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TGF-beta is a signal that keeps immune cells out of tumours, but blocking it throughout the body caused bleeding and heart toxicity and sank bintrafusp alfa. Tethering the blocker to tumour stroma with a FAP anchor, a collagen-binding domain or a protease-activated mask could give the benefit without the harm.
Systemic TGF-beta blockade, including the PD-L1-TGF-beta trap bintrafusp alfa, failed largely on a narrow therapeutic index with bleeding and cardiac toxicity. Localisation strategies (a FAP-anchored trap, a collagen-binding domain fusion, or a protease-activated masked format) restrict activity to stroma-rich tumour tissue, and masked antibody formats are already in clinical trials.
Two bottleneck pages and 32 idea pages on OnCo cite this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing pages listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
One of the most cited reviews Europe PMC returns for PD-L1 in Bladder & urothelial cancer, so it is a natural first reading for anyone weighing the idea it is linked from. The record was linked automatically by title and abstract; read the abstract above and the paper itself before relying on any figure.
One of the most cited reviews Europe PMC returns for PD-L1 in Bladder & urothelial cancer, so it is a natural first reading for anyone weighing the idea it is linked from. The record was linked automatically by title and abstract; read the abstract above and the paper itself before relying on any figure.
One of the most cited reviews Europe PMC returns for PD-L1 in Bladder & urothelial cancer, so it is a natural first reading for anyone weighing the idea it is linked from. The record was linked automatically by title and abstract; read the abstract above and the paper itself before relying on any figure.
Shares Estimation of the Percentage of US Patients With Cancer Who Are Eligible for and Respond to Checkpoint Inhibitor Immunotherapy Drugs, Desmoplasia (tumour stroma), Hot vs cold tumours, Cold tumours and the immunosuppressive microenvironment.
Shares Estimation of the Percentage of US Patients With Cancer Who Are Eligible for and Respond to Checkpoint Inhibitor Immunotherapy Drugs, Hot vs cold tumours, Cold tumours and the immunosuppressive microenvironment, Pancreatic ductal adenocarcinoma.
Shares Estimation of the Percentage of US Patients With Cancer Who Are Eligible for and Respond to Checkpoint Inhibitor Immunotherapy Drugs, Desmoplasia (tumour stroma), FAP, Cold tumours and the immunosuppressive microenvironment.
Shares Estimation of the Percentage of US Patients With Cancer Who Are Eligible for and Respond to Checkpoint Inhibitor Immunotherapy Drugs, Hot vs cold tumours, Cold tumours and the immunosuppressive microenvironment, Bladder & urothelial cancer.
Shares Estimation of the Percentage of US Patients With Cancer Who Are Eligible for and Respond to Checkpoint Inhibitor Immunotherapy Drugs, Hot vs cold tumours, Cold tumours and the immunosuppressive microenvironment, Bispecific antibodies.
Shares Estimation of the Percentage of US Patients With Cancer Who Are Eligible for and Respond to Checkpoint Inhibitor Immunotherapy Drugs, Hot vs cold tumours, Cold tumours and the immunosuppressive microenvironment, Pancreatic ductal adenocarcinoma.
Shares Estimation of the Percentage of US Patients With Cancer Who Are Eligible for and Respond to Checkpoint Inhibitor Immunotherapy Drugs, Hot vs cold tumours, Cold tumours and the immunosuppressive microenvironment, Pancreatic ductal adenocarcinoma.
Shares Estimation of the Percentage of US Patients With Cancer Who Are Eligible for and Respond to Checkpoint Inhibitor Immunotherapy Drugs, FAP, Hot vs cold tumours, Cold tumours and the immunosuppressive microenvironment.