Round up of member activity
It’s only through community discussion and debate that we can collectively update, evolve and improve the framework. So, a big thank you to all who have added their ideas already!
As we know, cancer immunity is a rapidly evolving field of research. And so, keeping the framework up to date – improving on what’s included and adding new data when it gets published - will only be achieved through a collective effort from everyone involved.
Here’s a quick round up of ideas have been added to the framework so far:
- Step 1 – Release of cancer-cell antigens:
Mutational burden, mismatch repair deficiency, radiotherapy, viral antigens, reactive oxygen species (ROS), neoantigens, cancer associated antigens
- Step 2 – Cancer antigen presentation:
TNF-α, exercise induced IL-6, photoimmune IL-6 ARNTL, 1,25(OH)2D3 (vitamin D3), endotoxin response, HMGCR inhibitors, traditional Chinese medicine, NOD2, TLR, FcyRIII, NF-κB, inflammasome pathway, ATG16L, calreticulin
- Step 3 – Priming and activation of T-cells:
STING agonists, IKZF3, HLA type, vitamin A, 1,25(OH)2D3 (vitamin D3), TCR, age-related loss of TCR diversity, RANKL, glucocorticoids, NSAIDs, HMGCR inhibitors, antigen immunogenicity
- Step 4 – Trafficking of T cells to tumours:
Heat shock proteins, HMGB1, sitagliptin
- Step 5 – Infiltration of T cells into tumours:
FAS ligand, anti-VEGF, CAFs/collagen, TGF-β, VEGF, chemokines, LOX, sitagliptin, metronomic cyclophosphamide, immunogenic cell death inhibitors (ICD) inducers, next-generation DC vaccines
- Step 6 – Recognition of cancer cells by T cells:
Antigen expression, MHC class I expression, TAP-1, BRAF, KRAS, B2M, MEKi
- Step 7 – Killing of cancer cells:
JAK-STAT, RANKL, hypoxia, IDO-1, PD-L1, exercise-induced IL-10, anti-CTLA4, A2A, persistent antigen encounter, TGF-β, chemotherapy, radiotherapy, targeted therapy, photodynamic therapy, pro-apoptotic BCL2 family members, anti-apoptotic BCL2 family members
Spot any you know lots about? – please do add your comments on that specific factor
Also, a couple of members have posed some specific questions over the last week:
- On step 7, on the anti-BCL2 family members factors, Jose asks:
"What criteria drive the selection of a cell-death pathway in immunotherapy?"
- On step 5, chemokines, Veronika asks:
"How come chemokines are noted down with negative effects? The CXCR3/CXCR3 ligand axis, for instance, has been shown to recruit T and NK cells into tumors in mouse studies and has been associated with T cell infiltration in several human studies."
Are you an expert on these topics – can you help answer their questions?
Don’t be shy - please go to the website (on a computer rather than mobile) and add to or comment on the interactive framework. All contributions are welcome, no matter how big or small!
Please see our ‘how to’ post if you need a quick reminder about what you need to do.