Panel Discussion: Cutting Cancer Off At The Knees: Analysing the Preclinical Potential of Reprogramming/Repolarising Pro-Tumour Immune Cells
Time: 5:00 pm
day: Day One
The aggression of tumours is hugely linked with tumour survival mechanisms resulting in high-grade tumours. Assessing the implication of suppressor cells on the progression of tumours. Tumour-associated macrophages (TAMs) make up around 50% of the solid mass in a variety of human solid cancers (e.g., lung, breast and pancreatic) which are polarised into the M2 phenotype and support immune suppression, tumour growth, angiogenesis, metastasis, and therapeutic resistance. Myeloid-derived suppressor cells (MDSCs) are activated under pathological conditions and can induce further immunosuppressive cells and inhibit the antitumoral immune response, therefore posing a great immunotherapy target however, this panel is going to discuss the potential of repolarising these cells to aid in the antitumoral immune response thereby improving preclinical and translational success.
This panel will discuss:
- The immune suppressive phenotype: insight into whether it’s fixed or flexible?
- Can the suppressive phenotype be reverted e.g. for example macrophage reprogramming from M2 to M1?
- Discussion around both immunosuppressive tumour-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs)
- The efficacy of targeting folate-targeted Toll-like receptor 7 agonist (FA-TLR7-1A) for reverting the inflammatory phenotype. Off target effects/Systemic activation concerns?
- How does this help us improve our translatability into clinic?
- Implications of blocking tumour-derived granulocyte-macrophage colony-stimulating factor (GM-CSF) on TAMs, resulting in anti-tumour T-cell immunity leading to tumour regression