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neutropenia","drugs":4,"maxGrade3":28,"maxAnyGrade":76,"examples":[{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"},{"id":"tarlatamab","kind":"drug","name":"Tarlatamab","route":"/drugs/tarlatamab/"},{"id":"tebentafusp","kind":"drug","name":"Tebentafusp","route":"/drugs/tebentafusp/"}]},{"group":"Nausea or vomiting","drugs":4,"maxGrade3":1.6,"maxAnyGrade":22,"examples":[{"id":"tarlatamab","kind":"drug","name":"Tarlatamab","route":"/drugs/tarlatamab/"},{"id":"tebentafusp","kind":"drug","name":"Tebentafusp","route":"/drugs/tebentafusp/"},{"id":"zanidatamab","kind":"drug","name":"Zanidatamab","route":"/drugs/zanidatamab/"}]},{"group":"Rash, itching or skin reactions","drugs":4,"maxGrade3":26,"maxAnyGrade":86,"examples":[{"id":"amivantamab","kind":"drug","name":"Amivantamab","route":"/drugs/amivantamab/"},{"id":"glofitamab","kind":"drug","name":"Glofitamab","route":"/drugs/glofitamab/"},{"id":"talquetamab","kind":"drug","name":"Talquetamab","route":"/drugs/talquetamab/"}]}],"drugsWithToxicity":14},"resistance":[{"id":"egfr-tki","drugClass":"EGFR tyrosine kinase inhibitors (osimertinib)","tldr":"Lung cancers on osimertinib escape by mutating the drug's binding site, switching on a bypass receptor (MET), or changing cell type entirely.","route":"/resistance/#egfr-tki","exemplars":[{"id":"osimertinib","kind":"drug","name":"Osimertinib","route":"/drugs/osimertinib/"},{"id":"amivantamab","kind":"drug","name":"Amivantamab","route":"/drugs/amivantamab/"}],"mechanisms":[{"name":"On-target EGFR C797S","category":"on-target","categoryLabel":"On-target","how":"Mutation of the cysteine that osimertinib binds covalently; abolishes drug binding while EGFR stays active.","frequency":"~7 to 15% after first-line osimertinib","route":"/resistance/#egfr-tki-on-target-egfr-c797s"},{"name":"MET amplification / bypass","category":"bypass","categoryLabel":"Bypass","how":"Amplified MET signals to PI3K/MAPK independently of EGFR.","frequency":"~15 to 20%","route":"/resistance/#egfr-tki-met-amplification-bypass"},{"name":"Histologic transformation","category":"lineage","categoryLabel":"Lineage switch","how":"Conversion to small-cell lung cancer (RB1/TP53 co-loss) or squamous histology; EGFR mutation persists but the cell no longer depends on it.","frequency":"~5 to 15%","route":"/resistance/#egfr-tki-histologic-transformation"},{"name":"Pre-existing minor resistant clones","category":"other","categoryLabel":"Other","how":"Small subclones that already carry a resistance route expand under single-agent TKI; adding chemotherapy up front kills them before they take over.","route":"/resistance/#egfr-tki-pre-existing-minor-resistant-clones"}],"sources":[{"label":"FLAURA2 (NEJM 2023)","url":"https://www.nejm.org/doi/full/10.1056/NEJMoa2306434"}]},{"id":"bcma-directed","drugClass":"BCMA-directed therapy (CAR-T, bispecifics, ADC)","tldr":"Myeloma escapes BCMA drugs by deleting or mutating the target, or by exhausting the T cells that were supposed to do the killing.","route":"/resistance/#bcma-directed","exemplars":[{"id":"ciltacabtagene-autoleucel","kind":"drug","name":"Ciltacabtagene autoleucel","route":"/drugs/ciltacabtagene-autoleucel/"},{"id":"teclistamab","kind":"drug","name":"Teclistamab","route":"/drugs/teclistamab/"},{"id":"belantamab-mafodotin","kind":"drug","name":"Belantamab mafodotin","route":"/drugs/belantamab-mafodotin/"}],"mechanisms":[{"name":"BCMA antigen loss (biallelic TNFRSF17 deletion, extracellular mutations)","category":"antigen","categoryLabel":"Antigen loss","how":"Deletion or mutation removes or alters the epitope; more common after bispecifics than CAR-T.","frequency":"~10 to 30% after bispecifics","route":"/resistance/#bcma-directed-bcma-antigen-loss-biallelic-tnfrsf17-deletion-extracellular-mutations"},{"name":"T-cell exhaustion and low fitness","category":"immune-evasion","categoryLabel":"Immune evasion","how":"Prior lines, high tumour burden, and continuous bispecific dosing exhaust T cells; CAR-T products from heavily pretreated patients expand