The first 60 days: Secondary and therapy-related acute myeloid leukaemia

Below, week by week, is what OnCo's record of Secondary and therapy-related acute myeloid leukaemia says about the first two months: the order is typical, the timing is yours to ask about. Secondary acute myeloid leukaemia grows out of an earlier marrow disorder or follows chemotherapy or radiotherapy for another cancer. It resists standard treatment more than other leukaemias; a liposomal form of the two classic chemotherapy drugs, CPX-351, lengthens life in fit older patients, and transplant is the only route to cure. Sections appear only where the record has something to say. Orientation, not medical advice.

Weeks 1 to 2

What happens now

Staging tests establish exactly what and where the cancer is. Everything else follows from the answers.

Newly diagnosed, fit for intensive chemotherapy, age 60 to 75 NCCN Guidelines: Acute Myeloid Leukemia
CPX-351 induction (Study 301) followed by allogeneic transplant in remission; 7+3 where CPX-351 is unavailable.
CPX-351 (liposomal daunorubicin-cytarabine)CPX-351 Study 301 Cytarabine + anthracycline ('7+3')Allogeneic stem cell transplantation
Newly diagnosed, unfit for intensive chemotherapy NCCN Guidelines: Acute Myeloid Leukemia
Venetoclax plus azacitidine or decitabine; hypomethylating agent alone for TP53-mutated disease where venetoclax adds little; trials.
Venetoclax Azacitidine Decitabine VIALE-A

Biomarkers your report may list

TP53 mutation and allelic state Complex or monosomal karyotype Myelodysplasia-related mutations (SRSF2, SF3B1, ASXL1, RUNX1, U2AF1, EZH2, BCOR, STAG2)KMT2A rearrangement Prior clonal haematopoiesis ELN 2022 risk group

Ask which of these were tested and what the results were; see the report reader for what each value means.

Weeks 1 to 3

Who is on your team

These specialties appear in the standard of care for this cancer. In most centres they meet weekly as a tumour board to agree each plan; you can ask when yours was discussed and what was decided.

A second opinion from a centre that treats many similar cases is normal, not rude; the standard of care tells you what to compare it against.

Weeks 2 to 6

Decisions coming up

Each row is a setting from the standard of care, in the order it usually arises. Not all will apply to you; your stage and biomarkers decide which do. The guideline grade, where recorded, says how strong the evidence is.

1.Consolidation and relapse NCCN Guidelines: Acute Myeloid Leukemia
Allogeneic transplant is the only curative option; genotype-directed drugs where a FLT3, IDH or KMT2A target exists.
Allogeneic stem cell transplantation Gilteritinib Ivosidenib Revumenib

Every visit

Questions to ask at each visit

Generated from this cancer's standard of care, biomarkers and open problems. Take the group that matches where you are. To tick, add your own and print, open the one-page appointment sheet.

Newly diagnosed

What is my exact diagnosis, stage, and grade, and which tests established them?Everything else follows from an accurate stage and subtype.
Which biomarkers have been tested on my tumour (for example TP53 mutation and allelic state, Complex or monosomal karyotype, Myelodysplasia-related mutations, KMT2A rearrangement, Prior clonal haematopoiesis), and what were the results?These results decide eligibility for targeted therapy, immunotherapy, and trials.
Which subtype is my cancer, and does that change the recommended treatment?Recognised subtypes for this cancer include Secondary AML arising from myelodysplastic syndromes or CMML, Post-MPN blast phase, Therapy-related AML after alkylating agents or radiotherapy.
Is germline (inherited) genetic testing recommended for me or my family?Inherited variants can change treatment and matter for relatives.

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

For my situation (newly diagnosed, fit for intensive chemotherapy, age 60 to 75), which of the standard options do you recommend and why?Guideline options include: CPX-351 induction (Study 301) followed by allogeneic transplant in remission; 7+3 where CPX-351 is unavailable.
Am I a candidate for CPX-351 (liposomal daunorubicin-cytarabine), Cytarabine + anthracycline ('7+3'), and what side effects should I expect?Knowing the expected toxicities helps you plan work, family, and supportive care.
How do the results of CPX-351 Study 301 apply to someone like me?Trial populations differ from individual patients; ask how closely you match.

