Interrogating Cancer Drivers via CRISPR: Mutant TP53 as a Therapeutic Target in Hypodiploid B-cell Acute Lymphoblastic Leukemia

Speaker: Ernesto Diaz-Flores, PhD
Associate Professor, University of California San Francisco

Watch this webinar to learn how Dr. Flores was able to go from 1%–2% lentiviral transduction efficiency to >95% in hard-to-transduce hypodiploid cell lines and primary cells. Dr. Flores presents how he was able to quickly and gently enrich transduced clones to allow such high transduction efficiency and the generation of knockouts for further studies.

About: Ernesto Diaz-Flores, Ph.D.

University of California, San Francisco
San Francisco, CA

As a leukemia researcher, Dr. Flores’ ultimate goal is to find new cures for high-risk leukemia through an understanding of the mechanisms mediating leukemogenesis. During his time as assistant professor at the University of California, San Francisco, he has identified B-cell lymphoma 2 (BCL-2) as a promising therapeutic target and validated venetoclax as an effective drug against this leukemia. These studies contributed to the first clinical trial of venetoclax in pediatric acute lymphoblastic leukemia (ALL). In follow-up work, Dr. Flores provides evidence for a highly effective combinatorial therapy (Pariury et al., submitted) as well as biomarkers or response to inotuzumab immunotherapy (Benhert et al., submitted). His current work focuses on studying pharmacological and immunotherapeutic opportunities for targeting mutant p53 in the context of acute leukemia. This work represents a new paradigm in the field of p53 and hypodiploid leukemia and is expected to bring novel treatments to the clinic.

Applications: Oncology, Cell Line Development

Key takeaways:

• Learn how 1%-2% lentiviral transduction efficiency was successfully increased to >95% in hard-to-transduce cell lines and primary cells
• See data demonstrating the successful generation of isogenic hypodiploid cell lines that were p53 deficient with knock-in p53 wildtype or mutant alleles.