poorly.","route":"/resistance/#bcma-directed-t-cell-exhaustion-and-low-fitness"},{"name":"Soluble BCMA decoy","category":"pharmacology","categoryLabel":"Pharmacology","how":"Shed BCMA binds drug in circulation.","route":"/resistance/#bcma-directed-soluble-bcma-decoy"}],"sources":[{"label":"CARTITUDE-4 (NEJM 2023)","url":"https://www.nejm.org/doi/full/10.1056/NEJMoa2303379"}]},{"id":"cd19-car-t","drugClass":"CD19 CAR-T","tldr":"Leukaemia and lymphoma relapse after CD19 CAR-T either without CD19 (the target is gone) or with it (the CAR-T cells are gone or exhausted).","route":"/resistance/#cd19-car-t","exemplars":[{"id":"axicabtagene-ciloleucel","kind":"drug","name":"Axicabtagene ciloleucel","route":"/drugs/axicabtagene-ciloleucel/"},{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"}],"mechanisms":[{"name":"CD19-negative relapse","category":"antigen","categoryLabel":"Antigen loss","how":"Alternative splicing, mutation, or lineage switch (to myeloid) removes the CD19 epitope.","frequency":"~30 to 50% of relapses in ALL, less in lymphoma","route":"/resistance/#cd19-car-t-cd19-negative-relapse"},{"name":"CD19-positive relapse from poor CAR-T persistence","category":"pharmacology","categoryLabel":"Pharmacology","how":"Limited expansion or early loss of CAR-T cells; 4-1BB products persist longer than CD28.","route":"/resistance/#cd19-car-t-cd19-positive-relapse-from-poor-car-t-persistence"},{"name":"Immunosuppressive microenvironment and T-cell exhaustion","category":"immune-evasion","categoryLabel":"Immune evasion","how":"PD-1 upregulation, TGF-β, and myeloid suppression in lymphoma.","route":"/resistance/#cd19-car-t-immunosuppressive-microenvironment-and-t-cell-exhaustion"}],"sources":[{"label":"ZUMA-7 OS (NEJM 2023)","url":"https://www.nejm.org/doi/full/10.1056/NEJMoa2301665"}]}],"papers":[{"id":"paper-angerilli-her2-ihc-cish-biliary-hum-pathol-2026","kind":"paper","name":"HER2 status in extrahepatic cholangiocarcinoma and gallbladder carcinoma: concordance between immunohistochemistry and chromogenic in situ hybridization in 140 cases","route":"/key-papers/paper-angerilli-her2-ihc-cish-biliary-hum-pathol-2026/","year":2026,"journal":"Human Pathology","paperType":"observational","tldr":"In 140 resected bile duct and gallbladder cancers scored by the rules used in the zanidatamab trial, about one in ten was HER2-positive; every strongly stained tumour had extra gene copies, some weakly stained ones did too, and staining was often patchy.","via":[{"id":"zanidatamab","kind":"drug","name":"Zanidatamab","route":"/drugs/zanidatamab/"}]},{"id":"paper-angerilli-her2-gallbladder-extrahepatic-concordance-hum-pathol-2026","kind":"paper","name":"HER2 status in extrahepatic cholangiocarcinoma and gallbladder carcinoma: Concordance between immunohistochemistry and chromogenic in situ hybridization in 140 Cases","route":"/key-papers/paper-angerilli-her2-gallbladder-extrahepatic-concordance-hum-pathol-2026/","year":2026,"journal":"Human Pathology","paperType":"observational","tldr":"In 140 resected bile duct and gallbladder cancers tested the way the zanidatamab trial did, about one in eleven was HER2-positive, and the HER2 signal was often patchy, present in under half the tumour cells.","via":[{"id":"zanidatamab","kind":"drug","name":"Zanidatamab","route":"/drugs/zanidatamab/"}]},{"id":"paper-aall1731-blinatumomab-children-nejm-2025","kind":"paper","name":"Children's Oncology Group AALL1731: blinatumomab added to chemotherapy for children with standard-risk B-cell ALL","route":"/key-papers/paper-aall1731-blinatumomab-children-nejm-2025/","year":2025,"journal":"New England Journal of Medicine","paperType":"rct","tldr":"Two courses of blinatumomab added to standard chemotherapy cut relapses in children with average- or higher-risk standard-risk leukaemia, raising three-year disease-free survival from 88% to 96%.","via":[{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"},{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"},{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]},{"id":"paper-enrgy-zenocutuzumab-nrg1-fusion-positive-cancer-nejm-2025","kind":"paper","name":"eNRGy: