Chronic myeloid leukaemia, accelerated and blast phase
Prepared with OnCo (onco.cc/prep/cml-advanced-phase/). Orientation, not medical advice; your team knows your case.
My details
What I know, what is unclear, changes to discuss
Saved in this browserMy questions
17 on the sheet- 1.What is my exact diagnosis, stage, and grade, and which tests established them?
- 2.Which biomarkers have been tested on my tumour (for example Blast percentage in blood and marrow, Basophil percentage and platelet count, Additional chromosomal abnormalities, BCR::ABL1 kinase domain mutations including T315I, Blast lineage by flow cytometry), and what were the results?
- 3.Which subtype is my cancer, and does that change the recommended treatment?
- 4.Is germline (inherited) genetic testing recommended for me or my family?
- 5.For my situation (accelerated phase), which of the standard options do you recommend and why?
- 6.Am I a candidate for Dasatinib, Nilotinib, Bosutinib or related drugs, and what side effects should I expect?
- 7.How do the results of The Study for CML Who Failed Prior TKIs or With T315I Mutation or Ph+ ALL Who Failed Prior TKIs or With T315I Mutation and Open-label Study of Asciminib for CML-CP or CML-AP Patients With T315I Mutation Who Are Resistant, Intolerant or Ineligible to Ponatinib. apply to someone like me?
- 8.For my situation (myeloid blast phase), which of the standard options do you recommend and why?
- 9.Am I a candidate for Ponatinib, Dasatinib, Cytarabine + anthracycline ('7+3') or related drugs, and what side effects should I expect?
- 10.For my situation (lymphoid blast phase), which of the standard options do you recommend and why?
- 11.Am I a candidate for Dasatinib, Ponatinib, Blinatumomab or related drugs, and what side effects should I expect?
- 12.For my situation (consolidation), which of the standard options do you recommend and why?
- 13.Are there clinical trials I could join, for example of Ponatinib, Asciminib, Olverembatinib, Blinatumomab?
- 14.Would a second opinion at a high-volume centre change anything, and can you help arrange it?
- 15.What supportive care (symptom control, nutrition, exercise, mental health, financial help) is available from the start?
- 16.I read that “Blast phase remains largely fatal without transplant, and few patients reach it in remission”. How does that affect my plan?
- 17.I read that “Trials are tiny because progression has become rare”. How does that affect my plan?
The words I may hear
- Tyrosine kinase inhibitor (TKI): Pills that block the on-switch enzyme (a kinase) that a particular cancer depends on: imatinib for CML, osimertinib for EGFR lung cancer, ibrutinib for CLL.
- Philadelphia chromosome (Ph+, BCR::ABL1): A swapped piece between chromosomes 9 and 22 that fuses two genes into BCR::ABL1, a runaway kinase.
- Drug resistance (primary and acquired): Why cancer drugs stop working: the tumour either never depended on the target or evolves around the block.
- Conditioning regimen (myeloablative, reduced-intensity): The chemotherapy (with or without whole-body radiation) given in the days before a stem cell transplant to destroy the diseased marrow and, for donor transplants, suppress the patient's immune system so the graft is not rejected.
- Blasts (leukaemic blast cells): Immature blood cells that should mature in the marrow but in acute leukaemia multiply without growing up.
- Allogeneic stem cell transplant (allo-SCT): Replacing a patient's blood system with a donor's: chemotherapy wipes out the marrow, donor stem cells rebuild it, and the donor's immune cells hunt down leftover leukaemia.
Tests and results to bring
Biomarker results to ask for: Blast percentage in blood and marrow, Basophil percentage and platelet count, Additional chromosomal abnormalities (clonal evolution), BCR::ABL1 kinase domain mutations including T315I, Blast lineage by flow cytometry (myeloid or lymphoid), ASXL1, RUNX1, IKZF1 and TP53 mutations, Donor availability.
Scans and tests linked to this cancer: Cytogenetics and FISH.
Bring copies of scan reports, pathology and blood results, and a list of every medicine and supplement.
The treatments I may be offered
- Accelerated phase: Second- or third-generation tyrosine kinase inhibitor at full dose guided by mutation testing (dasatinib, nilotinib, bosutinib, ponatinib for T315I, olverembatinib where approved); allogeneic transplant if response is poor or clonal evolution progresses. (Dasatinib, Nilotinib, Bosutinib, Ponatinib, Olverembatinib, Asciminib, The Study for CML Who Failed Prior TKIs or With T315I Mutation or Ph+ ALL Who Failed Prior TKIs or With T315I Mutation, Open-label Study of Asciminib for CML-CP or CML-AP Patients With T315I Mutation Who Are Resistant, Intolerant or Ineligible to Ponatinib., Allogeneic stem cell transplantation)
- Myeloid blast phase: Tyrosine kinase inhibitor (ponatinib or dasatinib) with 7+3-type or hypomethylating agent and venetoclax induction, then allogeneic transplant in second chronic phase. (Ponatinib, Dasatinib, Cytarabine + anthracycline ('7+3'), Cytarabine, Azacitidine, Venetoclax, Allogeneic stem cell transplantation)
- Lymphoid blast phase: Dasatinib or ponatinib with ALL-type chemotherapy or with blinatumomab, central nervous system prophylaxis, then allogeneic transplant. (Dasatinib, Ponatinib, Blinatumomab, Cyclophosphamide, Allogeneic stem cell transplantation, BCR::ABL1 TKI + blinatumomab (chemotherapy-free Ph+ ALL))
- Consolidation: Allogeneic stem cell transplant for every eligible patient in second chronic phase, with tyrosine kinase inhibitor maintenance after transplant. (Allogeneic stem cell transplantation, Allogeneic stem cell transplant (allo-SCT), Conditioning regimen (myeloablative, reduced-intensity))
From the standard of care recorded for this cancer; which apply depends on your stage and biomarkers. Ask which the team recommends and why.