Open evaluation: can you get a good answer here?
One hundred questions a patient, carer, clinician, or analyst might ask, each with a grounded expected answer and a rubric of must-mention points. The same rubric scores OnCo, a search engine, or an AI assistant. Scores are published here in public, every run.
Leaderboard
| System | Date | Mean | Factual | Procedural | Reasoning | Method |
|---|---|---|---|---|---|---|
| OnCo (search-retrieval proxy, top 8 entities) | 2026-09-08 | 84% | 86% | 62% | 85% | For each question: MiniSearch retrieval over the site index; rubric coverage of tldr+summary of the top entities. 1 point per rubric item met, normalised to 0-1. |
OnCo's own run is a deliberately hard retrieval proxy: it scores only the TL;DR and summary text of the top eight search hits, with no reasoning layer. A human reading the linked pages would score higher; that gap is part of what the benchmark measures.
Score another system
1. Download the questions: benchmark.json (also in the repo at src/data/benchmark.ts).
2. Ask each question to the system under test, verbatim, and save the answers as { "<question id>": "answer text", … }.
3. Run npm run bench:score -- answers.json "System name" and open a pull request with the generated file in public/eval/. The rubric is public; the only judgement is substring matching, so scores are reproducible and disputable.
The questions
| # | Question | Category | Level | Grounded in | OnCo |
|---|---|---|---|---|---|
| tnbc-01 | Which TROP2 ADCs are approved for first-line metastatic triple-negative breast cancer? Expected answer and rubricSacituzumab govitecan (Trodelvy), as monotherapy for PD-1-ineligible patients (ASCENT-03) and with pembrolizumab for PD-L1 CPS ≥10 disease (ASCENT-04), and datopotamab deruxtecan (Datroway) for PD-1/PD-L1-ineligible patients (TROPION-Breast02), both approved in 2026.
| Factual | 1 | Sacituzumab govitecanDatopotamab deruxtecanASCENT-03ASCENT-04 / KEYNOTE-D19TROPION-Breast02 | 4/4 |
| tnbc-02 | What does 'triple-negative' mean in breast cancer? Expected answer and rubricThe tumour lacks the three receptors other breast cancers can be treated through: oestrogen receptor, progesterone receptor, and HER2 (IHC 0-1+ or 2+/ISH-negative).
| Factual | 1 | Triple-negative breast cancer (TNBC)HER2Estrogen receptor (ERα) | 4/4 |
| tnbc-03 | What is the standard treatment for stage II-III triple-negative breast cancer today? Expected answer and rubricNeoadjuvant pembrolizumab with carboplatin/paclitaxel then anthracycline chemotherapy, surgery, and adjuvant pembrolizumab (KEYNOTE-522); adjuvant olaparib for germline BRCA carriers with residual disease (OlympiA); capecitabine for residual disease without BRCA.
| Factual | 2 | Triple-negative breast cancer (TNBC)KEYNOTE-522PembrolizumabOlaparibOlympiA | 5/5 |
| tnbc-04 | Did KEYNOTE-522 improve overall survival? Expected answer and rubricYes. Seven-year overall survival was 85.1% vs 77.2% (ASCO 2026 update); five-year EFS 81.2% vs 72.2%; pCR 64.8% vs 51.2%.
| Factual | 2 | KEYNOTE-522 | 4/4 |
| tnbc-05 | What is pathologic complete response and why does it matter in TNBC? Expected answer and rubricpCR means no invasive cancer is left in the breast and lymph nodes when the surgeon removes the tissue after pre-surgery treatment. In TNBC patients with pCR have around 90% five-year event-free survival, and trials now test giving less treatment after pCR.
| Factual | 1 | Pathologic complete response (pCR)OptimICE-pCR (A012103)Triple-negative breast cancer (TNBC) | 4/4 |
| tnbc-06 | Which trial showed the first overall survival benefit for a first-line ADC in triple-negative breast cancer? Expected answer and rubricTROPION-Breast02: datopotamab deruxtecan vs chemotherapy in first-line PD-1/PD-L1-ineligible metastatic TNBC, OS 23.7 vs 18.7 months.
| Factual | 2 | TROPION-Breast02Datopotamab deruxtecan | 4/4 |
| tnbc-07 | What is the first bispecific ADC to succeed in a phase 3 trial, and in which cancer? Expected answer and rubricIzalontamab brengitecan (iza-bren, BL-B01D1), an EGFR×HER3 bispecific ADC from SystImmune/BMS, met PFS and OS in previously treated TNBC (BL-B01D1-307, February 2026) and also in oesophageal squamous cell carcinoma.
| Factual | 2 | Izalontamab brengitecanBL-B01D1-307Bispecific ADC | 5/5 |
| tnbc-08 | Why does trastuzumab deruxtecan work in 'HER2-low' breast cancers that older HER2 drugs ignored? Expected answer and rubricIts cleavable linker releases a membrane-permeable topoisomerase-I payload (DXd) at high DAR, so a small amount of HER2 is enough to deliver drug and the payload diffuses to kill neighbouring cells (bystander effect); HER2-low is a delivery address, not a driver. DESTINY-Breast04 and -06 proved it.
| Reasoning | 2 | Trastuzumab deruxtecanHER2-low and HER2-ultralowBystander effect (ADC)DESTINY-Breast04 | 4/4 |
| tnbc-09 | Should a patient get a second ADC with the same kind of payload straight after the first one fails? Expected answer and rubricCaution: retrospective series (SATEEN, BRE-354) show shorter PFS for a second TOP1-payload ADC given back-to-back; resistance is at the payload level (SLFN11 loss, TOP1 mutations, ABCG2 efflux). Some data suggest interposing chemotherapy or switching payload class; prospective trials (TRADE-DXd) are pending.
