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CRISPR & RNAi Genetic Screening and other Methods for the Discovery of Oncogenic Vulnerabilities and Drug Resistance
April 12 @ 3:00 pm – 4:00 pm CDT
Join Cellecta experts at Exhibitor Spotlight Theater A on Tuesday, April 12 from 3:00 – 4:00 p.m. Register to attend in person here. Refreshments will be provided. Space is limited.
Moderator: Paul Diehl, PhD, COO, Cellecta
Speaker 1: Maria J. Ruiz-Echevarria, PhD
Associate Professor Stephenson Cancer Center Oklahoma Health Sciences Center Talk: Development of a multitargeted therapy for prostate cancer Relapse after first-line androgen deprivation therapy (ADT) is the main cause of mortality in patients with advanced prostate cancer (PCa). Key molecular mechanisms of resistance reveal continued activation of the androgen receptor (AR). To enable the development of multitargeted therapeutics for PCa, we have developed an unbiased RNA interference (RNAi)-based negative selection screen to identify shRNAs that cause toxicity in cellular models of relapsed disease after ADT, by targeting multiple AR-signaling components. The results emphasize the value of this screen for the identification of effective multitarget therapeutic modalities that maximize AR signaling inhibition with theoretically limited resistance profiles.
Speaker 2: Alex Chenchik, PhD
President and Chief Scientific Officer, Cellecta Talk: Immunophenotyping of TCR and BCR clonotypes T-cell receptor (TCR) and B-cell receptor (BCR) repertoire profiling holds great potential for understanding the disease mechanisms and development of new therapeutics for infectious disease, auto-immunity and immuno-oncology applications. However, this potential could be greatly improved by combining information about receptor clonotypes with immunophenotypes of T and B cells. To facilitate these studies, we developed a novel technology for combined profiling of all human TCR and BCR variable regions and phenotypic characterization of immune cells.
Register to attend in person here. Refreshments will be provided. Space is limited.