Yuki Muroyama, MD, PhD, of the University of Pennsylvania Perelman School of Medicine, discusses the interaction between the immune system and a novel marker—T-cell DNA damage and repair response—to understand how that interaction may affect immune cell biology and therapeutic response (Abstract 310).
Emily Z. Keung, MD, of The University of Texas MD Anderson Cancer Center, discusses the complex interactions of immune infiltrates and neoadjuvant immune checkpoint blockade (ICB) in patients with resectable soft-tissue sarcoma. These interactions may hold the key to understanding pathologic response to ICB and ICB resistance (Abstract 379).
Yevgeniy R. Semenov, MD, of Massachusetts General Hospital and Harvard Medical School, discusses new findings suggesting cutaneous adverse events such as vitiligo, lichenoid dermatitis, and psoriasis—which often occur in patients with cancer who receive immune checkpoint inhibitors—may be strongly associated with response to therapy and a 22% reduction in mortality (Abstract 814).
John M. Kirkwood, MD, of the University of Pittsburgh Medical Center, discusses phase Ib findings on the combination of vidutolimod plus pembrolizumab, as well as vidutolimod monotherapy, both of which showed clinical activity in patients with PD-1 blockade–refractory melanoma. The duration of response with the combination therapy was substantially longer. Phase II studies are ongoing (Abstract 950).
Hans Wildiers, MD, of University Hospitals Leuven, discusses the final results from the phase IIb AIPAC study, which suggested that eftilagimod added to paclitaxel may be of benefit to patients older than 65 years with hormone receptor–positive, HER2-negative metastatic breast cancer after endocrine-based therapy. Eftilagimod, which is a first-in-class antigen presenting cell activator, appeared to increase circulating CD4/CD8 T cells, which correlated to improved overall survival (Abstract 948).
Kim A. Reiss, MD, of the University of Pennsylvania, discusses results of a phase I trial of a CAR-M engineered macrophage cancer therapy, known as CT-0508, for patients with solid tumors that overexpress HER2. CAR-M, designed to exploit the natural role of macrophages to initiate an antitumor response, is currently under study at multiple clinical sites (Abstract 951).