| Reasoning | 3 | Caution: TOP1 ADC immediately after TOP1 ADCADC sequencingPayload-class switching as the rule for ADC sequencing | 4/4 |
| tnbc-10 | What questions should someone newly diagnosed with triple-negative breast cancer ask before surgery? Expected answer and rubricWhether chemo-immunotherapy before surgery (KEYNOTE-522) is planned and why; germline BRCA testing; PD-L1 and HER2-low status; TIL score; clinical trial options; fertility preservation; breast-conserving versus mastectomy and sentinel node approach; what response (pCR/RCB) will mean for treatment afterwards.
| Procedural | 2 | Triple-negative breast cancer (TNBC)KEYNOTE-522Germline (hereditary) testingTumour-infiltrating lymphocytes (TILs)Pathologic complete response (pCR)Residual cancer burden (RCB) | 4/5 |
| tnbc-11 | Does the TROP2 level measured on a biopsy tell you whether Trodelvy will work? Expected answer and rubricNot reliably. ASCENT showed benefit regardless of TROP2 IHC, so no companion diagnostic is required; expression is heterogeneous and archival tissue may not reflect current status. TROP2 PET tracers are being developed to map expression across the body and over time.
| Reasoning | 3 | TROP2ASCENTTROP2 PETTROP2 PET to choose and sequence TROP2 ADCs | 3/4 |
| breast-12 | What was the first PROTAC ever approved and for what? Expected answer and rubricVepdegestrant (Veppanu, Arvinas/Pfizer), an oral oestrogen receptor degrader, approved in 2026 for ESR1-mutated ER+/HER2- advanced breast cancer (VERITAC-2).
| Factual | 2 | VepdegestrantPROTACs & molecular glues (targeted protein degradation)VERITAC-2 | 4/4 |
| breast-13 | Which CDK4/6 inhibitors are approved after surgery for early hormone-positive breast cancer, and on what trials? Expected answer and rubricAbemaciclib (monarchE, high-risk node-positive) and ribociclib (NATALEE, stage II-III including node-negative).
| Factual | 2 | AbemaciclibRibociclibmonarchENATALEE | 4/4 |
| breast-14 | What can a 21-gene test tell a woman with early hormone-positive breast cancer? Expected answer and rubricOncotype DX gives a recurrence score; TAILORx showed women with a score of 25 or below (over 50) get no benefit from chemotherapy and can safely skip it; RxPONDER extended this to 1-3 positive nodes in postmenopausal women.
| Factual | 1 | Oncotype DXHR-positive / HER2-negative breast cancer | 4/4 |
| breast-15 | In what setting did T-DXd move into early-stage HER2-positive breast cancer in 2026? Expected answer and rubricNeoadjuvant (DESTINY-Breast11, T-DXd followed by THP, pCR 67.3% vs 56.3%) and post-neoadjuvant residual disease (DESTINY-Breast05, beating T-DM1), both approved Q2 2026.
| Factual | 2 | Trastuzumab deruxtecanDESTINY-Breast11HER2-positive breast cancer | 4/4 |
| lung-16 | Which biomarkers must be tested at diagnosis of advanced non-small-cell lung cancer? Expected answer and rubricEGFR, ALK, ROS1, BRAF V600E, MET exon 14/amplification, RET, NTRK, KRAS G12C, HER2 mutations, and PD-L1 TPS.
| Factual | 2 | Non-small-cell lung cancerEGFRALKKRASPD-L1 | 5/5 |
| lung-17 | What is the standard adjuvant treatment after resection of EGFR-mutant lung cancer and what did it do to survival? Expected answer and rubricThree years of osimertinib (ADAURA): DFS HR 0.20 in stage II-IIIA and OS HR 0.49, five-year OS 88% vs 78%.
| Factual | 2 | OsimertinibADAURA | 1/4 |
| lung-18 | Which regimen beat osimertinib in first-line EGFR-mutant lung cancer? Expected answer and rubricAmivantamab plus lazertinib (MARIPOSA): PFS 23.7 vs 16.6 months and an OS benefit of more than a year.
| Factual | 2 | AmivantamabMARIPOSA | 4/4 |
| lung-19 | What is the first T-cell engager to improve survival in a common solid tumour? Expected answer and rubricTarlatamab (Imdelltra), DLL3×CD3, in second-line small-cell lung cancer: OS 13.6 vs 8.3 months in DeLLphi-304.
| Factual | 2 | TarlatamabDeLLphi-304Small-cell lung cancer | 4/4 |
| lung-20 | Why did the first KRAS inhibitors need an EGFR antibody added in colorectal cancer but not in lung cancer? Expected answer and rubricColorectal epithelium has strong EGFR-driven adaptive feedback that reactivates MAPK within hours of KRAS G12C inhibition, so monotherapy response is ~10%; adding cetuximab or panitumumab (CodeBreaK 300, KRYSTAL-1) raises it to 30-45%.
| Reasoning | 3 | KRAS G12C inhibitor + anti-EGFR antibody (colorectal)CodeBreaK 300SotorasibAdagrasib | 3/4 |
| lung-21 | Which drug beat pembrolizumab head to head on progression-free survival in lung cancer? Expected answer and rubricIvonescimab, a PD-1×VEGF bispecific (Akeso/Summit): PFS 11.1 vs 5.8 months in PD-L1-positive first-line NSCLC (HARMONi-2, China).
| Factual | 2 | IvonescimabVEGF / VEGFRPD-1 | 4/4 |
| lung-22 | What is the longest progression-free survival ever reported for a targeted pill in metastatic lung cancer? Expected answer and rubricLorlatinib in ALK-positive NSCLC (CROWN): five-year PFS about 60% versus 8% for crizotinib.