efficacy of zenocutuzumab in NRG1 fusion-positive cancer","route":"/key-papers/paper-enrgy-zenocutuzumab-nrg1-fusion-positive-cancer-nejm-2025/","year":2025,"journal":"New England Journal of Medicine","paperType":"observational","tldr":"Zenocutuzumab, an antibody that grips HER2 and HER3 at once so the NRG1 growth signal cannot get through, shrank tumours in about three in ten patients whose cancers carried an NRG1 fusion, with responses lasting close to a year, and did best in pancreatic cancer. It became the first drug approved for a pancreatic cancer driver alteration.","via":[{"id":"zenocutuzumab","kind":"drug","name":"Zenocutuzumab","route":"/drugs/zenocutuzumab/"}]},{"id":"paper-harmoni-2-lancet-2025","kind":"paper","name":"HARMONi-2: ivonescimab, a PD-1 x VEGF bispecific, beats pembrolizumab head-to-head in PD-L1-positive lung cancer","route":"/key-papers/paper-harmoni-2-lancet-2025/","year":2025,"journal":"The Lancet","paperType":"rct","tldr":"In the first randomised trial to beat pembrolizumab directly, a single antibody that blocks both PD-1 and VEGF nearly doubled the time to progression in PD-L1-positive lung cancer, though survival data were still immature.","via":[{"id":"ivonescimab","kind":"drug","name":"Ivonescimab","route":"/drugs/ivonescimab/"},{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"}]},{"id":"paper-mondaca-erbb2-gallbladder-us-chile-jco-go-2024","kind":"paper","name":"Clinical and genomic characterization of ERBB2-altered gallbladder cancer: exploring differences between an American and a Chilean cohort","route":"/key-papers/paper-mondaca-erbb2-gallbladder-us-chile-jco-go-2024/","year":2024,"journal":"JCO Global Oncology","paperType":"observational","tldr":"In 260 gallbladder cancer patients from New York and Santiago, HER2 gene changes were found in about one in seven at both centres, split between extra copies and point mutations, and patients with them lived longer.","via":[{"id":"zanidatamab","kind":"drug","name":"Zanidatamab","route":"/drugs/zanidatamab/"}]},{"id":"paper-e1910-blinatumomab-mrd-negative-all-nejm-2024","kind":"paper","name":"ECOG-ACRIN E1910: adding blinatumomab to chemotherapy for adults with B-cell ALL already in MRD-negative remission","route":"/key-papers/paper-e1910-blinatumomab-mrd-negative-all-nejm-2024/","year":2024,"journal":"New England Journal of Medicine","paperType":"rct","tldr":"Giving the bispecific blinatumomab to adults whose leukaemia was already undetectable after chemotherapy raised three-year survival from 68% to 85%.","via":[{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"},{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"},{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]},{"id":"paper-mariposa-nejm-2024","kind":"paper","name":"MARIPOSA: amivantamab plus lazertinib versus osimertinib as first treatment for EGFR-mutated lung cancer","route":"/key-papers/paper-mariposa-nejm-2024/","year":2024,"journal":"New England Journal of Medicine","paperType":"rct","tldr":"Combining an EGFR-MET bispecific antibody with a third-generation EGFR pill beat osimertinib alone, delaying progression by about seven months and later improving survival, at the cost of more side effects.","via":[{"id":"amivantamab","kind":"drug","name":"Amivantamab","route":"/drugs/amivantamab/"},{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"}]},{"id":"paper-zhu-clin-transl-sci","kind":"paper","name":"Translational findings support regimen selection for first-in-human study of ubamatamab (MUC16 × CD3 bispecific antibody) in patients with recurrent ovarian cancer","route":"/key-papers/paper-zhu-clin-transl-sci/","year":2024,"journal":"Clinical and translational science","paperType":"basic","tldr":"Paper cited by one treatment page and one target page, indexed on Europe PMC as PubMed record 39652449 and published in Clinical and translational science; the citing pages link this DOI, which is how the record was matched.","via":[{"id":"ubamatamab","kind":"drug","name":"Ubamatamab","route":"/drugs/ubamatamab/"}]},{"id":"paper-aall1331-low-risk-hogan-jco-2023","kind":"paper","name":"AALL1331: