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Inhibitor Checkpoint, HLA Variation - Coggle Diagram
Inhibitor Checkpoint
IC basics :
What are Immune Checkpoints ? :
molecules (PD-1, CTLA-4...) that are really good to prevent auto-immune diseases but that are not really helpfull to fight against cancer
What is the idea of block immune checkpoint ?
To block the brakes allowing immune system to do its job and attack cancer cells
Does it work in real life ?
Durvalumab
anti-PD-L1 Since February 2016 for Stage III non-small-cell lung cancer (NSCLC)
Avelumab
anti-PD-L1 Since March 2017 for histologically confirmed metastatic Merkel cell carcinoma
Ipilimumab
anti-CTLA-4 Since August 2010 for stage 3 or 4 malignant melanoma
Cemiplimab
anti-PD-1 Since September 2018 for metastatic cutaneous squamous cell carcinoma
Atezolizumab
anti-PD-L1 Since October 2016 for stage III-B or IV nonsquamous and squamous NSCLC
Pembrolizumab
anti-PD-1 Since October 2016 for Stage IV nonsquamous and squamous NSCLC
Nivolumab
anti-PD-1 Since March 2015 for Stage III-B or IV Squamous NSCLC
IC therapy combination
Can we combine them with other therapies?
Oncolytic virus: what are they?
Genetically modified viruses that infect and kill cancer cells
Why combine them with IC therapy?
To enhance immune response
To make make tumor cells more recognizable to the immune system
Oncogenic pathway inhibitors
Drugs that block pathways that help tumors grow (MAPK, PI3K...)
Why combine them with IC therapy?
To make tumors cells more vulnerable
To help immune cells get into the tumor
HLA-I genotype strongly influences checkpoint inhibitor outcomes
Heterozygosity = broader antigen presentation = better survival
Integration of HLA genotyping into precision oncology
HLA Variation
