Vivek Subbiah, MD, of The University of Texas MD Anderson Cancer Center, discusses data on selpercatinib that showed promising activity across a variety of RET fusion–positive cancers, including treatment-refractory gastrointestinal malignancies. This analysis highlights the need for genomic profiling to identify actionable oncogenic drivers.
Dennis J. Slamon, MD, PhD, of the UCLA David Geffen School of Medicine, reflects on the ways in which breast cancer research pioneered the targeted treatment approach, as understanding of the basic biology of tumors deepened and new pathways were uncovered. He sees a future ripe with possibilities for new molecular targets to further improve outcomes for patients with breast cancer and other types of tumors.
Michel Sadelain, MD, PhD, of Memorial Sloan Kettering Cancer Center, discusses the challenges in developing CAR T-cell therapy, as well as the progress being made, such as creating hybrid CAR and T-cell receptors that should enable T cells to recognize much lower levels of antigens. The field, he says, is poised to take on a range of solid tumors to extend the successes in hematologic malignancies.
Matthew J. Matasar, MD, of Memorial Sloan Kettering Cancer Center, discusses phase III results of the CHRONOS-3 trial, which showed that copanlisib plus rituximab led to a 48% reduction in the risk of disease progression or death compared with placebo plus rituximab in patients with relapsed indolent non-Hodgkin lymphoma (Abstract CT001).
Ralph R. Weichselbaum, MD, of the University of Chicago, discusses oligometastasis as a part of the metastatic spectrum where ablative therapies, such as surgery or stereotactic body radiotherapy, may be curative alone or with systemic agents, as well as some potential biomarkers to guide treatment selection.
Linda T. Vahdat, MD, MBA, of Memorial Sloan Kettering Cancer Center, discusses results of a phase II trial designed to test the concept that targeting the tumor microenvironment by depleting copper may prevent metastases, essentially disrupting the infrastructure that contributes to tumor spread.