Newly diagnosed, unfit for intensive chemotherapy

For my situation (newly diagnosed, unfit for intensive chemotherapy), which of the standard options do you recommend and why?Guideline options include: Venetoclax plus azacitidine or decitabine; hypomethylating agent alone for TP53-mutated disease where venetoclax adds little; trials.
Am I a candidate for Venetoclax, Azacitidine, Decitabine, and what side effects should I expect?Knowing the expected toxicities helps you plan work, family, and supportive care.
How do the results of VIALE-A apply to someone like me?Trial populations differ from individual patients; ask how closely you match.

Consolidation and relapse

For my situation (consolidation and relapse), which of the standard options do you recommend and why?Guideline options include: Allogeneic transplant is the only curative option; genotype-directed drugs where a FLT3, IDH or KMT2A target exists.
Am I a candidate for Gilteritinib, Ivosidenib, Revumenib, and what side effects should I expect?Knowing the expected toxicities helps you plan work, family, and supportive care.

Any stage

Are there clinical trials I could join, for example of CPX-351 (liposomal daunorubicin-cytarabine), Venetoclax, myeloMATCH, Which patients' blood clones will become leukaemia after treatment??Trials are how the next standard of care is set; asking early keeps options open.
Would a second opinion at a high-volume centre change anything, and can you help arrange it?Rare or high-stakes decisions benefit from a centre that treats many similar patients.
What supportive care (symptom control, nutrition, exercise, mental health, financial help) is available from the start?Supportive care improves quality of life and helps patients complete treatment.
I read that “No regimen produces durable remissions in TP53-mutated AML”. How does that affect my plan?Open problems are where trials and second opinions matter most.
I read that “Whether CPX-351 helps patients under 60 or those fit enough for transplant regardless of induction”. How does that affect my plan?Open problems are where trials and second opinions matter most.

Weeks 3 to 8

Trials to ask about

Trials open now for this cancer in OnCo, largest phase first. Joining a trial is a decision like any other: ask what the comparison arm is, whether a placebo is used, and what happens if you leave. The cancer page searches ClinicalTrials.gov live for more.

myeloMATCHPlatform trial · recruiting · NCT05564390Newly diagnosed AML and MDS: genomic screening at diagnosis assigns patients to tiered, biomarker-defined sub-studies from induction through MRD-guided consolidation and maintenance

From day one

Help that costs nothing

Much of what helps in the first weeks is free if you know to ask: testing, helplines, rides and lodging, second opinions, trial travel.

Any time

What to read next

Words this page and the cancer page use

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.
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.
Alkylating agents and therapy-related myeloid neoplasms: Alkylating chemotherapy can damage a blood stem cell in a way that shows up years later as myelodysplastic syndrome or acute myeloid leukaemia.
Topoisomerase II inhibitors and the shorter latency: Etoposide and the anthracyclines can cause a leukaemia too, but a different one: it arrives after about two years rather than six, it starts as acute leukaemia without a myelodysplastic phase, and it carries a balanced break in a chromosome rather than a missing piece.
Hypomethylating agents (azacitidine, decitabine): Low-intensity chemotherapy that strips chemical 'off' switches (methyl groups) from DNA so silenced genes can be read again.
SF3B1 mutation: SF3B1 is a splicing gene whose mutation makes the marrow produce red cells with iron-stuffed mitochondria (ring sideroblasts); in myelodysplastic syndrome it defines a low-risk subtype with anaemia that responds to luspatercept, whereas in CLL and uveal melanoma the same mutation has different, mostly adverse or delayed-relapse, meaning.
ELN 2022 risk classification: The three-tier system (favourable, intermediate, adverse) that decides how aggressively an adult with AML is treated and whether a transplant is recommended.
TP53-mutated (p53-abnormal): Loss of the p53 'guardian of the genome', the most commonly mutated gene in cancer.
Secondary malignancy (therapy-related cancer): A new, different cancer caused by the treatment of the first one: leukaemia after alkylating chemotherapy or PARP inhibitors, solid tumours in irradiated tissue decades later, and rarely T-cell lymphoma after CAR-T.

Every term links to the glossary.