Electra D. Paskett, PhD, of The Ohio State University, discusses various factors that may contribute to cancer such as socioeconomic status, discrimination, violence, and access to health care. When clinicians identify these factors and intervene with access to services, it may be possible to improve outcomes for their patients (Abstract SY33).
Josh Neman, PhD, of the Keck School of Medicine, University of Southern California, discusses the distribution of brain metastasis to preferential brain regions that vary according to cancer subtype, how neurotransmitters respond, and the ways in which the central nervous system acclimates (Abstract SY32).
Yaqi Zhao, MSc, of St. Jude Children’s Research Hospital, discusses findings from the phase III INO-VATE trial, which showed that inotuzumab ozogamicin reduced the signs and symptoms of acute lymphoblastic leukemia associated with a variety of gene and chromosome changes. Future studies may confirm which patients are more likely to benefit from this agent (Abstract CT027).
Charles L. Sawyers, MD, of Memorial Sloan Kettering Cancer Center, discusses the battle against treatment resistance and how to overcome it, as well as the power of observational clinical data in precision oncology, derived largely from his experience with Project GENIE, and the role of genetic ancestry (Abstract PL02).
Timothy A. Yap, MBBS, PhD, of The University of Texas MD Anderson Cancer Center, discusses results from a phase Ib expansion trial of the safety and efficacy of the oral ataxia telangiectasia and Rad3-related (ATR) inhibitor elimusertib in advanced solid tumors with DNA damage response defects. Elimusertib is a selective inhibitor of ATR, a key regulator of responses to DNA damage and replication stress, with antitumor activity in preclinical models of various solid tumors and lymphoma (Abstract CT006).
David A. Barbie, MD, of Dana-Farber Cancer Institute, discusses his laboratory’s studies, showing that malignant pleural mesothelioma, an inflamed cancer type with marginal response to immune checkpoint blockade, demonstrated high tumor cell STING expression and response to STING agonists in combination with natural killer cell therapies ex vivo. STING is the tumor cell stimulator of interferon genes (Abstract 4168).
