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The immunotherapy roadmap is a 130-year arc from injecting bacteria into tumours to releasing immune brakes, and now to designing the immune response itself with vaccines, engagers, and cells.
The immunotherapy roadmap covers a 130-year arc that starts with Coley's toxins, BCG for bladder cancer, interferon and IL-2 and sipuleucel-T, an era of sporadic cures and scepticism. The checkpoint revolution followed with ipilimumab, nivolumab, pembrolizumab and atezolizumab and the Nobel Prize to Allison and Honjo, then immunotherapy moved into earlier lines, combinations, T-cell engagers and TIL. The emerging step is engineered immunity: personalised mRNA vaccines, PD-1 and VEGF bispecifics, ADC plus IO, oncolytic viruses, TCR-T and in vivo CAR, with interception vaccines as the speculative end. The route links checkpoint inhibitors, T-cell engagers, CAR-T, TIL and STING agonists, and the cold-tumour and response-prediction bottlenecks.
The prehistory runs from Coley's toxins (1891) through BCG for bladder cancer (1976) and interferon and IL-2 (1980s-90s) to sipuleucel-T (2010). The era brings sporadic cures, high toxicity and scepticism.
Ipilimumab (2011), nivolumab and pembrolizumab (2014) and atezolizumab (2016) are approved; the tumour-agnostic MSI-H approval follows (2017) and the Nobel Prize goes to Allison and Honjo (2018). Durable responses follow across >15 tumour types.
Immunotherapy moves earlier and into combinations: neoadjuvant/adjuvant IO in melanoma, NSCLC, TNBC, bladder; IO + chemo, IO + VEGF, IO + IO (LAG-3); T-cell engagers in myeloma and lymphoma; and the first solid-tumour engager (tarlatamab) and TIL (lifileucel).
Numbers are from the trial as recorded here; see the source links in the table below. This is orientation, not medical advice: ask your team how closely the trial population matches you.
Personalised mRNA vaccines pass phase 3 (intismeran, 2026); PD-1×VEGF bispecifics challenge pembrolizumab; ADC + IO becomes first line; oncolytic virus RP1 approved; TCR-T and solid-tumour CAR-T approvals; in vivo CAR first-in-human.
Off-the-shelf shared-neoantigen vaccines for KRAS and TP53; interception vaccines in high-risk carriers; myeloid-reprogramming drugs that make cold tumours hot; immune-PET-guided IO selection; engineered cytokines with tumour-restricted activity.
Every era's records, trial outcomes and papers, and every watch item, as JSON.
Probability ranges are named estimates that the claim is borne out on roughly a five-year horizon. They are meant to be argued with: propose a revision with your name and reasoning via a pull request to src/data/confidence.ts.
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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.
For the minority of patients whose tumours express a lot of PD-L1, a single antibody outperforms chemotherapy and is far easier to take. The word minority is the point: the same drug in the same disease at lower PD-L1 gives much less.
Shares TIL therapy, Oncolytic viruses, Hot vs cold tumours, Personalised neoantigen (mRNA) vaccines.
Shares INTerpath-001 (V940-001), RNA neoantigen vaccines prime long-lived CD8+ T cells in pancreatic cancer, Personalised neoantigen (mRNA) vaccines, Cold tumours and the immunosuppressive microenvironment.
Shares Vusolimogene oderparepvec, Cytokines & engineered cytokines, Oncolytic viruses, Cold tumours and the immunosuppressive microenvironment.
Shares INTerpath-001 (V940-001), Personalised neoantigen (mRNA) vaccines, Ipilimumab, Nivolumab.
Shares STING & innate immune agonists, Hot vs cold tumours, Cold tumours and the immunosuppressive microenvironment, No one can predict who responds to immunotherapy.
Shares Lifileucel, TIL therapy, Hot vs cold tumours, Personalised neoantigen (mRNA) vaccines.
Shares Relatlimab + nivolumab, CheckMate 067, Ipilimumab, Nivolumab.
Shares Cytokines & engineered cytokines, Hot vs cold tumours, Cold tumours and the immunosuppressive microenvironment, No one can predict who responds to immunotherapy.