blinatumomab added to chemotherapy in low-risk first relapse of childhood B-ALL","route":"/key-papers/paper-aall1331-low-risk-hogan-jco-2023/","year":2023,"journal":"Journal of Clinical Oncology","paperType":"rct","tldr":"In children with a late, low-risk relapse of leukaemia, adding three blocks of blinatumomab did not change survival overall, but for the two thirds whose relapse involved the bone marrow it cut relapses and deaths enough to become their new standard.","via":[{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"}]},{"id":"paper-blinatumomab-infant-all-van-der-sluis-nejm-2023","kind":"paper","name":"Blinatumomab added to chemotherapy in infant KMT2A-rearranged acute lymphoblastic leukaemia","route":"/key-papers/paper-blinatumomab-infant-all-van-der-sluis-nejm-2023/","year":2023,"journal":"New England Journal of Medicine","paperType":"observational","tldr":"Adding a single course of the bispecific antibody blinatumomab after induction chemotherapy in infants with KMT2A-rearranged leukaemia raised two-year disease-free survival from a historical 49 percent to 82 percent, the first major advance in infant leukaemia in decades.","via":[{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"}]},{"id":"paper-dellphi-301-nejm-2023","kind":"paper","name":"DeLLphi-301: tarlatamab, a DLL3-targeting T-cell engager, in previously treated small-cell lung cancer","route":"/key-papers/paper-dellphi-301-nejm-2023/","year":2023,"journal":"New England Journal of Medicine","paperType":"rct","tldr":"A bispecific antibody that pulls T cells onto small-cell lung cancer cells produced responses in 40% of patients whose cancer had come back after chemotherapy, lasting far longer than any previous drug in this setting.","via":[{"id":"tarlatamab","kind":"drug","name":"Tarlatamab","route":"/drugs/tarlatamab/"},{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"},{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]},{"id":"paper-epcore-nhl-1-epcoritamab-jco-2023","kind":"paper","name":"EPCORE NHL-1: epcoritamab, a subcutaneous CD20 x CD3 bispecific, in relapsed large B-cell lymphoma including after CAR-T","route":"/key-papers/paper-epcore-nhl-1-epcoritamab-jco-2023/","year":2023,"journal":"Journal of Clinical Oncology","paperType":"translational","tldr":"In EPCORE NHL-1, the off-the-shelf bispecific antibody epcoritamab, injected under the skin, produced responses in 63% of 157 patients with relapsed large B-cell lymphoma, including the 39% whose CAR-T had failed. Cytokine release syndrome occurred in half, mostly mild, and the drug won accelerated approval in 2023.","via":[{"id":"epcoritamab","kind":"drug","name":"Epcoritamab","route":"/drugs/epcoritamab/"},{"id":"glofitamab","kind":"drug","name":"Glofitamab","route":"/drugs/glofitamab/"},{"id":"mosunetuzumab","kind":"drug","name":"Mosunetuzumab","route":"/drugs/mosunetuzumab/"},{"id":"odronextamab","kind":"drug","name":"Odronextamab","route":"/drugs/odronextamab/"}]},{"id":"paper-magnetismm-3-elranatamab-natmed-2023","kind":"paper","name":"MagnetisMM-3: elranatamab, a second BCMA bispecific, with a switch to fortnightly dosing after response","route":"/key-papers/paper-magnetismm-3-elranatamab-natmed-2023/","year":2023,"journal":"Nature Medicine","paperType":"translational","tldr":"Elranatamab produced responses in 61% of heavily pretreated myeloma patients and showed that dosing can be thinned to every two weeks once patients respond.","via":[{"id":"elranatamab","kind":"drug","name":"Elranatamab","route":"/drugs/elranatamab/"},{"id":"talquetamab","kind":"drug","name":"Talquetamab","route":"/drugs/talquetamab/"},{"id":"teclistamab","kind":"drug","name":"Teclistamab","route":"/drugs/teclistamab/"},{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"}]},{"id":"paper-harding-lancet-oncol","kind":"paper","name":"Zanidatamab for HER2-amplified, unresectable, locally advanced or metastatic biliary tract cancer (HERIZON-BTC-01): a multicentre, single-arm, phase 2b study","route":"/key-papers/paper-harding-lancet-oncol/","year":2023,"journal":"The Lancet Oncology","paperType":"observational","tldr":"Paper