| Factual | 2 | LorlatinibALK | 4/4 |
| prostate-23 | What is theranostics and what is the best-known example? Expected answer and rubricUsing the same targeting molecule for a diagnostic scan and a treatment: PSMA PET shows where prostate cancer is, and 177Lu-PSMA-617 (Pluvicto) delivers radiation to the same target.
| Factual | 1 | TheranosticsPSMA PETLutetium-177 vipivotide tetraxetanPSMA | 4/4 |
| prostate-24 | What did the VISION trial show? Expected answer and rubric177Lu-PSMA-617 plus standard care improved overall survival (15.3 vs 11.3 months, HR 0.62) in PSMA-positive metastatic castration-resistant prostate cancer after ARPI and taxane.
| Factual | 2 | VISIONLutetium-177 vipivotide tetraxetan | 3/4 |
| prostate-25 | Why might an alpha-emitting PSMA drug work after lutetium PSMA has stopped working? Expected answer and rubricAlpha particles (actinium-225) deposit far more energy over 50-100 µm, causing clustered double-strand breaks independent of oxygen and cell cycle, so beta-resistant, hypoxic, or small-volume disease can still be killed; retrospective series show PSA responses in about half after 177Lu failure. Supply of Ac-225 and salivary toxicity are the limits.
| Reasoning | 3 | Beta radioligand → alpha radioligandTargeted alpha therapyActinium-225 PSMA agentsAlpha vs beta emitters | 4/4 |
| prostate-26 | What is the first FDA-cleared AI pathology tool that predicts treatment benefit, and in which cancer? Expected answer and rubricArteraAI Prostate (de novo authorisation, August 2025) predicts prognosis and benefit from short-term androgen deprivation with radiotherapy in localised prostate cancer.
| Factual | 2 | ArteraAI ProstateDigital pathology & AI | 4/4 |
| bladder-27 | What regimen replaced platinum chemotherapy as first-line treatment for advanced bladder cancer, and how big was the effect? Expected answer and rubricEnfortumab vedotin plus pembrolizumab (EV-302): OS 31.5 vs 16.1 months, HR 0.47.
| Factual | 2 | Enfortumab vedotinEV-302 / KEYNOTE-A39Bladder & urothelial cancer | 4/4 |
| bladder-28 | What was the first cancer drug approved on the basis of a blood test for leftover disease? Expected answer and rubricAtezolizumab for ctDNA-positive muscle-invasive bladder cancer after cystectomy (IMvigor011, using Signatera), approved Q2 2026; DFS HR 0.64, OS HR 0.59.
| Factual | 2 | AtezolizumabIMvigor011SignateraMRD / molecular residual disease testing | 4/4 |
| gi-29 | Which cancer gene was called undruggable for forty years and what changed? Expected answer and rubricKRAS. In 2013 a covalent pocket was found in the G12C mutant; sotorasib (2021) and adagrasib followed, and pan-RAS(ON) inhibitors such as daraxonrasib are now in phase 3 for pancreatic cancer.
| Factual | 2 | KRASKRAS & RAS inhibitorsSotorasibDaraxonrasibKRAS roadmap: undruggable → G12C → pan-RAS | 4/4 |
| gi-30 | What is daraxonrasib and where does it stand? Expected answer and rubricRevolution Medicines' pan-RAS(ON) tri-complex inhibitor; phase 3 RASolute 302 in second-line pancreatic cancer (reported OS benefit, HR 0.40 per the pancreatic spike), with first-line and NSCLC phase 3 trials ongoing.
| Factual | 2 | DaraxonrasibRevolution MedicinesPancreatic ductal adenocarcinoma | 4/4 |
| gi-31 | What did the dostarlimab rectal cancer study show? Expected answer and rubricIn mismatch-repair-deficient locally advanced rectal cancer, dostarlimab alone produced a complete clinical response in 100% of patients, sustained in more than 40 patients by 2025, allowing surgery and radiation to be avoided.
| Factual | 2 | DostarlimabMicrosatellite instability (MSI-H) / mismatch repair deficiency (dMMR)Colorectal cancer | 4/4 |
| gi-32 | Can a blood test decide who needs chemotherapy after colon cancer surgery? Expected answer and rubricYes in stage II: the DYNAMIC trial used ctDNA to guide adjuvant chemotherapy, halving its use (15% vs 28%) with non-inferior recurrence-free survival (93.5% vs 92.4% at two years).
| Reasoning | 2 | DYNAMICMRD / molecular residual disease testingCirculating tumour DNA (ctDNA) | 4/4 |
| gi-33 | What was the first approval in nearly thirty years specific to locally advanced pancreatic cancer? Expected answer and rubricOptune Pax (tumour treating fields) with gemcitabine/nab-paclitaxel, approved Q1 2026 on PANOVA-3.
| Factual | 2 | Optune / Optune Pax (TTFields)Tumour treating fields (TTFields)Pancreatic ductal adenocarcinoma | 4/4 |
| gi-34 | Which new target has an approved antibody, an approved CAR-T in China, and ADCs in phase 3 for gastric cancer? Expected answer and rubricClaudin 18.2: zolbetuximab (Vyloy), satricabtagene autoleucel (satri-cel, CARsgen, China), and ADCs such as CMG901/AZD0901.
| Factual | 2 | Claudin 18.2Satricabtagene autoleucelSonesitatug vedotinGastric & gastro-oesophageal junction cancer | 4/4 |
| gi-35 | Why is pancreatic cancer so hard to treat with immunotherapy? Expected answer and rubricIt is immunologically cold: dense desmoplastic stroma blocks drug and T-cell entry, low mutational burden gives few neoantigens, and an immunosuppressive myeloid microenvironment. Vaccines (autogene cevumeran) and RAS inhibitors that may increase antigen presentation are the main hopes.
