Date, Time & Venue
- 31st January 2025, 13:30-14:30
- Venue: CCII Bristol Myers Squibb Building (Bldg. No 2), NITORI Hall (1F)
- On-site participation, admission free
- Organizer: Centre for Cancer Immunotherapy and Immunobiology (CCII)
Speaker
Dr. Soki Kashima
Postdoctoral Associate
Department of Medical Oncology
Yale Cancer Center
Yale School of Medicine
Abstract
The immunobiology of renal cell carcinoma (RCC) is distinct from that of other immunotherapy-responsive cancers. While RCC lesions exhibit signs of high-level inflammation, intratumoral CD8 T cell infiltration paradoxically correlates with poorer prognosis. Conventional biomarkers of ICI-response, such as tumor mutational burden and PD-L1 expression, have failed to prove as predictive biomarkers in RCC patients. These findings highlight the necessity for further investigation into the mechanisms driving antitumor immunity and inflammation within the RCC tumor microenvironment (TME). In this study, we sought to elucidate the mechanisms and employed single-cell RNA sequencing to investigate how the interferon signaling axis modulates immune cell populations within the RCC TME. Subsequently, we conducted a dissection of the TME using pre- and post-ICI treatment samples, and further identified specific myeloid cell populations associated with ICI response in RCC. The results of our study suggest a critical mechanism of anti-tumor resistance mediated by specific myeloid cells and the interferon signaling. These findings underscore the need for novel strategies that target the specific myeloid populations to overcome ICI resistance in RCC.