cited by one cancer page, indexed on Europe PMC as PubMed record 37276871 and published in The Lancet Oncology; the citing page links this DOI, which is how the record was matched.","via":[{"id":"zanidatamab","kind":"drug","name":"Zanidatamab","route":"/drugs/zanidatamab/"}]},{"id":"paper-majestec-1-teclistamab-nejm-2022","kind":"paper","name":"MajesTEC-1: teclistamab, an off-the-shelf BCMA bispecific antibody, in heavily pretreated myeloma","route":"/key-papers/paper-majestec-1-teclistamab-nejm-2022/","year":2022,"journal":"New England Journal of Medicine","paperType":"translational","tldr":"A ready-made antibody that pulls T cells onto myeloma cells produced responses in 63% of patients after a median of five prior therapies, without the wait for cell manufacturing.","via":[{"id":"elranatamab","kind":"drug","name":"Elranatamab","route":"/drugs/elranatamab/"},{"id":"talquetamab","kind":"drug","name":"Talquetamab","route":"/drugs/talquetamab/"},{"id":"teclistamab","kind":"drug","name":"Teclistamab","route":"/drugs/teclistamab/"},{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"}]},{"id":"paper-monumental-1-talquetamab-nejm-2022","kind":"paper","name":"MonumenTAL-1: talquetamab, a GPRC5D-directed bispecific antibody for relapsed multiple myeloma","route":"/key-papers/paper-monumental-1-talquetamab-nejm-2022/","year":2022,"journal":"New England Journal of Medicine","paperType":"observational","tldr":"Talquetamab, an antibody that pulls T cells onto a new myeloma target called GPRC5D, produced responses in about seven in ten heavily pretreated patients, including those already treated with BCMA-directed therapy.","via":[{"id":"mcla-129","kind":"drug","name":"MCLA-129","route":"/drugs/mcla-129/"},{"id":"talquetamab","kind":"drug","name":"Talquetamab","route":"/drugs/talquetamab/"}]},{"id":"paper-aall1331-brown-jama-2021","kind":"paper","name":"AALL1331: blinatumomab versus chemotherapy consolidation in high- and intermediate-risk first relapse of childhood B-ALL","route":"/key-papers/paper-aall1331-brown-jama-2021/","year":2021,"journal":"JAMA","paperType":"rct","tldr":"Children whose leukaemia relapsed did better when two cycles of the antibody blinatumomab replaced intensive chemotherapy before transplant: more were alive two years later and far fewer had serious infections, although the disease-free survival difference did not reach the trial's statistical threshold.","via":[{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"}]},{"id":"paper-ino-vate-inotuzumab-all-nejm-2016","kind":"paper","name":"INO-VATE: inotuzumab ozogamicin, a CD22 antibody-drug conjugate, versus chemotherapy for relapsed adult B-cell ALL","route":"/key-papers/paper-ino-vate-inotuzumab-all-nejm-2016/","year":2016,"journal":"New England Journal of Medicine","paperType":"rct","tldr":"A CD22 antibody-drug conjugate produced complete remission in 81% of adults with relapsed ALL compared with 29% on chemotherapy, at the cost of liver toxicity in about one in ten.","via":[{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"}]}],"eras":[{"roadmap":{"id":"cell-therapy-roadmap","kind":"roadmap","name":"Cell therapy roadmap: CD19 CAR-T → solid tumours → in vivo CAR","route":"/roadmaps/cell-therapy-roadmap/"},"era":"2017-2022","title":"CD19 and BCMA CAR-T approved","status":"historic","step":2,"route":"/roadmaps/cell-therapy-roadmap/#story-step-1","refs":[{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"},{"id":"teclistamab","kind":"drug","name":"Teclistamab","route":"/drugs/teclistamab/"}]},{"roadmap":{"id":"gallbladder-cancer-roadmap","kind":"roadmap","name":"Gallbladder cancer roadmap: from a chance finding at gallstone surgery to a disease with its own trials","route":"/roadmaps/gallbladder-cancer-roadmap/"},"era":"2017-2025","title":"HER2: the first target where gallbladder cancer leads","status":"current","step":8,"route":"/roadmaps/gallbladder-cancer-roadmap/#story-step-7","refs":[{"id":"zanidatamab","kind":"drug","name":"Zanidatamab","route":"/drugs/zanidatamab/"}]},{"roadmap":{"id":"immunotherapy-roadmap","kind":"roadmap","name":"Immunotherapy