| Reasoning | 3 | Pancreatic ductal adenocarcinomaHot vs cold tumoursAutogene cevumeranFAP | 1/4 |
| io-36 | What fraction of advanced melanoma patients on nivolumab plus ipilimumab are alive at ten years? Expected answer and rubricAbout 43% overall survival (CheckMate 067), with melanoma-specific survival around 52%.
| Factual | 2 | CheckMate 067NivolumabIpilimumab | 4/4 |
| io-37 | What was the first personalised cancer vaccine to win a phase 3 trial? Expected answer and rubricIntismeran autogene (V940/mRNA-4157, Moderna/Merck) with pembrolizumab in resected stage IIB-IV melanoma: INTerpath-001 met recurrence-free and distant-metastasis-free survival, announced 19 August 2026.
| Factual | 2 | Intismeran autogeneINTerpath-001 (V940-001)Personalised neoantigen (mRNA) vaccines | 4/4 |
| io-38 | How is a personalised mRNA cancer vaccine made? Expected answer and rubricThe tumour and normal DNA are sequenced, software predicts up to 34 neoantigens unique to the tumour, a patient-specific mRNA encoding them is manufactured in lipid nanoparticles over about six weeks, and it is given with a PD-1 blocker.
| Factual | 2 | Personalised neoantigen (mRNA) vaccinesNeoantigenIntismeran autogene | 4/5 |
| io-39 | What is the first approved TIL therapy and how well does it work? Expected answer and rubricLifileucel (Amtagvi, Iovance), approved 2024 for anti-PD-1-refractory melanoma: response rate about 31%, with roughly a third of responders still responding at five years.
| Factual | 2 | LifileucelTIL therapy | 4/4 |
| io-40 | What are the main side effects of checkpoint inhibitors and how are they handled? Expected answer and rubricImmune-related adverse events such as colitis, thyroid problems, rash, hepatitis, and pneumonitis, most common with CTLA-4 plus PD-1 combinations; treated with steroids and sometimes other immunosuppressants, some endocrine effects are permanent.
| Procedural | 2 | Immune-related adverse events (irAEs)Immune checkpoint inhibitors | 3/4 |
| io-41 | Why did TIGIT-blocking antibodies fail despite promising early data? Expected answer and rubricPhase 3 trials (SKYSCRAPER-01, -02 and others) did not add benefit to PD-(L)1 blockade in NSCLC and SCLC; phase 2 signals did not reproduce, and the roles of Fc-effector function and patient selection remain debated.
| Reasoning | 3 | TIGITCaution: TIGIT + PD-(L)1 blockade | 4/4 |
| io-42 | What does 'hot' versus 'cold' tumour mean? Expected answer and rubricHot tumours are full of immune cells and tend to respond to immunotherapy; cold tumours have kept the immune system out (immune-excluded or immune-desert), such as pancreatic, prostate, glioblastoma, and most HR+ breast cancers.
| Factual | 1 | Hot vs cold tumours | 4/4 |
| heme-43 | What is CAR-T and which cancers is it approved for? Expected answer and rubricA patient's T cells are engineered with a synthetic receptor, multiplied, and returned. Approved CD19 products treat B-cell lymphomas and leukaemias; BCMA products treat multiple myeloma; the first solid-tumour approval (Claudin 18.2, gastric) is in China.
| Factual | 1 | CAR-T cell therapyCD19BCMA | 4/4 |
| heme-44 | What were the first checkpoint inhibitor and the first ADC ever approved? Expected answer and rubricIpilimumab (2011) was the first checkpoint inhibitor; gemtuzumab ozogamicin (Mylotarg, 2000) was the first ADC, withdrawn in 2010 and re-approved in 2017.
| Factual | 2 | IpilimumabGemtuzumab ozogamicinADC roadmap: from Mylotarg to bispecific and dual-payload ADCs | 2/4 |
| heme-45 | What is the first menin inhibitor and who is it for? Expected answer and rubricRevumenib (Revuforj, Syndax), approved 2024 for relapsed KMT2A-rearranged acute leukaemia and 2025 for NPM1-mutant AML.
| Factual | 2 | RevumenibMenin | 4/4 |
| heme-46 | How did CAR-T change second-line treatment of large B-cell lymphoma? Expected answer and rubricZUMA-7 showed axicabtagene ciloleucel beats standard chemotherapy plus transplant for early relapse; CAR-T is now second-line standard, curing around 40% of relapsed patients.
| Factual | 2 | Axicabtagene ciloleucelDiffuse large B-cell lymphoma | 4/4 |
| heme-47 | Why does venetoclax work in leukaemia? Expected answer and rubricIt blocks BCL-2, the protein that stops leukaemia cells from self-destructing, so the built-in death programme (apoptosis) can run; used in CLL (fixed duration with obinutuzumab) and AML (with azacitidine).
| Reasoning | 2 | VenetoclaxBCL-2Intrinsic apoptosis (BCL-2 family) | 2/4 |
| img-48 | What is the difference between a CT scan and a PET scan? Expected answer and rubricCT is a fast 3D X-ray showing size and shape; PET shows biology by tracking where a radioactive tracer accumulates (for example glucose uptake with FDG or a specific protein such as PSMA). PET/CT combines both.
| Factual | 1 | CT (computed tomography)PET (positron emission tomography)PET/CTFDG PET | 3/4 |
| img-49 | What does a FAPI PET scan see that an FDG scan often misses? Expected answer and rubricThe activated fibroblasts (FAP) in tumour stroma, present in more than 90% of epithelial cancers, giving high contrast in pancreatic, gastric, HCC, and peritoneal disease where FDG is weak; it is not yet approved.
| Factual | 2 | FAPI PETFAP | 4/4 |
| img-50 | What is the Galleri test and where does it stand with the FDA? Expected answer and rubricGRAIL's methylation-based multi-cancer early detection blood test for more than 50 cancers; PMA submitted January 2026 on PATHFINDER 2 and NHS-Galleri data, FDA advisory committee 23 September 2026. NHS-Galleri missed its primary stage III-IV reduction endpoint (stage IV fell ~14%).
