Loading
A review of why immune drugs fail in pancreatic cancer: the tumour's own driver genes build immune suppression from the start, single agents do nothing, and the proposed answer is to combine antigen delivery, T-cell support and stromal reprogramming.
Pancreatic ductal adenocarcinoma is among the most immune-resistant tumour types; its genomic landscape shaped by oncogenic drivers promotes immune suppression from the earliest stages of tumour inception and subverts adaptive T-cell immunity. Single-agent immune modulators have been clinically ineffective and multi-modal therapies targeting mechanisms of resistance are likely needed. The review covers strategies to confer antigen specificity, enhance T-cell effector function and neutralise immunosuppressive elements of the tumour microenvironment.
The clearest statement of why the corpus records so many negative immunotherapy trials here, and of the design logic behind the vaccine and agonist combinations now in trials.
Shares Immune exclusion, Cold tumours: immune deserts and exclusion, Hot vs cold tumours, PD-1 / PD-L1 immune checkpoint & T-cell activation.
Shares Hot vs cold tumours, PD-1 / PD-L1 immune checkpoint & T-cell activation, Pancreatic ductal adenocarcinoma.
Shares Robert H. Vonderheide, Abramson Cancer Center, University of Pennsylvania, Pancreatic ductal adenocarcinoma.
Shares Cold tumours: immune deserts and exclusion, The cancer-immunity cycle.
Shares Hot vs cold tumours, PD-1 / PD-L1 immune checkpoint & T-cell activation, Pancreatic ductal adenocarcinoma.
Shares Immune exclusion, The cancer-immunity cycle, Pancreatic ductal adenocarcinoma.
Shares Hot vs cold tumours, PD-1 / PD-L1 immune checkpoint & T-cell activation, Pancreatic ductal adenocarcinoma.
Shares Hot vs cold tumours, PD-1 / PD-L1 immune checkpoint & T-cell activation, Pancreatic ductal adenocarcinoma.