roadmap: Coley's toxins → checkpoint inhibitors → engineered immunity","route":"/roadmaps/immunotherapy-roadmap/"},"era":"2018-2024","title":"Earlier lines and combinations","status":"current","step":3,"route":"/roadmaps/immunotherapy-roadmap/#story-step-2","refs":[{"id":"tarlatamab","kind":"drug","name":"Tarlatamab","route":"/drugs/tarlatamab/"}]},{"roadmap":{"id":"immunotherapy-roadmap","kind":"roadmap","name":"Immunotherapy roadmap: Coley's toxins → checkpoint inhibitors → engineered immunity","route":"/roadmaps/immunotherapy-roadmap/"},"era":"2024-2027","title":"Engineered immunity arrives","status":"emerging","step":4,"route":"/roadmaps/immunotherapy-roadmap/#story-step-3","refs":[{"id":"ivonescimab","kind":"drug","name":"Ivonescimab","route":"/drugs/ivonescimab/"}]},{"roadmap":{"id":"paediatric-oncology-roadmap","kind":"roadmap","name":"Paediatric oncology roadmap: cooperative-group cures → engineered immunity → drugs developed for children first","route":"/roadmaps/paediatric-oncology-roadmap/"},"era":"2014-2026","title":"Engineered immunity, children first","status":"current","step":3,"route":"/roadmaps/paediatric-oncology-roadmap/#story-step-2","refs":[{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"}]},{"roadmap":{"id":"targeted-therapy-roadmap","kind":"roadmap","name":"Targeted therapy roadmap: imatinib → designed for resistance → the undruggable drivers fall","route":"/roadmaps/targeted-therapy-roadmap/"},"era":"2021-2026","title":"The undruggable drivers fall","status":"current","step":4,"route":"/roadmaps/targeted-therapy-roadmap/#story-step-3","refs":[{"id":"amivantamab","kind":"drug","name":"Amivantamab","route":"/drugs/amivantamab/"}]}],"ideas":[{"id":"idea-transplant-free-ph-all","kind":"idea","name":"Transplant-free Ph-positive ALL for MRD-negative adults","route":"/ideas/idea-transplant-free-ph-all/","maturity":"being-tested-at-scale","tldr":"If a pill plus immunotherapy makes the leukaemia undetectable, can most adults safely skip a bone-marrow transplant?","via":[{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"}]},{"id":"idea-bio1-upfront-bypass-combination","kind":"idea","name":"Add the second drug on day one when the escape route is predictable","route":"/ideas/idea-bio1-upfront-bypass-combination/","maturity":"early-clinical","tldr":"If most tumours escape a drug by the same back-up route, blocking that route from the start may prevent resistance rather than chase it.","via":[{"id":"amivantamab","kind":"drug","name":"Amivantamab","route":"/drugs/amivantamab/"}]},{"id":"idea-biomarker-quadruplet-gastric","kind":"idea","name":"Biomarker-directed first-line quadruplets in gastric cancer","route":"/ideas/idea-biomarker-quadruplet-gastric/","maturity":"early-clinical","tldr":"Stomach cancer now has three add-on biomarkers (HER2, PD-L1, Claudin 18.2) that often overlap. Test whether combining two add-ons beats picking one.","via":[{"id":"zanidatamab","kind":"drug","name":"Zanidatamab","route":"/drugs/zanidatamab/"}]},{"id":"idea-ctdna-guided-dlbcl-frontline","kind":"idea","name":"ctDNA-guided escalation and de-escalation in frontline DLBCL","route":"/ideas/idea-ctdna-guided-dlbcl-frontline/","maturity":"early-clinical","tldr":"Use an ultra-sensitive blood test after two cycles to decide who needs more than R-CHOP and who can stop early.","via":[{"id":"epcoritamab","kind":"drug","name":"Epcoritamab","route":"/drugs/epcoritamab/"}]},{"id":"idea-menin-infant-all","kind":"idea","name":"Menin inhibitors for infant KMT2A-rearranged ALL","route":"/ideas/idea-menin-infant-all/","maturity":"early-clinical","tldr":"Infant leukaemia is driven almost entirely by KMT2A fusions, which menin inhibitors were built to attack. Add them to the new blinatumomab-containing backbone.","via":[{"id":"blinatumomab","kind":"drug","name":"Blinatumomab","route":"/drugs/blinatumomab/"}]},{"id":"idea-gbc-reflex-her2-testing-advanced-biliary","kind":"idea","name":"Reflex HER2 testing of every advanced gallbladder and extrahepatic biliary cancer","route":"/ideas/idea-gbc-reflex-her2-testing-advanced-biliary/","maturity":"early-clinical","tldr":"Between