| Factual | 2 | GalleriMulti-cancer early detection (MCED)NHS-GalleriPATHFINDER 2 | 4/4 |
| img-51 | What is positive predictive value and why does it matter for a cancer screening blood test? Expected answer and rubricThe chance that a positive result is truly cancer. With a low-prevalence disease even a highly specific test yields many false positives; Galleri's PPV in PATHFINDER 2 was around 40-60%, so roughly half of positives lead to a diagnostic workup that finds no cancer.
| Reasoning | 2 | Positive predictive value (PPV)Multi-cancer early detection (MCED)Galleri | 4/4 |
| img-52 | What is a liquid biopsy used for in cancer care today? Expected answer and rubricA blood test reading tumour DNA fragments: to genotype a tumour when tissue is scarce, to track resistance mutations (EGFR T790M, ESR1), to detect minimal residual disease after surgery, and, experimentally, to screen for cancer.
| Factual | 1 | Liquid biopsy (ctDNA)Circulating tumour DNA (ctDNA)MRD / molecular residual disease testing | 2/4 |
| img-53 | How could a TROP2 PET scan change how ADCs are used? Expected answer and rubricIt would map antigen expression across all lesions and over time, potentially selecting patients, choosing between TROP2 ADCs, and detecting antigen loss at progression to guide a switch to a different target, as PSMA PET does for Pluvicto. First-in-human tracers exist; no outcome data yet.
| Reasoning | 3 | TROP2 PETTROP2 PET to choose and sequence TROP2 ADCsTROP2 PET → TROP2 ADC selection | 4/4 |
| tech-54 | What are the three parts of an antibody-drug conjugate and what does each do? Expected answer and rubricAn antibody that finds the tumour cell, a linker that holds the payload in the blood and releases it inside the cell, and a payload, a very potent chemotherapy such as a topoisomerase-I inhibitor.
| Factual | 1 | Antibody-drug conjugate (ADC)Payload (ADC)Linker (ADC) | 4/4 |
| tech-55 | What is the bystander effect in ADCs? Expected answer and rubricA released, membrane-permeable payload diffuses out of the targeted cell and kills neighbouring cells that lack the antigen; requires a cleavable linker and permeable payload (DXd, MMAE, SN-38), explaining T-DXd's activity in HER2-low disease and T-DM1's lack of it.
| Factual | 2 | Bystander effect (ADC)Trastuzumab deruxtecanTrastuzumab emtansine | 4/4 |
| tech-56 | What is drug-to-antibody ratio and why does it matter? Expected answer and rubricThe number of payload molecules per antibody, typically 2-8. Higher DAR delivers more drug per binding event (T-DXd about 8) but increases hydrophobicity and clearance unless hydrophilic linkers are used.
| Factual | 2 | Drug-to-antibody ratio (DAR)Site-specific conjugation & linker chemistry | 4/4 |
| tech-57 | What is synthetic lethality and what is the proven clinical example? Expected answer and rubricTwo genes where losing either alone is survivable but losing both kills the cell; tumours with BRCA loss die when PARP is inhibited, the basis of olaparib and other PARP inhibitors.
| Factual | 2 | Synthetic lethalityPARP inhibitorsBRCA1 / BRCA2 (HRD) | 4/4 |
| tech-58 | How does a PROTAC differ from a conventional inhibitor? Expected answer and rubricRather than blocking a protein's active site it recruits an E3 ubiquitin ligase to tag the protein for destruction by the proteasome, removing the whole protein including scaffolding functions, catalytically and at sub-stoichiometric doses.
| Reasoning | 2 | PROTACs & molecular glues (targeted protein degradation)Vepdegestrant | 1/4 |
| tech-59 | What is in vivo CAR-T and why is it exciting? Expected answer and rubricTargeted lipid nanoparticles or viral vectors deliver CAR-encoding mRNA or DNA to T cells inside the patient, avoiding manufacturing, lymphodepletion, and wait time and allowing redosing; first-in-human data in 2025-26 show B-cell depletion. AbbVie bought Capstan for up to $2.1B.
| Factual | 2 | In vivo CAR-TCAR-T cell therapy | 4/4 |
| tech-60 | What is a bispecific ADC and why might it beat a normal one? Expected answer and rubricIts antibody binds two different tumour antigens (for example EGFR and HER3), improving avidity, internalisation, and tumour selectivity and hitting cells that express either antigen, addressing heterogeneity; iza-bren is the first with positive phase 3 data.
| Reasoning | 2 | Bispecific ADCIzalontamab brengitecan | 4/4 |
| tech-61 | What is FLASH radiotherapy? Expected answer and rubricDelivering a full radiation dose in under a second at ultra-high dose rates (>40 Gy/s), which spares normal tissue in animal models; first-in-human trials (FAST-01/02, Varian) show feasibility but the clinical benefit is unproven.
| Factual | 2 | FLASH radiotherapy | 4/4 |
| tech-62 | What is brachytherapy and where is it essential? Expected answer and rubricPlacing a radioactive source directly inside or next to the tumour; essential in cervical cancer, used in prostate (seeds or HDR), breast, skin, and eye melanoma.
| Factual | 1 | BrachytherapyCervical cancerProstate cancer | 4/4 |
| tech-63 | What is the difference between lutetium-177 and actinium-225 as therapeutic isotopes? Expected answer and rubric177Lu emits beta particles (range 1-10 mm, crossfire helps bulky heterogeneous tumours, marrow toxicity, 6.7-day half-life); 225Ac emits alpha particles (range 50-100 µm, very high energy, oxygen-independent clustered DNA damage, good for micrometastases, daughter redistribution and supply constraints).
