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Secondary and therapy-related acute myeloid leukaemia: the decisions you may face

3 treatment settings, 3 with more than one named option. Each section lays out the options the standard of care names, what each is for, the trials behind them with their recorded results, the side effects and cautions on record, and questions to ask. Built from the cancer page's standard-of-care rows; nothing here is advice for your case.

Advanced, first line

Newly diagnosed, fit for intensive chemotherapy, age 60 to 75

CPX-351 induction (Study 301) followed by allogeneic transplant in remission; 7+3 where CPX-351 is unavailable.

The options, in plain words

The two old chemotherapy drugs packed together into tiny fat bubbles at a fixed ratio, which doubled five-year survival in older adults with high-risk AML.

The intensive chemotherapy that has induced remission in fit AML patients since 1973: seven days of one drug, three of another. Still the backbone that targeted drugs are added to.

Allogeneic stem cell transplantation replaces a patient's blood system with a donor's after conditioning chemotherapy, so donor immune cells hunt down leukaemia left behind. It remains the only cure for adverse-risk acute myeloid leukaemia, high-risk acute lymphoblastic leukaemia and Richter transformation, at the price of graft-versus-host disease.

  • Curative for otherwise incurable leukaemia
  • Graft-versus-leukaemia is an antigen-agnostic immune therapy
The evidence behind it
The main trade-offs on record
  • Treatment-related mortality 10-20%
  • Chronic GVHD
  • Relapse remains the main cause of failure
Questions to ask about this decision
  1. Between CPX-351 (liposomal daunorubicin-cytarabine), Cytarabine + anthracycline ('7+3') and Allogeneic stem cell transplantation, which do you recommend for me, and what about my case would make you choose differently?
    Why: Guidelines list several reasonable options; the choice turns on details of your tumour, your health and your priorities.
  2. What is each option trying to achieve: cure, long control, or relief of symptoms, and over what time?
    Why: The aim shapes how much side effect and disruption is worth accepting.
  3. How closely do I match the people in CPX-351 Study 301, and does that change what the results mean for me?
    Why: Trial populations are selected; age, fitness, prior treatment and biomarkers all affect how far results carry.
  4. What happens if I delay, or decline this step for now? Is the decision reversible?
    Why: Some decisions can wait for a second opinion or a trial slot; others cannot. Knowing which is part of the choice.
  5. Does your recommendation follow the current guideline (NCCN Guidelines: Acute Myeloid Leukemia), and if it departs from it, why?
    Why: Departures from guidelines are sometimes right for an individual; they should be explained.
  6. For my situation (newly diagnosed, fit for intensive chemotherapy, age 60 to 75), which of the standard options do you recommend and why?
    Why: Guideline options include: CPX-351 induction (Study 301) followed by allogeneic transplant in remission; 7+3 where CPX-351 is unavailable.
  7. Am I a candidate for CPX-351 (liposomal daunorubicin-cytarabine), Cytarabine + anthracycline ('7+3'), and what side effects should I expect?
    Why: Knowing the expected toxicities helps you plan work, family, and supportive care.
  8. How do the results of CPX-351 Study 301 apply to someone like me?
    Why: Trial populations differ from individual patients; ask how closely you match.

Add these to your appointment list, or take the full question set for this cancer.

Special situations

Newly diagnosed, unfit for intensive chemotherapy

Venetoclax plus azacitidine or decitabine; hypomethylating agent alone for TP53-mutated disease where venetoclax adds little; trials.

The options, in plain words

A pill that removes the survival shield from leukaemia cells, enabling chemotherapy-free, time-limited treatment for CLL.

A gentle chemotherapy that switches silenced genes back on. With venetoclax it became the standard for older people with AML who cannot take intensive treatment.

Decitabine (Dacogen) is an infusion that loosens the chemical silencing of genes in myelodysplastic syndromes and acute myeloid leukaemia, helping the bone marrow work again. An oral version combined with cedazuridine has its own record.

The evidence behind it
  • Newly diagnosed AML unfit for intensive chemotherapy: venetoclax + azacitidine vs placebo + azacitidine

    OS 14.7 vs 9.6 months, HR 0.66; CR 36.7% vs 17.9%.

    Overall survival (median) (months): Venetoclax + azacitidine 14.7 (n=286) vs Placebo + azacitidine 9.6 (n=145) · HR 0.66 · source
The main trade-offs on record
  • Take with a meal and water. Avoid grapefruit, Seville oranges and starfruit.
  • Reduce by 50% in severe impairment.
Side effectAny gradeGrade 3+
Neutropenia · VIALE-A combination arm-42%

Rates from the label or pivotal trial as recorded on the product page; each grade 3+ figure links to its source.

