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Chronic myeloid leukaemia is caused by BCR::ABL1, arising from the Philadelphia chromosome. Treatment is directed at that fusion, and response is measured by quantifying the transcript on an international standardised scale. Because the measurement is precise and standardised, management is unusually well defined by milestones.
Also called CML, Chronic myeloid leukemia.
Start here
CML is defined by a single genetic event and monitored by measuring that event over time, which makes molecular response at defined milestones the central organising fact of the whole disease.
Chronic myeloid leukaemia is caused by BCR::ABL1, arising from the Philadelphia chromosome. Treatment is directed at that fusion, and response is measured by quantifying the transcript on an international standardised scale. Because the measurement is precise and standardised, management is unusually well defined by milestones.
01Before any molecular question
Usually established first: phase (chronic, accelerated or blast phase), confirmation of BCR::ABL1, and the specific transcript type. Most patients present in chronic phase, often found on a routine blood count.
Usually already established
02
The divisions below are not labels. Each one changes what the treatment discussion is actually about.
Chronic phase
Where most patients present, and where treatment aims for deep molecular response and long-term control.
Accelerated phase
An intermediate state requiring a different discussion.
Blast phase
Behaves like an acute leukaemia and is managed accordingly.
Treatment-free remission candidates
Patients in sustained deep molecular response for whom stopping treatment under close monitoring may be discussed.
03What is discussed
BCR::ABL1 is the defining alteration. The transcript type matters because it determines whether standardised quantitative monitoring is possible; atypical transcripts require different monitoring approaches. Response is reported on the International Scale, and milestones at defined time points guide whether treatment is working. At resistance, kinase domain mutation testing identifies specific alterations, and the T315I mutation in particular requires a different agent from all the others.
BCR::ABL1
The defining alteration, and the thing measured to follow the disease.
Transcript type
Determines whether standardised quantitative monitoring is possible.
Kinase domain mutations
Tested at resistance. T315I in particular changes which agents can work.
Additional chromosomal abnormalities
Their appearance can signal progression.
This is not an exhaustive list, and which markers are relevant depends on the individual case. Not every marker listed is assessed in every patient.
04What is tested, and from what
Diagnosis is confirmed by detecting BCR::ABL1. Quantitative monitoring on the International Scale is then performed at regular intervals, and the results are compared against defined milestones. Kinase domain mutation testing is performed when response is inadequate or lost, and not routinely otherwise. Consistency of the testing laboratory matters, because trends over time are what is being interpreted.
CML is not an inherited disease in any practical sense. The BCR::ABL1 fusion is an acquired event in a blood-forming cell, and germline testing is not part of the pathway.
Cancer genetics and hereditary riskPeripheral blood is used directly for quantitative monitoring, which makes CML the clearest example in oncology of a disease managed by a blood-based molecular measurement over years.
More on ctDNA monitoring05The timing question
Testing that arrives after the decision it was meant to inform has already been made is a common and avoidable problem. This is the sequence in which molecular information tends to become relevant.
06Take these to your team
When a decision is being made
Questions worth raising with a treating team.
At progression, recurrence or resistance
The molecular picture at diagnosis is not always the molecular picture later.
07What shapes eligibility
Trial activity includes newer agents for resistant disease and treatment-free remission strategies. Eligibility is usually written in terms of prior agents, mutation status and depth of molecular response.
| Term | What it means |
|---|---|
| BCR::ABL1 | The fusion gene that causes CML, produced by the Philadelphia chromosome. |
| International Scale | A standardised way of reporting BCR::ABL1 levels so results are comparable between laboratories. |
| Molecular response | How far the BCR::ABL1 level has fallen. Reported as MR3, MR4, MR4.5 and so on. |
| Treatment-free remission | Stopping treatment in patients with sustained deep response, under close monitoring. |
| T315I | A specific resistance mutation that most agents cannot overcome. |
These are the services most often relevant to this cancer. Which of them applies is a clinical question, not an automatic one.
This entry is educational. It describes what is commonly discussed in this cancer, not what should happen for any individual. Which of it applies depends on the specific diagnosis, stage, prior treatment and the person themselves. Nothing here is a recommendation, and no list of biomarkers here is exhaustive. Decisions belong with a treating team who know the whole case.
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