The first 60 days: Chronic myeloid leukaemia (CML)
Chronic myeloid leukaemia is a blood cancer driven by a single fused gene, BCR-ABL1, and the model for oncogene-targeted treatment: imatinib in 2001 and the tyrosine kinase inhibitors that followed turned it into a condition most people live with long-term. About half of patients with a sustained deep molecular response can now stop treatment altogether. Below, week by week, is what OnCo's record of Chronic myeloid leukaemia (CML) says about the first two months: the order is typical, the timing is yours to ask about. Sections appear only where the record has something to say. Orientation, not medical advice.
What happens now
Staging tests establish exactly what and where the cancer is. Everything else follows from the answers.
Ask which of these were tested and what the results were; see the report reader for what each value means.
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.
- Medical oncologistNamed in the standard of care for: Chronic phase, first line, Resistance or intolerance, Blast phase.
- Transplant and cell therapy teamNamed in the standard of care for: Resistance or intolerance, Blast phase.
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.
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.Chronic phase, first lineNCCN category Category 1 (imatinib, dasatinib, nilotinib, bosutinib, asciminib), NCCN Guidelines: CML; ELN 2020 recommendations
Imatinib 400 mg, or a second-generation TKI (dasatinib, nilotinib, bosutinib), or asciminib (ASC4FIRST, approved 2024). Choice by comorbidity and treatment goal; monitor BCR-ABL1 IS at 3, 6, 12 months against ELN milestones.
Treatment-free remission attempt after ≥3-5 years of TKI and ≥2 years of MR4 or better, with monthly PCR for the first six months (EURO-SKI); restart on loss of MMR.
TKI plus acute-leukaemia-type induction (ponatinib or dasatinib with chemotherapy), then allogeneic HSCT.
Switch TKI guided by mutation analysis; ponatinib or asciminib for T315I; allogeneic HSCT if two or more TKIs fail or in advanced phase.
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 BCR-ABL1 by RT-qPCR on the International Scale, ABL1 kinase-domain mutations, ELTS score at diagnosis, Additional cytogenetic abnormalities, Cardiovascular risk profile), 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 Chronic phase, Accelerated phase, Blast phase.
- Is germline (inherited) genetic testing recommended for me or my family?Inherited variants can change treatment and matter for relatives.
Chronic phase, first line
- For my situation (chronic phase, first line), which of the standard options do you recommend and why?Guideline options include: Imatinib 400 mg, or a second-generation TKI (dasatinib, nilotinib, bosutinib), or asciminib (ASC4FIRST, approved 2024). Choice by comorbidity and treatment goal; monitor BCR-ABL1 IS at 3, 6, 12 months against ELN milestones.
- Am I a candidate for Imatinib, Dasatinib, Nilotinib or related drugs, and what side effects should I expect?Knowing the expected toxicities helps you plan work, family, and supportive care.
Resistance or intolerance
- For my situation (resistance or intolerance), which of the standard options do you recommend and why?Guideline options include: Switch TKI guided by mutation analysis; ponatinib or asciminib for T315I; allogeneic HSCT if two or more TKIs fail or in advanced phase.
- Am I a candidate for Ponatinib, Asciminib, Bosutinib, and what side effects should I expect?Knowing the expected toxicities helps you plan work, family, and supportive care.
Sustained deep molecular response
- For my situation (sustained deep molecular response), which of the standard options do you recommend and why?Guideline options include: Treatment-free remission attempt after ≥3-5 years of TKI and ≥2 years of MR4 or better, with monthly PCR for the first six months (EURO-SKI); restart on loss of MMR.
Blast phase
- For my situation (blast phase), which of the standard options do you recommend and why?Guideline options include: TKI plus acute-leukaemia-type induction (ponatinib or dasatinib with chemotherapy), then allogeneic HSCT.
- Am I a candidate for Ponatinib, Dasatinib, 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 Asciminib, Allogeneic stem cell transplantation?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 “Blast-phase CML: median survival still under a year”. How does that affect my plan?Open problems are where trials and second opinions matter most.
