Within this project we will investigate the impact of caspase-independent cell death elicited by chemotherapy or targeted therapy on the inflammatory response. The project is based on the observation that elevated sub-lethal levels of caspase activity contribute to the oncogenic state in SCLC and may suppress inflammatory response genes. The team will seek to analyze the mechanistic principles of caspase-dependent inflammatory signaling during therapeutic stress and activation status of the immune cell infiltrate on the single cell level in vivo. Furthermore, they will explore, to which extent combination therapies can be used to elicit synergistic effects by enhancing immunogenicity. The team will collaborate with teams that are focused on the understanding of inflammatory signaling in SCLC patients (A04, A05, A09, C01, C05, C08) and with those that aim at identifying SCLC-specific vulnerabilities (A01, A05, A07, B01, B05, C04).