MembersBon Federica, BSc Student
Calcinotto Arianna, Group Leader
Elia Angela Rita, Research Assistant
Mukherjee Siddhartha, PhD Student
Nüesch Manuel, PhD Student
The genome of cancer cells is littered with mutations (errors in individual nucleotides), some of which might contribute to growth of the cancer by acting tumor-promoting genes called oncogenes.
Potentially oncogenic mutations accumulating throughout life, in apparently normal tissues, can be recognized and killed by the immune system. However, cancer-related inflammation is a double-edged sword. On the one hand, the inflammatory factors can trigger the immune-surveillance leading to the elimination of tumor cells; on the other hand, there is emerging evidence suggesting that inflammation acts as pro-tumorigenic factor. Therefore, the immune response in the tumor can be both a tumor suppressor and –promoter depending on cell-, tissue- and cancer context.
Our research focuses on a different way of conceiving immunotherapy, blocking factors produced by immune cells that act as nourishment/triggers for tumor growth, progression and as causes of therapy resistance in cancer.
A major current interest of the lab is identifying the mechanisms underlying the contribution of the innate immune cells in regulating later stages of tumor progression and favoring therapy resistance in breast cancer. Our ultimate goal is the generation of a cellular engineered humanized breast cancer mouse model platform to study human tumor immune responses and test new combined immunotherapy approaches in vivo at much greater resolution than what is possible with current systems with the final aim to apply these discoveries to the clinic and develop novel therapeutic options and illuminate our understanding of the spectrum of interactions in the tumor microenvironment.
- IL-23 secreted by myeloid cells drives castration-resistant prostate cancer.
Calcinotto A, et al. Nature. 2018 doi: 10.1038/s41586-018-0266-0.
- Microbiota-driven interleukin-17-producing cells and eosinophils synergize to accelerate multiple myeloma progression.
Calcinotto A, et al, Nat Commun. 2018 doi: 10.1038/s41467-018-07305-8.
- Modifications of the mouse bone marrow microenvironment favor angiogenesis and correlate with disease progression from asymptomatic to symptomatic multiple myeloma.
Calcinotto A, et al, Oncoimmunology. 2015
- Modulation of microenvironment acidity reverses anergy in human and murine tumor-infiltrating T lymphocytes.
Calcinotto A, et al, Cancer Res. 2012 doi: 10.1158/0008-5472.CAN-11-1272.
- Targeting TNF-α to neoangiogenic vessels enhances lymphocyte infiltration in tumors and increases the therapeutic potential of immunotherapy.
Calcinotto A, et al, J Immunol. 2012 doi: 10.4049/jimmunol.1101877. Epub 2012 Feb 8