- I read that “Predicting who can stop TKI safely; second TFR attempts”. How does that affect my plan?Open problems are where trials and second opinions matter most.
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.
- A Phase 3 Study for the Efficacy and Safety of Radotinib in CP-CML Patients With Failure or Intolerance to Previous TKIsPhase 3 · recruiting · NCT03459534A Phase 3 Multinational, Multi-center, Single-arm, Open-label Study for the Efficacy and Safety of Radotinib in Ph+ Chronic Phase Chronic Myeloid Leukemia Patients With Failure or Intolerance to Previous TKIs Therapy Including Imatinib
- A Study of Oral Asciminib Versus Other TKIs in Adult Patients With Newly Diagnosed Ph+ CML-CPPhase 3 · active · NCT04971226A Phase III, Multi-center, Open-label, Randomized Study of Oral Asciminib Versus Investigator Selected TKI in Patients With Newly Diagnosed Philadelphia Chromosome Positive Chronic Myelogenous Leukemia in Chronic Phase
- A Study to Investigate Tolerability and Efficacy of Asciminib (Oral) Versus Nilotinib (Oral) in Adult Participants (≥18 Years of Age) With Newly Diagnosed Philadelphia Chromosome Positive Chronic Myelogenous Leukemia in Chronic Phase (Ph+ CML-CP)Phase 3 · active · NCT05456191A Phase IIIb, Multi-center, Open-label, Randomized Study of Tolerability and Efficacy of Oral Asciminib Versus Nilotinib in Patients With Newly Diagnosed Philadelphia Chromosome Positive Chronic Myelogenous Leukemia in Chronic Phase.
- Randomized Evaluation of Radotinib Versus Imatinib in Phase III Study for Efficacy With Chinese Patients (RERISE China)Phase 3 · active · NCT03722420A Phase III, Multi-center, Open-Label, Randomized Study of the Efficacy of Radotinib Versus Imatinib in Newly Diagnosed Philadelphia Chromosome Positive (Ph+) Chronic Myeloid Leukemia Chinese Patients in Chronic Phase
- Study of Olverembatinib (HQP1351) in Patients With CML-CPPhase 3 · recruiting · NCT06423911A Global, Multicenter, Open Label, Randomized, Phase 3 Registrational Study of Olverembatinib (HQP1351) in Patients With Chronic Phase Chronic Myeloid Leukemia (CML-CP)
Much of what helps in the first weeks is free if you know to ask: testing, helplines, rides and lodging, second opinions, trial travel.
- Chronic myeloid leukaemia (CML): the full pageChronic myeloid leukaemia is a blood cancer driven by a single fused gene, BCR-ABL1, and the model for oncogene-targeted treatment: imatinib in 2001 and the tyrosine kinase inhibitors that followed turned it into a condition most people live with long-term. About half of patients with a sustained deep molecular response can now stop treatment altogether.
- One-page appointment sheetYour questions, the words you may hear, what to bring, and space for the answers. Print it.
- Treatment sequencingWhich treatment tends to follow which, line by line.
- NavigatorStandard of care for your stage, what you have tried, and trials near you.
- Drug resistance (primary and acquired): Why cancer drugs stop working: the tumour either never depended on the target or evolves around the block.
- Oncogene addiction: When a cancer depends so completely on one mutated gene that blocking it collapses the tumour.
- Aneuploidy and chromosomal instability as the cause of cancer: The oldest theory of cancer, from Theodor Boveri in 1914: tumours arise from cells with the wrong number or arrangement of chromosomes.
- Somatic mutation theory of cancer: The standard account: cancer begins when a single body cell picks up mutations in the genes that control growth, and its descendants inherit them.
- Clonal evolution and the ecological view of cancer: A tumour is a population of cells that mutate, compete and are selected, exactly as species are, and treatment is one more selective pressure.
- Minimal / molecular residual disease (MRD): Cancer still present after treatment but too small to see on scans, detected by blood or marrow tests.
Every term links to the glossary.