| Factual | 2 | Alpha vs beta emittersRadioligand therapy (beta emitters)Targeted alpha therapy | 4/4 |
| tech-64 | Why is actinium-225 supply a problem? Expected answer and rubricIt is made in tiny quantities from a legacy thorium-229 stockpile or accelerators; commercial-scale expansion is a 3-5 year effort (TerraPower's Philadelphia plant aims for a 20-fold increase), so phase 3 alpha trials and future launches are gated by production.
| Reasoning | 2 | TerraPower IsotopesTargeted alpha therapyOrano MedITM Isotope Technologies Munich | 4/4 |
| tech-65 | What is tumour treating fields and which cancers is it approved for? Expected answer and rubricWearable electrode arrays delivering alternating electric fields that disrupt cell division; approved for glioblastoma, mesothelioma, NSCLC after platinum, and (2026) locally advanced pancreatic cancer.
| Factual | 1 | Tumour treating fields (TTFields)Optune / Optune Pax (TTFields) | 4/4 |
| tech-66 | What are foundation models in pathology and what have they enabled? Expected answer and rubricVery large self-supervised models trained on millions of slides (Virchow, UNI, CONCH, Prov-GigaPath) that adapt to many tasks; they predict molecular status from H&E and power FDA-cleared tools such as ArteraAI Prostate and ArteraAI Breast.
| Factual | 2 | Pathology & radiology foundation modelsDigital pathology & AIArtera | 4/4 |
| path-67 | Explain the PI3K/AKT/mTOR pathway in one paragraph and name approved drugs against it. Expected answer and rubricGrowth receptors activate PI3K (PIK3CA), which produces PIP3 and recruits AKT; PTEN reverses it; AKT releases mTORC1 to drive growth. Drugs: alpelisib and inavolisib (PI3Kα), capivasertib (AKT), everolimus (mTOR), gedatolisib (PI3K/mTOR, 2026).
| Factual | 2 | PI3K / AKT / mTORCapivasertibInavolisibGedatolisib | 5/5 |
| path-68 | Why does blocking BRAF alone cause problems that adding a MEK inhibitor fixes? Expected answer and rubricBRAF inhibitor monotherapy causes paradoxical MEK/ERK reactivation through CRAF dimers (and secondary skin cancers); blocking MEK downstream closes the escape and improves PFS and OS in melanoma.
| Reasoning | 3 | BRAF inhibitor + MEK inhibitorBRAFRAS / RAF / MEK / ERK (MAPK) | 4/4 |
| path-69 | What does the cGAS-STING pathway have to do with radiation and ADCs? Expected answer and rubricDNA damage from radiation, PARP inhibitors, and TOP1 payloads spills DNA into the cytoplasm; cGAS senses it, STING triggers type I interferon and chemokines that recruit and prime T cells, underlying immunogenic cell death, the abscopal effect, and ADC+IO synergy.
| Reasoning | 3 | cGAS–STING innate sensingAbscopal effectADC + checkpoint inhibitor | 4/4 |
| path-70 | What is oncogene addiction? Expected answer and rubricWhen a cancer depends so completely on one mutated gene that blocking it collapses the tumour, as with EGFR, ALK, BCR-ABL, KIT, and BRAF V600E; dramatic responses then acquired resistance.
| Factual | 1 | Oncogene addictionSmall-molecule kinase inhibitors | 4/4 |
| who-71 | Which hospital is ranked first in the world for oncology in 2026 and by whom? Expected answer and rubricMemorial Sloan Kettering Cancer Center, by Newsweek/Statista's World's Best Specialized Hospitals 2026; MD Anderson is second.
| Factual | 1 | Memorial Sloan Kettering Cancer CenterMD Anderson Cancer CenterNewsweek/Statista World's Best Specialized Hospitals – Oncology | 1/4 |
| who-72 | How many NCI-designated cancer centers are there and what types? Expected answer and rubric74 as of 2026: 58 Comprehensive, 8 Clinical, 8 Basic Laboratory.
| Factual | 1 | NCI-Designated Cancer CentersNational Cancer Institute (NIH) | 2/4 |
| who-73 | Where was FAPI PET invented? Expected answer and rubricHeidelberg (University Hospital, DKFZ/NCT; Haberkorn, Giesel, Kratochwil), which also ran the first-in-human 225Ac-PSMA therapy.
| Factual | 2 | Heidelberg University Hospital / NCT / DKFZFAPI PET | 1/4 |
| who-74 | Which company owns Trodelvy and how did it get it? Expected answer and rubricGilead Sciences, through its $21 billion acquisition of Immunomedics in 2020.
| Factual | 1 | Gilead Sciences (incl. Kite)Sacituzumab govitecan | 0/4 |
| who-75 | Which company develops sacituzumab tirumotecan and who holds ex-China rights? Expected answer and rubricSichuan Kelun-Biotech developed sac-TMT (approved in China 2024); Merck holds ex-Greater-China rights and runs the TroFuse phase 3 programme; FDA priority voucher July 2026.
| Factual | 2 | Sacituzumab tirumotecanSichuan Kelun-BiotechMerck & Co. (MSD) | 4/4 |
| who-76 | Where can I look up whether a specific tumour mutation has an approved drug? Expected answer and rubricOncoKB (MSK, FDA-recognised levels of evidence) and CIViC (open, community-curated); cBioPortal to see mutation frequency; ClinicalTrials.gov for trials.
| Procedural | 1 | OncoKBCIViCcBioPortal for Cancer GenomicsClinicalTrials.gov | 1/4 |
| who-77 | What is DepMap for? Expected answer and rubricThe Broad Institute's Cancer Dependency Map: genome-wide CRISPR and drug screens across more than 1,000 cancer cell lines showing which genes each line cannot live without, the source of synthetic-lethal targets like PRMT5/MTAP.