Questions to ask about this decision
  1. Between Venetoclax, Azacitidine and Decitabine, which do you recommend for me, and what about my case would make you choose differently?
    Why: Guidelines list several reasonable options; the choice turns on details of your tumour, your health and your priorities.
  2. What is each option trying to achieve: cure, long control, or relief of symptoms, and over what time?
    Why: The aim shapes how much side effect and disruption is worth accepting.
  3. How closely do I match the people in VIALE-A, and does that change what the results mean for me?
    Why: Trial populations are selected; age, fitness, prior treatment and biomarkers all affect how far results carry.
  4. Which side effects of Azacitidine are most likely for me, which are reversible, and which would make us stop?
    Why: The recorded rates below come from labels and trials; your own risk depends on dose, other medicines and your health.
  5. What happens if I delay, or decline this step for now? Is the decision reversible?
    Why: Some decisions can wait for a second opinion or a trial slot; others cannot. Knowing which is part of the choice.
  6. Does your recommendation follow the current guideline (NCCN Guidelines: Acute Myeloid Leukemia), and if it departs from it, why?
    Why: Departures from guidelines are sometimes right for an individual; they should be explained.
  7. For my situation (newly diagnosed, unfit for intensive chemotherapy), which of the standard options do you recommend and why?
    Why: Guideline options include: Venetoclax plus azacitidine or decitabine; hypomethylating agent alone for TP53-mutated disease where venetoclax adds little; trials.
  8. Am I a candidate for Venetoclax, Azacitidine, Decitabine, and what side effects should I expect?
    Why: Knowing the expected toxicities helps you plan work, family, and supportive care.
  9. How do the results of VIALE-A apply to someone like me?
    Why: Trial populations differ from individual patients; ask how closely you match.

Add these to your appointment list, or take the full question set for this cancer.

Second line

Consolidation and relapse

Allogeneic transplant is the only curative option; genotype-directed drugs where a FLT3, IDH or KMT2A target exists.

The options, in plain words

Allogeneic stem cell transplantation replaces a patient's blood system with a donor's after conditioning chemotherapy, so donor immune cells hunt down leukaemia left behind. It remains the only cure for adverse-risk acute myeloid leukaemia, high-risk acute lymphoblastic leukaemia and Richter transformation, at the price of graft-versus-host disease.

  • Curative for otherwise incurable leukaemia
  • Graft-versus-leukaemia is an antigen-agnostic immune therapy

A single pill that beats salvage chemotherapy for relapsed FLT3-mutated AML, and the backbone of the triplets now being tested in frontline disease.

The first drug to block a mutant metabolic enzyme in cancer. With azacitidine it tripled survival in IDH1-mutated AML that could not take intensive chemotherapy.

Revumenib (Revuforj) is the first menin inhibitor (2024), for acute leukaemias with KMT2A rearrangements or NPM1 mutations.

The evidence behind it

No trial record is attached to this row yet. The trials tab lists what is recruiting and the landmark trials for this cancer.

The main trade-offs on record
  • Treatment-related mortality 10-20%
  • Chronic GVHD
  • Relapse remains the main cause of failure
Side effectAny gradeGrade 3+
Differentiation syndrome · Boxed warning3%-
  • Known QT prolongation. Avoid other QT-prolonging drugs where possible; check ECG and correct potassium and magnesium before and during treatment.

Rates from the label or pivotal trial as recorded on the product page; each grade 3+ figure links to its source.

Side effectAny gradeGrade 3+
Differentiation syndrome · AGILE combination arm14%-
  • Known QT prolongation. Avoid other QT-prolonging drugs where possible; check ECG and correct potassium and magnesium before and during treatment.

Rates from the label or pivotal trial as recorded on the product page; each grade 3+ figure links to its source.

  • Known QT prolongation. Avoid other QT-prolonging drugs where possible; check ECG and correct potassium and magnesium before and during treatment.
Questions to ask about this decision
  1. Between Allogeneic stem cell transplantation, Gilteritinib, Ivosidenib and the other options, which do you recommend for me, and what about my case would make you choose differently?
    Why: Guidelines list several reasonable options; the choice turns on details of your tumour, your health and your priorities.
  2. What is each option trying to achieve: cure, long control, or relief of symptoms, and over what time?
    Why: The aim shapes how much side effect and disruption is worth accepting.
  3. Which side effects of Gilteritinib or Ivosidenib are most likely for me, which are reversible, and which would make us stop?
    Why: The recorded rates below come from labels and trials; your own risk depends on dose, other medicines and your health.
  4. What happens if I delay, or decline this step for now? Is the decision reversible?
    Why: Some decisions can wait for a second opinion or a trial slot; others cannot. Knowing which is part of the choice.
  5. Does your recommendation follow the current guideline (NCCN Guidelines: Acute Myeloid Leukemia), and if it departs from it, why?
    Why: Departures from guidelines are sometimes right for an individual; they should be explained.
  6. For my situation (consolidation and relapse), which of the standard options do you recommend and why?
    Why: Guideline options include: Allogeneic transplant is the only curative option; genotype-directed drugs where a FLT3, IDH or KMT2A target exists.
  7. Am I a candidate for Gilteritinib, Ivosidenib, Revumenib, and what side effects should I expect?
    Why: Knowing the expected toxicities helps you plan work, family, and supportive care.

Add these to your appointment list, or take the full question set for this cancer.

How to read this page. Options and results come from OnCo records with their sources; the settings are the standard-of-care rows on the cancer page, and the lines of therapy are on the sequencing grid. Where a setting names one path, the choice is usually about timing, trials and where to be treated: see expert centres. OnCo is orientation, not medical advice.