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Despite the fact that our knowledge about mechanisms responsible for cancer had enormously increased over the last decades, this has not been translated into a significant impact on mortality of cancer patients. Before, cancer treatment was solely based on therapies such as surgery, chemotherapy and radiotherapy, but since a couple of years, immunotherapy is getting into the picture. The immune system plays an important role in the control of cancer, but the immune responses are in most cases not strong enough to keep tumor growth under control. Cytotoxic T lymphocytes (CTL) need to be boosted to efficiently suppress tumor growth. Any successful immunotherapy must aim to enhance effector mechanisms, whilst reduce the suppressive mechanisms.

Oncolytic viruses (OVs) are designed to replicate selectively within infected cancer cells, and cause cell death leading to the release of mature virions that then subsequently can infect neighbouring cells. Although direct lysis of tumor cells by OVs will contribute to overall anti-tumor effect, there is mounting evidence that targeted infection of tumor cells with OVs has the potential to generate potent anti-tumor immune responses, both innate and adaptive. Although the molecular and cellular mechanisms resulting in the stimulation of the immune system are not yet fully known, it is highly likely that the mode of inducing tumor cell death is an important contributing factor. While OVs will certainly lower tumor burden, it remains to be addressed experimentally whether the immune response elicited by OVs is sufficient to improve other therapies like checkpoint therapy or other strategies like delivery of dendritic cells (DCs) to enhance the magnitude of the immune response.

Therefore, we study the role of and the interactions between the immune system and (immunogenic) cell death of melanoma after treatment with HSV-1 derived oncolytic viruses (eventually in combination with checkpoint inhibitors or DCs) in 2D and 3D models.


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