one in eleven and one in five gallbladder cancers is HER2-positive and two HER2 drugs are now approved, but testing still happens only when someone asks. Making it automatic on every advanced biliary diagnosis, on resection tissue where it exists, would find the patients the trials were built for.","via":[{"id":"zanidatamab","kind":"drug","name":"Zanidatamab","route":"/drugs/zanidatamab/"}]},{"id":"idea-bio2-intracavitary-immunotherapy","kind":"idea","name":"Treat the body cavity, not the bloodstream, for surface spread","route":"/ideas/idea-bio2-intracavitary-immunotherapy/","maturity":"early-clinical","tldr":"Intracavitary immunotherapy targets cancer that coats the lining of the abdomen or chest, which drugs given by drip barely reach. Delivering it straight into the cavity gives far higher local doses.","via":[{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]},{"id":"idea-bio2-tumour-anchored-tgfbeta-trap","kind":"idea","name":"Anchor a TGF-beta trap in the tumour stroma so it cannot act everywhere","route":"/ideas/idea-bio2-tumour-anchored-tgfbeta-trap/","maturity":"preclinical-evidence","tldr":"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.","via":[{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"}]},{"id":"idea-bio1-pmhc-bispecifics-public-drivers","kind":"idea","name":"Antibodies that see mutant KRAS and p53 fragments displayed on the cell surface","route":"/ideas/idea-bio1-pmhc-bispecifics-public-drivers/","maturity":"preclinical-evidence","tldr":"Cells chop up their internal proteins and display the pieces on their surface. That means even undruggable proteins inside the cell can be attacked from outside by the immune system.","via":[{"id":"tebentafusp","kind":"drug","name":"Tebentafusp","route":"/drugs/tebentafusp/"},{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"},{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]},{"id":"idea-bio2-myeloid-engager-bispecific","kind":"idea","name":"Bispecific antibodies that engage macrophages instead of T cells","route":"/ideas/idea-bio2-myeloid-engager-bispecific/","maturity":"preclinical-evidence","tldr":"Drugs that grab T cells and drag them onto tumours work well in blood cancers. The same trick aimed at tumour-eating cells might work where T cells are absent.","via":[{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"}]},{"id":"idea-bio2-antigen-presentation-triage","kind":"idea","name":"Check whether a tumour can still show itself to the immune system","route":"/ideas/idea-bio2-antigen-presentation-triage/","maturity":"preclinical-evidence","tldr":"Some tumours have broken the machinery that displays their identity to immune cells. Those patients cannot benefit from most immunotherapy and should be routed elsewhere.","via":[{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]},{"id":"idea-efflux-agnostic","kind":"idea","name":"Efflux-agnostic therapy for mesenchymal TNBC","route":"/ideas/idea-efflux-agnostic/","maturity":"preclinical-evidence","tldr":"Some tumours pump out every drug. Use treatments the pumps cannot touch: radiation, radioligands, immune cells, and payloads designed to evade them.","via":[{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]},{"id":"idea-bio2-cxcr4-mobilise-then-kill","kind":"idea","name":"Flush dormant cells out of bone marrow, then kill them","route":"/ideas/idea-bio2-cxcr4-mobilise-then-kill/","maturity":"preclinical-evidence","tldr":"Sleeping cancer cells hide in bone marrow where drugs cannot reach them. Pushing them into the bloodstream on purpose, then treating, might clear them.","via":[{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]},{"id":"idea-sclc-subtype-directed","kind":"idea","name":"Subtype-directed therapy for SCLC (ASCL1 / NEUROD1 / POU2F3 / inflamed)","route":"/ideas/idea-sclc-subtype-directed/","maturity":"preclinical-evidence","tldr":"Small-cell lung cancer is at least four diseases under the microscope's uniform appearance. Treat each by its transcription-factor subtype.","via":[{"id":"tarlatamab","kind":"drug","name":"Tarlatamab","route":"/drugs/tarlatamab/"}]},{"id":"idea-prame-tcr-beyond-a02","kind":"idea","name":"TCR