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Acute lymphoblastic leukaemia is classified by lineage and by genetic subtype. Treatment follows extended multi-phase protocols, and response measured as residual disease at specified points in those protocols drives subsequent decisions. Several genetic subtypes carry direct treatment implications, and central nervous system involvement is addressed routinely rather than only when symptomatic.
Also called ALL, Acute lymphoblastic leukemia, B-cell ALL, T-cell ALL.
Start here
ALL is managed on long, precisely staged protocols, and measurable residual disease at defined time points is the single most informative measurement, more so than almost any baseline feature.
Acute lymphoblastic leukaemia is classified by lineage and by genetic subtype. Treatment follows extended multi-phase protocols, and response measured as residual disease at specified points in those protocols drives subsequent decisions. Several genetic subtypes carry direct treatment implications, and central nervous system involvement is addressed routinely rather than only when symptomatic.
01Before any molecular question
Usually established first: lineage (B-cell or T-cell) by immunophenotype, cytogenetics, and the presence of BCR::ABL1. Central nervous system status is assessed at diagnosis. Age is a major determinant of protocol choice, and the boundary between paediatric and adult approaches has shifted, with paediatric-inspired protocols now used in young adults.
Usually already established
02
The divisions below are not labels. Each one changes what the treatment discussion is actually about.
B-cell ALL, Philadelphia chromosome positive
Defined by BCR::ABL1. Targeted agents are central to the treatment discussion.
B-cell ALL, Philadelphia-like
A genetically diverse group with a similar expression pattern but without BCR::ABL1. Requires specific testing to identify, and is often missed without it.
B-cell ALL, other subtypes
Including hyperdiploid, ETV6::RUNX1, KMT2A-rearranged and TCF3::PBX1 disease, each with distinct implications.
T-cell ALL
Including early T-cell precursor ALL, which is recognised as a distinct higher-risk entity.
Relapsed or refractory disease
Where immune-based approaches and trial options become central.
03What is discussed
BCR::ABL1 defines Philadelphia chromosome positive disease and must be identified at diagnosis. Philadelphia-like ALL involves a range of kinase-activating alterations including CRLF2 rearrangement, ABL class fusions and JAK pathway alterations, and identifying it requires specific testing that is not part of standard cytogenetics. KMT2A rearrangements, ETV6::RUNX1, TCF3::PBX1, IKZF1 deletion and hypodiploidy all carry risk implications. In T-cell ALL, NOTCH1 alterations are common. TP53 alteration and hypodiploidy are associated with less favourable outcomes.
BCR::ABL1
Defines Philadelphia positive disease. Identified at diagnosis and central to treatment.
Philadelphia-like signature
A group requiring specific testing to detect. Easily missed by standard cytogenetics alone.
CRLF2, ABL class fusions, JAK pathway
The alterations underlying Philadelphia-like disease.
IKZF1
Deletion carries risk implications.
KMT2A
Rearrangements define a distinct group, particularly in infants.
Measurable residual disease
Not a gene, but the most informative single measurement in this disease.
CD19, CD20, CD22
Surface markers relevant to immune-based treatment approaches.
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
Immunophenotyping and cytogenetics establish the diagnosis. BCR::ABL1 testing is urgent. Philadelphia-like ALL requires specific additional testing that is not part of standard cytogenetics, and this is a recognised gap in practice. Measurable residual disease is assessed at protocol-defined time points using flow cytometry or molecular methods, and these time points are specified in advance rather than chosen ad hoc.
Inherited predisposition is recognised, including germline PAX5, ETV6, IKZF1 and TP53 alterations, and Down syndrome carries a substantially increased risk. Constitutional mismatch repair deficiency is also associated. As in AML, germline evaluation matters before a sibling is used as a stem cell donor. Prompts include a family history of haematological malignancy or a striking personal history.
Cancer genetics and hereditary riskMeasurable residual disease monitoring in blood and marrow is the established equivalent of liquid biopsy in this disease, and it is one of the most mature applications of molecular monitoring anywhere in oncology.
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
Eligibility is written by subtype, measurable residual disease status, prior therapy and surface marker expression. Because protocols are long and precisely staged, the exact point in treatment matters for eligibility.
| Term | What it means |
|---|---|
| Lineage | Whether the leukaemia arises from B-cells or T-cells. The first classification step. |
| Philadelphia chromosome | A specific chromosomal rearrangement producing BCR::ABL1. |
| Philadelphia-like | Disease that behaves like Philadelphia positive ALL without carrying that rearrangement. Requires specific testing. |
| Measurable residual disease | Disease remaining below the level a microscope can detect. The key measurement in ALL. |
| CNS prophylaxis | Treatment directed at the central nervous system given routinely, because standard treatment does not reach it well. |
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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