• Metabolic theory of cancer: from Warburg to oncometabolites: Otto Warburg noticed a century ago that cancer cells ferment glucose even when oxygen is plentiful and concluded that damaged respiration causes cancer.
• 7+3 induction chemotherapy: The classic first treatment for acute myeloid leukaemia, unchanged since 1973: seven days of continuous cytarabine plus three days of an anthracycline, given in hospital.
• FLT3-ITD allelic ratio: How much of the FLT3 gene in the leukaemia carries the internal duplication, measured as the ratio of mutant to normal copies.
• Epigenetic progenitor theory: cancer without a first mutation: The proposal that cancer begins not with a mutation but with a reversible change in how genes are switched on and off in a stem or progenitor cell, which then makes later mutations more likely and more dangerous.
• Cancer stem cell theory and phenotypic plasticity: The idea that a tumour is organised like a tissue, with a small pool of stem-like cells that renew it and a bulk that cannot, so killing the bulk shrinks the tumour but the stem-like cells regrow it.
• AML with myelodysplasia-related gene mutations (AML-MR): Eight genes (ASXL1, BCOR, EZH2, RUNX1, SF3B1, SRSF2, STAG2, U2AF1 and ZRSR2) are almost never mutated in leukaemia that arises out of nowhere but are typical of leukaemia that grew out of a smouldering marrow disorder; finding one on the diagnostic gene panel labels the AML as myelodysplasia-related, puts it in the adverse-risk group and changes the chemotherapy chosen.
• Ageing tissue and clonal fields: cancer as a disease of old tissue: Sequencing of healthy skin, gullet and blood shows that by middle age they are patchworks of mutant clones, many carrying classic cancer mutations, yet cancer stays rare until old age.
• MRD-negative complete remission: MRD-negative complete remission means not just no leukaemia visible under the microscope, but none detectable with tests a thousand times more sensitive.
• From a clone in the blood to a leukaemia: what is known, and what is done: Chemotherapy and radiotherapy select for blood stem cells carrying particular mutations, and in a small minority one of those clones becomes a leukaemia.
• Induction therapy: The first, most intensive block of treatment, intended to knock the cancer into remission.

Diagnosis and risk assignment: Marrow morphology, flow, karyotype/FISH, rapid FLT3/NPM1/IDH testing (results within days), NGS panel; ELN 2022 risk; fitness assessment. Menin-inhibitor and FLT3-inhibitor eligibility depends on these results.

Biomarker results to ask for: FLT3-ITD/TKD, NPM1, IDH1/2, KMT2A, TP53, CD33, ELN risk, MRD, ELN 2022 genetic risk group, FLT3-ITD and TKD (midostaurin, quizartinib, gilteritinib), NPM1 (favourable risk without FLT3-ITD; MRD marker; menin inhibitor eligibility), IDH1 / IDH2 (ivosidenib, olutasidenib, enasidenib), KMT2A rearrangement (revumenib), TP53 and complex karyotype (adverse; venetoclax less effective), CD33 (gemtuzumab), CD123 (tagraxofusp, pivekimab), Measurable residual disease (flow, NPM1 qPCR, NGS) after cycles 2 and before transplant, Karyotype/FISH at diagnosis, Myelodysplasia-related mutation set.

Scans and tests linked to this cancer: Comprehensive genomic profiling, Cytogenetics and FISH, Flow cytometers, Multiparameter flow cytometry MRD, NGS-based MRD (clonoSEQ and molecular MRD), G8 geriatric screening tool.

Bring copies of scan reports, pathology and blood results, and a list of every medicine and supplement.

• Fit, favourable or intermediate risk, CD33-positive: 7+3 plus fractionated gemtuzumab ozogamicin (ALFA-0701); high-dose cytarabine consolidation; MRD-guided transplant for intermediate risk. (Gemtuzumab ozogamicin, ALFA-0701, Cytarabine + anthracycline ('7+3'))
• Fit: 7+3 ± targeted agent; consolidation; allogeneic transplant by risk. (Gemtuzumab ozogamicin, Cytotoxic chemotherapy)
• Unfit: Azacitidine + venetoclax. (Venetoclax)
• Fit, FLT3-mutated: 7+3 plus midostaurin (ITD or TKD) or quizartinib (ITD only), consolidation with continued inhibitor, allogeneic transplant for most FLT3-ITD in CR1, post-transplant FLT3-inhibitor maintenance if MRD-positive. (Cytarabine + anthracycline ('7+3'), Midostaurin, Quizartinib, RATIFY (CALGB 10603), QuANTUM-First, Allogeneic stem cell transplantation)
• Fit, secondary or therapy-related AML: CPX-351 induction (Study 301) then transplant in CR1; alternatives include 7+3 or venetoclax-based therapy in trials. (CPX-351 (liposomal daunorubicin-cytarabine), CPX-351 Study 301, Allogeneic stem cell transplantation)
• Fit, adverse risk (TP53, complex karyotype, MDS-related): Intensive induction or venetoclax-azacitidine to remission, then allogeneic transplant as the only realistic cure; clinical trial strongly preferred; TP53-mutated disease has no effective targeted therapy after the magrolimab and eprenetapopt failures. (Allogeneic stem cell transplantation, Venetoclax, Azacitidine, Magrolimab)
• Unfit for intensive chemotherapy (most patients over 75): Venetoclax + azacitidine (VIALE-A) or venetoclax + oral decitabine-cedazuridine (ASCERTAIN-V, 2026); ivosidenib + azacitidine if IDH1-mutated (AGILE); low-dose cytarabine + venetoclax as an alternative. Continue until progression; consider transplant in responders who become fit. (Venetoclax, Azacitidine, Decitabine + cedazuridine (oral), Ivosidenib, VIALE-A, AGILE, ASCERTAIN-V)
• Acute promyelocytic leukaemia: ATRA + arsenic trioxide without chemotherapy for standard risk (cure >95%); ATRA + arsenic + idarubicin or gemtuzumab for high risk. Differentiation syndrome prophylaxis. (Differentiation syndrome)
• Relapsed: Genotype-directed: gilteritinib, IDH inhibitors, menin inhibitors; transplant. (Revumenib)
• Relapsed or refractory, FLT3-mutated: Gilteritinib monotherapy (ADMIRAL) or gilteritinib + venetoclax/azacitidine, then transplant; quizartinib in Japan. (Gilteritinib, ADMIRAL, Allogeneic stem cell transplantation)
• Relapsed or refractory, IDH-mutated: Ivosidenib or olutasidenib (IDH1), enasidenib (IDH2), often with azacitidine or venetoclax; differentiation-syndrome monitoring. (Ivosidenib, Olutasidenib, Enasidenib, Differentiation syndrome)
• Relapsed or refractory, NPM1-mutated or KMT2A-rearranged: Menin inhibitor: revumenib (KMT2Ar 2024; NPM1 2025) or ziftomenib (NPM1, November 2025), as a bridge to transplant; triplets with venetoclax-azacitidine in trials. (Revumenib, Ziftomenib, AUGMENT-101, KOMET-001, Menin inhibitor + venetoclax + azacitidine)
• Maintenance after intensive therapy: Oral azacitidine (Onureg) for patients not transplanted (QUAZAR AML-001); FLT3 inhibitor maintenance after transplant in FLT3-ITD (MORPHO for MRD-positive); menin inhibitor maintenance in trials. (Azacitidine, Gilteritinib, Quizartinib, QUAZAR AML-001, MORPHO)

From the standard of care recorded for this cancer; which apply depends on your stage and biomarkers. Ask which the team recommends and why.