therapeutics for non-HLA-A*02 patients","route":"/ideas/idea-prame-tcr-beyond-a02/","maturity":"preclinical-evidence","tldr":"Today's T-cell-receptor drugs only work for people with one tissue type. Building versions for the other common types would roughly double who can be treated.","via":[{"id":"brenetafusp","kind":"drug","name":"Brenetafusp","route":"/drugs/brenetafusp/"},{"id":"tebentafusp","kind":"drug","name":"Tebentafusp","route":"/drugs/tebentafusp/"},{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]},{"id":"idea-bio2-transferrin-shuttle-adc","kind":"idea","name":"Use the brain's own transport door to carry antibody drugs across","route":"/ideas/idea-bio2-transferrin-shuttle-adc/","maturity":"preclinical-evidence","tldr":"The brain imports iron through the transferrin receptor. Antibody shuttle domains that bind that receptor raise brain exposure roughly ten to fifty-fold in primates and are already used in clinical Alzheimer's antibodies; the same engineering could carry antibody-drug conjugates or T-cell engagers to brain metastases.","via":[{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"},{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]},{"id":"idea-bio1-molecular-progression-add-on","kind":"idea","name":"Add a drug when the blood test turns, without stopping the one that works","route":"/ideas/idea-bio1-molecular-progression-add-on/","maturity":"speculative","tldr":"When a resistance mutation first appears in the blood, the current drug is often still controlling most of the tumour. Adding a second drug rather than swapping may keep both under control.","via":[{"id":"amivantamab","kind":"drug","name":"Amivantamab","route":"/drugs/amivantamab/"}]},{"id":"idea-fund-academic-adc-bispecific-platform","kind":"idea","name":"An open engineering platform for academic ADCs and bispecifics","route":"/ideas/idea-fund-academic-adc-bispecific-platform/","maturity":"speculative","tldr":"Academic labs find new tumour targets but cannot turn an antibody into an antibody-drug conjugate or a bispecific without licensed linker and payload technology. A shared platform would provide that at no cost for first trials.","via":[{"id":"bispecific-antibody","kind":"technology","name":"Bispecific antibodies","route":"/technologies/bispecific-antibody/"},{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]},{"id":"idea-bio1-cfrna-plasticity-tracking","kind":"idea","name":"Detect tumours changing cell type from RNA in the blood","route":"/ideas/idea-bio1-cfrna-plasticity-tracking/","maturity":"speculative","tldr":"Some cancers escape treatment by changing into a different kind of cell that the drug no longer affects. Tumour RNA in blood could show this shift months before a biopsy would.","via":[{"id":"tarlatamab","kind":"drug","name":"Tarlatamab","route":"/drugs/tarlatamab/"}]},{"id":"idea-bispecific-vs-car-t-second-line","kind":"idea","name":"Head-to-head bispecific vs CAR-T in second-line LBCL","route":"/ideas/idea-bispecific-vs-car-t-second-line/","maturity":"speculative","tldr":"Nobody has directly compared an off-the-shelf bispecific with CAR-T in the same patients; a trial would settle where each belongs.","via":[{"id":"epcoritamab","kind":"drug","name":"Epcoritamab","route":"/drugs/epcoritamab/"},{"id":"glofitamab","kind":"drug","name":"Glofitamab","route":"/drugs/glofitamab/"},{"id":"t-cell-engager","kind":"technology","name":"T-cell engagers (bispecific)","route":"/technologies/t-cell-engager/"}]}],"manufacturing":{"sites":[{"id":"abzena-sanford","name":"Abzena Sanford","operator":"Abzena","operatorRoute":"/companies/abzena/","ownership":"cdmo","city":"Sanford, North 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section is read from existing corpus records and names them (from, via, exemplars, refs); a section with nothing behind it is empty. Medicines of a format are the open drug engine's (/pipeline/engine/); technologies are listed in src/lib/modular-formats.ts. CC BY-NC 4.0, attribute Data from OnCo (onco.cc). Not medical advice."}