Please note: AABB reserves the right to make updates to this program.
Thursday, February 8, 2018
2:00 – 3:00 PM (ET) 7:00 – 8:00 PM (GMT)
Master Program Number: 18EL-311 (see program format numbers below under Registration)
Educational Track: Technical/Clinical
Topic: Cellular Therapies
Intended Audience: Director, Laboratory Staff, Managers/Supervisors, Medical Directors, Nurses, Physicians, Scientists, Students (MD, MT, SBB), Technologists
Teaching Level: Intermediate to Advanced
Director/Moderator: David Stroncek, MD, Chief, Cell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, MD
Speakers: Elizabeth Allen, MD, Associate Medical Director, Transfusion Medicine, UC San Diego Health, San Diego, CA; Steven Highfill, PhD, Director, Research and Product Development, Cell Processing Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, MD
After participating in this educational activity, participants should be able to:
- Identify the steps involved with producing CAR T cells.
- List the reason why too few autologous T cells are collected or too few CAR T cells are produced.
- Discuss methods being used to ensure that an adequate quantity of CD3+ cells are collected.
- Discuss modifications being made to the CAR T cells manufacturing process to improve manufacturing yields.
Chimeric Antigen Receptor (CAR) T cells are an important immerging new cancer immunotherapy. They have been found to be clinically effective for many types of hematological cancers and the clinical application of these therapies is growing rapidly. Typically, CAR T cell therapies are made from autologous peripheral blood mononuclear cells (PBMC) collected by apheresis; the cells are produced at a centralized manufacturing facility; and the final CAR T cell product is shipped to an academic health center where it is infused. However, PBMC collection and CAR T cell manufacturing are not always successful.
Two experts will present their work related to the collection of autologous PBMC concentrates and the manufacture of CAR T cells. The typical collection and manufacturing process will be discussed as will common problems associated with PBMC collection and CAR T cell production. Methods that are being used to ensure enough autologous T cells are collected and sufficient quantities of transduced T cells are produced will be reviewed.
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|Single Viewer: On-Demand||
|Group Viewing: Live||
|Group Viewing: On-Demand||
|Group Viewing: Live & On-Demand||
Dr. Elizabeth Allen attended the David Geffen School of Medicine at UCLA and completed a residency in Clinical Pathology at the University of California Irvine. She went on to her fellowship in Blood Banking/Transfusion Medicine at the National Institutes of Health, where she studied apheresis collections for CAR T cells and antibody formation in patients with sickle cell disease undergoing transplant. She is currently the associate medical director of Transfusion Medicine at the University of California San Diego.
Dr. Steven Highfill currently leads the Product Development group at the NIH Center for Cellular Engineering and is responsible for CMC related activities for cell therapy products. These activities include developing new cell manufacturing methods and optimizing current methods for Clinical Center Investigators. Dr. Highfill was formerly an investigator at Novartis where he managed multiple CAR T-cell programs targeting antigens on both hematologic and solid tumors. One of the primary focuses of his research was on desensitizing CAR T-cells to the suppressive tumor microenvironment. During his postdoctoral fellowship at the NCI, Dr. Highfill lead a research project that identified a major barrier for patients receiving PD1 checkpoint blockade therapy for sarcoma. Here, it was discovered that tumor-induced inhibitory myeloid cells limit the efficacy of anti-PD1 therapy, and this limitation could be reversed by preventing the migration of myeloid cells to the tumor (Science Translational Medicine 2014). Similarly, retinoic acid was used to differentiate inhibitory myeloid cells so that they lost their suppressive function, which allowed for an enhanced therapeutic benefit of GD2 CAR T-cells in a murine xenograft model of osteosarcoma (Cancer Immunol Res 2016).