| Factual | 2 | DepMap (Cancer Dependency Map)CRISPR functional genomicsBroad Institute of MIT and Harvard | 2/4 |
| who-78 | Which cooperative group ran the trial that put nivolumab into first-line Hodgkin lymphoma? Expected answer and rubricSWOG (S1826, nivolumab-AVD vs BV-AVD), leading to FDA approval in March 2026 for ages 12 and over.
| Factual | 2 | SWOG Cancer Research NetworkNivolumabHodgkin lymphoma | 4/4 |
| proc-79 | My relative has metastatic pancreatic cancer. How do we find a clinical trial? Expected answer and rubricAsk the oncologist about trials at the treating centre and referral to an NCI-designated or major academic centre; search ClinicalTrials.gov (status recruiting, condition pancreatic cancer, filter by location); OnCo's cancer page has a live recruiting-trials list; ask about RAS inhibitor trials such as daraxonrasib.
| Procedural | 1 | Pancreatic ductal adenocarcinomaClinicalTrials.govDaraxonrasibCancer Commons | 2/4 |
| proc-80 | What should I ask before starting an ADC such as Enhertu? Expected answer and rubricHow lung inflammation (ILD) will be monitored and what symptoms to report immediately; HER2 status and how it was scored; expected nausea, hair loss, and blood counts; dosing schedule (every three weeks); how response will be assessed and when; what comes next if it stops working.
| Procedural | 2 | Trastuzumab deruxtecanInterstitial lung disease (ILD) / pneumonitisHER2-low and HER2-ultralow | 4/5 |
| proc-81 | Who should have germline genetic testing when diagnosed with cancer? Expected answer and rubricAll patients with TNBC, ovarian, pancreatic, or metastatic prostate cancer, increasingly all breast cancer, and anyone with suggestive family history; results change surgery, drug choice (PARP inhibitors), and family screening.
| Procedural | 2 | Germline (hereditary) testingBRCA1 / BRCA2 (HRD)Triple-negative breast cancer (TNBC)Ovarian cancerPancreatic ductal adenocarcinomaProstate cancer | 5/5 |
| proc-82 | How do I get a second opinion for a rare cancer? Expected answer and rubricAsk your oncologist for referral to a high-volume centre (NCI-designated in the US, ESMO-accredited or national reference centres elsewhere); nonprofits such as Cancer Commons offer free navigation; bring pathology slides, genomic reports, and imaging; telemedicine second opinions exist.
| Procedural | 1 | Cancer CommonsNCI-Designated Cancer CentersMemorial Sloan Kettering Cancer Center | 1/4 |
| proc-83 | What is exercise oncology and is there real evidence? Expected answer and rubricStructured exercise during and after treatment; the CHALLENGE trial (2025) randomised colon cancer survivors and showed improved disease-free and overall survival, the first level-1 evidence, plus less fatigue and neuropathy.
| Factual | 1 | Exercise & lifestyle oncologyColorectal cancer | 4/4 |
| proc-84 | Does scalp cooling prevent hair loss from chemotherapy? Expected answer and rubricPartly: roughly half of patients on taxane-based regimens keep at least 50% of their hair with DigniCap or Paxman; it is less effective with anthracyclines and reimbursement varies.
| Factual | 1 | Scalp cooling | 4/4 |
| proc-85 | What does a 'Phase 3' trial mean compared with Phase 1? Expected answer and rubricPhase 1 tests safety and dose in a small group; Phase 2 looks for activity; Phase 3 randomises hundreds to thousands of patients against the current standard to prove benefit, the usual basis for full approval.
| Factual | 1 | Lines of therapyAccelerated approvalStandard of care | 2/4 |
| proc-86 | What is accelerated approval and what are its risks for patients? Expected answer and rubricFDA approval based on early evidence such as tumour shrinkage or pCR, conditional on a confirmatory trial; if confirmation fails the drug is withdrawn (atezolizumab in TNBC, belantamab in 2022, sacituzumab in bladder cancer), so benefit is not yet proven when prescribed.
| Reasoning | 2 | Accelerated approvalIMpassion130Belantamab mafodotin | 4/4 |
| pipe-87 | List the generations of ADC technology and what defined each. Expected answer and rubricFirst (gemtuzumab, 2000: unstable linker, heterogeneous); second (brentuximab 2011, T-DM1 2013: humanised antibodies, potent tubulin payloads, stable linkers, no bystander for T-DM1); third (T-DXd, sacituzumab, 2019-22: high-DAR TOP1 payloads with bystander effect); fourth emerging (bispecific, dual-payload, degrader, immune-stimulating, masked, radio-ADCs).
| Factual | 3 | ADC roadmap: from Mylotarg to bispecific and dual-payload ADCsAntibody-drug conjugate (ADC) | 3/4 |
| pipe-88 | What are the three approved or near-approved TROP2 ADCs and how do their payloads differ? Expected answer and rubricSacituzumab govitecan (SN-38, DAR ~7.6, hydrolysable linker), datopotamab deruxtecan (DXd, DAR ~4, GGFG cleavable linker), and sacituzumab tirumotecan (belotecan-derived T030, DAR ~7.4, stable linker; approved in China, US decision pending).
| Factual | 3 | Sacituzumab govitecanDatopotamab deruxtecanSacituzumab tirumotecanTROP2 ADC roadmap: sacituzumab govitecan → Dato-DXd → sac-TMT → bispecifics and PET | 4/4 |
| pipe-89 | Which oncology drugs were approved in the US in July 2026? Expected answer and rubricIsatuximab subcutaneous (Sarclisa Escena), pembrolizumab SC plus enfortumab vedotin, selpercatinib label update, gedatolisib (Revtorpyk), zidesamtinib (Jideytro), and a Pluvicto label expansion.
