigen-4 [CTLA-4]), has exhibited dramatic and durable responses across a spectrum of malignancies. However, the clinical potential of these antibodies in patients with GBM is not known. Here we systematically evaluated the antitumor efficacy of antibodies targeting the immune checkpoint molecules PD-1 and CTLA-4 when administered as single-agent therapies and in combination with (XRT-TMZ) in an EGFR-driven genetically engineered immunocompetent mouse model of GBM. Treatment with anti PD-1 and anti CTLA-4 antibodies resulted in a significant increase in survival when compared to either control untreated animals and XRT-TMZ treated mice. Our results support the clinical evaluation of immune checkpoint blockade as single agents.
Add to Calendar ▼2016-11-01 00:00:002016-11-02 00:00:00Europe/LondonCancer Immunotherapy and Biofluid Biopsies 2016Cancer Immunotherapy and Biofluid Biopsies 2016 in Boston, USABoston, USASELECTBIOenquiries@selectbiosciences.com
Add to Calendar ▼2016-11-02 09:30:002016-11-02 10:30:00Europe/LondonInsights into Immune Checkpoint Blockade Biology in EGFR-Driven Mouse Models of GlioblastomaCancer Immunotherapy and Biofluid Biopsies 2016 in Boston, USABoston, USASELECTBIOenquiries@selectbiosciences.com
