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'Hot' tumours are full of immune cells and respond to immunotherapy; 'cold' tumours have kept the immune system out.
Hot tumours are full of immune cells and tend to respond to immunotherapy, whereas cold tumours have kept the immune system out. Immunologists distinguish inflamed tumours, immune-excluded tumours in which T cells are held at the margin by TGF-β and stroma, and immune deserts. Pancreatic cancer, prostate cancer, glioblastoma and most HR-positive breast cancers are cold, and turning cold tumours hot is the goal of radiation, vaccines, ISACs, STING agonists and oncolytic viruses. The term is linked to the Immune checkpoint inhibitors, STING & innate immune agonists and Oncolytic viruses technologies and to Desmoplasia (tumour stroma), and it is referenced by the Pancreatic ductal adenocarcinoma and Glioma & glioblastoma entries, Miriam Merad and the bottleneck on cold tumours.
Showing the technology this term belongs to: Immune checkpoint inhibitors.
The glossary entry explains the word; the readout page carries the scoring rule, the thresholds approvals use, the companion diagnostics and the tests.
The strongest human evidence that a cancer vaccine can make durable T cells in a tumour with few mutations; the randomised phase 2 IMCODE003 (260 patients, primary completion listed for January 2031) is the test of whether that translates into fewer relapses.
The first credible response signal in microsatellite stable colorectal cancer, and the reason the field's attention has moved to Fc engineering and to excluding patients with active liver metastases, in whom responses are rare.
It is the strongest case that mutation burden is real biology in lung cancer and, at the same time, the clearest demonstration that its threshold is not fixed, which is why it never became a reliable selector.
It corrected a widely repeated simplification. An STK11 or KEAP1 mutation is not by itself a reason to expect immunotherapy to fail; it is a reason to expect it in a KRAS-mutant tumour, which is how the result should be read on a report.
It offers the first credible explanation for why only a minority of small-cell patients get a durable benefit from checkpoint blockade, and it introduces subtype switching, which would mean retesting at relapse rather than typing once.
One pathway page on OnCo cites 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 page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
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.
The reference for why pancreatic microenvironment trials read as a list of failures and what the field now means by remodelling rather than removing the stroma.
Shares Safety and activity of anti-PD-L1 antibody in patients with advanced cancer, Autophagy promotes immune evasion of pancreatic cancer by degrading MHC-I, Phase 2 trial of single agent ipilimumab (anti-CTLA-4) for locally advanced or metastatic pancreatic adenocarcinoma, Challenges and opportunities for pancreatic cancer immunotherapy.
Shares Block the complement signal that recruits tumour-protecting cells, Train the bone marrow to make better anti-tumour immune cells, Clear the suppressive neutrophils out of pancreatic tumours first, De-acidify the tumour so T cells can work in it.
Shares Map which tumour clones sit next to which immune cells before choosing therapy, Standards for spatial and multiplex tissue biomarkers before they reach the clinic, Binnewies 2018: understanding the tumour immune microenvironment for effective therapy, Grow tumour organoids together with the patient's own immune cells.
Shares Miriam Merad, Map which tumour clones sit next to which immune cells before choosing therapy, Standards for spatial and multiplex tissue biomarkers before they reach the clinic, Clear the suppressive neutrophils out of pancreatic tumours first.
Shares Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 immunotherapy in pancreatic cancer, Anchor a TGF-beta trap in the tumour stroma so it cannot act everywhere, What actually holds T cells at the tumour border?, Make every cold tumour hot: a coordinated programme to reprogramme immune-excluded tumours.
Shares Autophagy promotes immune evasion of pancreatic cancer by degrading MHC-I, Phase 2 trial of single agent ipilimumab (anti-CTLA-4) for locally advanced or metastatic pancreatic adenocarcinoma, Durvalumab with or without tremelimumab for patients with metastatic pancreatic ductal adenocarcinoma: a phase 2 randomized clinical trial, Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 immunotherapy in pancreatic cancer.
Shares Chen and Mellman 2013: the cancer-immunity cycle, Genetic mechanisms of immune evasion in colorectal cancer, Association of high tumor mutation burden in non-small cell lung cancers with increased immune infiltration and improved clinical outcomes of PD-L1 blockade across PD-L1 expression levels, RNA neoantigen vaccines prime long-lived CD8+ T cells in pancreatic cancer.
Shares Autophagy promotes immune evasion of pancreatic cancer by degrading MHC-I, CheckMate 143, Chen and Mellman 2013: the cancer-immunity cycle, Atezolizumab with or without cobimetinib versus regorafenib in previously treated metastatic colorectal cancer (IMblaze370).