| Factual | 3 | GedatolisibZidesamtinibLutetium-177 vipivotide tetraxetanSelpercatinibFDA Oncology Approvals (OCE) & Novel Drug Approvals | 0/4 |
| pipe-90 | What happened to tazemetostat in 2026? Expected answer and rubricIpsen withdrew Tazverik from all markets and indications on 9 March 2026 after SYMPHONY-1 showed excess secondary haematologic malignancies (5.7% vs none), and stopped its trials.
| Factual | 2 | EZH2 | 2/4 |
| pipe-91 | What is the readout calendar event on 23 September 2026? Expected answer and rubricThe FDA advisory committee (Molecular and Clinical Genetics Panel) reviewing GRAIL's Galleri multi-cancer early detection PMA.
| Factual | 1 | GalleriMulti-cancer early detection (MCED) | 1/4 |
| pipe-92 | Name three next-generation ADC concepts beyond bispecific antibodies. Expected answer and rubricDual-payload ADCs, degrader-antibody conjugates, immune-stimulating antibody conjugates, masked or conditionally active ADCs, peptide-drug conjugates, radio-ADCs.
| Factual | 2 | Dual-payload ADCDegrader-antibody conjugate (DAC)Immune-stimulating antibody conjugate (ISAC)Masked / conditionally active ADC | 1/4 |
| pipe-93 | Which company's PD-1×VEGF bispecific did BMS license, and for how much? Expected answer and rubricBioNTech's pumitamig (BNT327), in a 2025 deal valued at about $11 billion.
| Factual | 2 | BioNTechBristol Myers Squibb | 4/4 |
| pipe-94 | What is the rationale for combining an ADC with a checkpoint inhibitor, and where is it proven? Expected answer and rubricADC payloads cause immunogenic cell death and STING activation, releasing antigens and depleting suppressive myeloid cells; PD-1 blockade converts that priming into durable control. Proven in urothelial cancer (EV-302) and TNBC (ASCENT-04).
| Reasoning | 2 | ADC + checkpoint inhibitorEV-302 / KEYNOTE-A39ASCENT-04 / KEYNOTE-D19 | 3/4 |
| pipe-95 | Why do OnCo's institution rankings differ from research-output rankings? Expected answer and rubricOnCo's score sums Newsweek 2026 rank points, NCI designation points, and links in the corpus, so it measures clinical reputation plus documentation coverage, while Nature Index and SCImago count publications; both formulas are disclosed and neither measures clinical benefit.
| Reasoning | 2 | Newsweek/Statista World's Best Specialized Hospitals – OncologyNature Index – Healthcare and Cancer institutionsSCImago Institutions Rankings – Oncology | 4/4 |
| reason-96 | A patient with HER2-low, hormone-positive metastatic breast cancer has progressed on a CDK4/6 inhibitor and one chemotherapy. What are the ADC options and how would you order them? Expected answer and rubricT-DXd (DESTINY-Breast04/06) is generally first among ADCs for HER2-low disease; sacituzumab govitecan (TROPiCS-02) or Dato-DXd (TROPION-Breast01) later. Both classes carry TOP1 payloads, so cross-resistance is a concern and interposing chemotherapy is debated; consider ESR1/PIK3CA-directed options if endocrine-sensitive.
| Reasoning | 3 | Trastuzumab deruxtecanSacituzumab govitecanDatopotamab deruxtecanADC sequencingHR-positive / HER2-negative breast cancer | 4/4 |
| reason-97 | Why are mesenchymal or claudin-low triple-negative tumours hard to treat with any class of drug? Expected answer and rubricEMT programmes (ZEB1/2, SNAIL) confer stemness, apoptosis resistance, immune exclusion, and high ABC efflux transporters that pump out chemotherapy and ADC payloads (MMAE, DXd, SN-38), so efflux-independent approaches (radiation, radioligands, immune killing) are proposed.
| Reasoning | 3 | Epithelial–mesenchymal transition & drug effluxDrug efflux pumps (ABC transporters)Efflux-agnostic therapy for mesenchymal TNBCTriple-negative breast cancer (TNBC) | 4/4 |
| reason-98 | Is a positive ctDNA result after surgery a reason to start treatment right away? Expected answer and rubricIt depends on proof that intervening helps: in bladder cancer IMvigor011 showed atezolizumab improves survival in ctDNA-positive patients (now approved); in colon cancer DYNAMIC supports de-escalation for negatives; in breast cancer trials are ongoing and lead time without a proven intervention mainly causes anxiety.
| Reasoning | 3 | ctDNA MRD → adjuvant therapy decisionIMvigor011DYNAMICctDNA-triggered escalation in early TNBC | 3/4 |
| reason-99 | Why might personalised vaccines work better after surgery than in metastatic disease? Expected answer and rubricTumour burden is low so immune responses are not overwhelmed, there is time for the six-week manufacturing, immunosuppression from bulky disease is absent, and recurrence-free survival is a clean endpoint; INTerpath-001 tested exactly this adjuvant setting.
| Reasoning | 2 | Personalised neoantigen (mRNA) vaccinesINTerpath-001 (V940-001)Personalised neoantigen vaccine + PD-1 blockade | 3/4 |
| reason-100 | What single change would most improve outcomes across all cancers, and what evidence supports it? Expected answer and rubricPrevention and early detection: HPV vaccination has driven cervical cancer toward elimination in vaccinated cohorts, tobacco control and screening (mammography, colonoscopy, low-dose CT) have proven mortality benefits, and early-stage disease is where surgery cures; MCED blood tests aim to extend this but are unproven.
| Reasoning | 3 | HPV & HBV vaccinationPrevention & RiskEarly Detection & ScreeningMulti-cancer early detection (MCED)Early detection roadmap: organ screening → blood tests for many cancers | 3/4 |