Main unanswered questions identified by each working group
| WORKING GROUP | Main Questions |
|---|---|
| I. Germline GENETIC Contributions TO Cancer Immune Responsiveness | 1. Which are the key molecular mechanisms involved in anti-tumor immunity that might be modulated by germline genetic variants?2. Are common genetic polymorphisms associated with a differential spontaneous or treatment-induced anti-tumor immune response?3. How can we implement the study of host genetic diversity to identify novel biomarkers of responsiveness or toxicity to cancer immunotherapy? |
| II. Somatic GENETIC Contributions TO Cancer Immune Responsiveness | 1. Can our knowledge of how cancer-intrinsic features influence the tumor microenvironment help us optimize immunotherapy combinations?2. How do we harmonize biomarkers derived from different technologies in order to specifically tailor IO therapy for a patient and increase the likelihood of response?3. Will understanding the role of epigenetic re-programming downstream of molecular alterations in tumor cells reveal new opportunities to combat cancer immune-evasion strategies? |
| III. Transcriptional Changes Related to CIR | 1. Can we generate transcriptional signature with high predictive value for a specific tumor-immune microenvironment?2. Can transcriptional profiling be developed as a biomarker for the CIR?3. What technological advances do we need to dissect the tumor-immune microenvironment in space and time? |
| IV. Immunogenic Cell Death and Cancer Immune Responsiveness | 1. What are the key molecular events that occur during immunogenic cell death that prime a robust immune response and promote immunological memory?2. Which therapeutic strategies will more effectively promote ICD while minimizing off target inhibition of immune responses?3. How can detection of immunogenic cell death be routinely incorporated into clinical trials? |
| V. Experimental Models of the Immune Landscape of Cancer | 1. What are the current limitations of humanized PDX mouse models?2. What approaches can be undertaken towards more faithful models of human cancer-human myeloid cells interface?3. How to develop models that better model to reproduce tumor mutational load? |