HeyHippocratesBiomarkers, immunotherapy, subtype — a colleague who cites every call.
Clinical decision support that reasons like a medical oncologist while you decide: match the molecular marker, weigh immunotherapy eligibility, sequence the systemic therapy — with the decision rule and exactly what would change it. Built for verified oncologists.
Watch it think — in clinical oncology.
Two worked examples, reasoned the way it answers: the relevant clinical checks run, the answer is cited, the decision rule is explicit, and what is missing is flagged.
Newly diagnosed metastatic cutaneous melanoma, BRAF wild-type, ECOG 0, no autoimmune history — first-line systemic therapy?
BRAF wild-type metastatic melanoma with good performance status → first-line checkpoint immunotherapy. Anti-PD-1 (nivolumab or pembrolizumab), or a combination (nivolumab + ipilimumab, or nivolumab + relatlimab) for a higher response at the cost of more immune-related toxicity. Establish baseline organ and endocrine function, then monitor for immune-related adverse events throughout.
Decision ruleBRAF wild-type + fit → checkpoint immunotherapy first-line; combination for a higher response if the patient can tolerate the toxicity; a BRAF V600 mutation adds a targeted option.
Not established from this alone — BRAF/LDH status, brain metastases, autoimmune history and performance status change the regimen.
HR-positive, HER2-negative metastatic breast cancer, postmenopausal, PIK3CA-mutant, progressing on an aromatase inhibitor — next line?
HR+/HER2− disease is endocrine-driven: first-line is an aromatase inhibitor plus a CDK4/6 inhibitor. On progression with a PIK3CA mutation, alpelisib plus fulvestrant is guideline-supported; fulvestrant, everolimus-based therapy and, for a germline BRCA mutation, a PARP inhibitor are alternatives. Reserve chemotherapy for visceral crisis or clear endocrine resistance.
Decision ruleHR+/HER2− → endocrine therapy + CDK4/6 first-line; PIK3CA-mutant on progression → alpelisib + fulvestrant; chemotherapy only for visceral crisis or endocrine resistance.
Not established from this alone — prior lines of therapy, germline BRCA, visceral burden and menopausal status change the sequence.
Illustrative simulations. The physician always decides.
The answers oncologists actually look up.
The exact questions your field searches for — answered in the format the knowledge base speaks: the answer, the decision rule, what's missing, and the source.
Immunotherapy — which biomarkers predict checkpoint-inhibitor benefit?
Three biomarkers most often support a checkpoint inhibitor: PD-L1 expression (the threshold varies by tumor and assay), MSI-high / mismatch-repair-deficient status, and a high tumor mutational burden (≥10 mutations/Mb). MSI-H/dMMR and TMB-high are tumor-agnostic indications for pembrolizumab; PD-L1 is tumor-specific. None is perfect — clinical context still decides.NCCN · biomarker guidance
Decision ruleTest PD-L1, MSI/MMR and TMB before immunotherapy; MSI-H/dMMR or TMB-high → checkpoint inhibitor regardless of site; the PD-L1 threshold is tumor- and assay-specific.
Missing data: tumor type, the specific assay and cut-off, prior therapy and autoimmune history change eligibility.
Breast cancer — how does subtype drive treatment?
Systemic therapy follows the receptors. HR+/HER2− is endocrine-driven (endocrine therapy ± CDK4/6). HER2-positive is treated with HER2-directed therapy (trastuzumab ± pertuzumab, T-DM1, trastuzumab deruxtecan). Triple-negative relies on chemotherapy, adds immunotherapy when PD-L1-positive, and a PARP inhibitor with a germline BRCA mutation. Surgery (lumpectomy or mastectomy) and radiation are decided alongside.guideline synthesis
Decision ruleReceptor subtype sets the backbone: HR+ → endocrine ± CDK4/6; HER2+ → HER2-directed; TNBC → chemotherapy ± immunotherapy/PARP by PD-L1 and BRCA.
Missing data: stage, nodal status, germline BRCA, PD-L1 and menopausal status refine the plan.
Metastatic melanoma — first-line systemic therapy?
For most metastatic cutaneous melanoma, checkpoint immunotherapy is first-line: anti-PD-1 alone, or a combination (anti-PD-1 + anti-CTLA-4, or anti-PD-1 + anti-LAG-3) for a higher response at the cost of more toxicity. A BRAF V600 mutation adds BRAF/MEK-targeted therapy as an option, often reserved for rapidly progressive or high-burden disease.NCCN · melanoma
Decision ruleImmunotherapy first-line for most; combinations for a higher response if tolerated; a BRAF V600 mutation adds a targeted option, favored when a fast response is needed.
Missing data: BRAF status, LDH, brain metastases, the pace of disease and autoimmune history drive the choice.
HR-positive metastatic breast cancer — how do I sequence endocrine therapy?
First-line is an aromatase inhibitor (or fulvestrant) plus a CDK4/6 inhibitor. On progression, actionable biology guides the next line: a PIK3CA mutation → alpelisib + fulvestrant; other cases → fulvestrant, everolimus-based therapy, or a PARP inhibitor for a germline BRCA mutation. Chemotherapy is reserved for visceral crisis or clear endocrine resistance.guideline synthesis
Decision ruleEndocrine + CDK4/6 first-line; on progression, biomarker-match the next line (PIK3CA → alpelisib + fulvestrant); chemotherapy only for visceral crisis.
Missing data: prior endocrine exposure, PIK3CA and BRCA status, and visceral burden change the sequence.
What it knows in clinical oncology
Your whole practice, one specialist brain — grounded in specialist-written, cited knowledge.
A generalist medical-oncology colleague across breast, thoracic, GI, GU, melanoma and immuno-oncology — cited, non-directive, always with the decision rule.
Deep specialist agents for breast, thoracic, gastrointestinal, GU & melanoma and immuno-oncology — each its own specialist voice and knowledge base — plus your own uploaded materials.
Why not just use OpenEvidence or ChatGPT?
A large language model answers any clinical question with total confidence and no idea whether it is right. A search engine finds papers. HeyHippocrates reasons inside your specialty from a knowledge base a specialist in your field wrote and signed, and tells you the decision rule and what is missing.
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Questions oncologists ask
It reasons the way you do — subtype and biomarker first (HR/HER2, PD-L1, MSI/MMR, driver mutations), then guideline-supported sequencing — and always shows the reasoning, the decision rule and what would change it. The choice always stays your call.
Both. Fellows use it to pressure-test a plan and learn the decision rule; attendings use it as a fast, cited second opinion between clinics and tumor boards. Access is gated to verified physicians.
Breast, thoracic, gastrointestinal, GU & melanoma, and immuno-oncology each have their own deep specialist agent on the Pro plan, on top of the full general medical-oncology scope on Basic.
No. It is physician-facing clinical decision support — a cited thinking partner. It does not diagnose, does not treat, and gives no patient-facing advice. The decision always stays with you.
Every answer is grounded only in specialist-written, cited oncology knowledge — traceable to a named source — and always states the decision rule plus what data is missing, instead of a confident guess.