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Signature BLL+
More than 600 genes covering lymphoblastic leukaemia and the lymphoma overlap, with the Philadelphia-like detection, copy number and clonality that a routine karyotype does not deliver.
For lymphoblastic leukaemia at diagnosis or relapse, lymphoid disease with an unclear subtype, a suspected Philadelphia-like signature, and cases being assessed for a trial.
The lymphoid panel, built to find the subtype that standard cytogenetics misses.
More than 600 genes covering lymphoblastic leukaemia and the lymphoma overlap, with the Philadelphia-like detection, copy number and clonality that a routine karyotype does not deliver.
What it reports
Driver mutations
The gene changes that define the disease and assign its subtype.
Fusions and rearrangements
The structural events that drive lymphoid leukaemia and guide therapy.
Philadelphia-like signature
The kinase-activating alterations that standard cytogenetics does not detect.
Copy number and deletions
Including the deletions that carry risk implications of their own.
Lymphoma overlap genes
Because lymphoid disease does not always present as a clean leukaemia.
Risk-defining markers
Findings that inform how intensively the leukaemia is treated.
Clonality and MRD baseline
A reference point that later monitoring can be measured against.
Targetable findings
Alterations with a matched therapy or an accessible trial.
Before launch: Supply the Signature BLL+ gene list (SNV and InDel genes, fusion and rearrangement genes, and any copy-number or cytogenetic markers). Add it to _build/genes.py with a count assertion, then render it with genepanel() exactly as the solid-tumour pages do.
The timing question
When molecular information matters in blood cancer
Acute leukaemia moves faster than most solid tumours, so the order in which results arrive matters as much as what they say.
- At presentation, within hoursRuling out acute promyelocytic leukaemia is the immediate priority in a myeloid presentation, because it is a treatable emergency with a specific treatment.
- Within daysThe findings that change the first cycle. In myeloid disease these are reported ahead of the fuller panel rather than held back with it.
- Within one to two weeksFull risk classification, combining cytogenetics with the molecular findings, which informs the transplant discussion.
- Before a related donor is chosenGermline predisposition should be excluded, because an affected sibling would be an unsuitable donor. This is far easier to ask before transplant than after.
- Through treatmentMeasurable residual disease monitoring, measured against the baseline this test establishes.
- At relapseRepeat profiling, because the molecular picture commonly changes and targets that were absent at diagnosis can appear.
How it works
- Step 1Sample
Blood or bone marrow, collected by a qualified professional.
- Step 2Sequencing
An accredited laboratory reads the leukaemia’s DNA and fusions.
- Step 3Engine
Annotation, subtype assignment and matching to therapies and trials.
- Step 4KPCIRC sign-out
A tumour board authors and signs the decision.
Take these to your team
Questions worth raising
When a decision is being made
Questions worth raising with a treating team.
- Has the lineage been established, and is the panel being used the right one for it?
- In a myeloid presentation, has acute promyelocytic leukaemia been ruled out as an immediate priority?
- Will the findings that change the first cycle arrive before that cycle starts?
- Has full risk classification used cytogenetics and molecular findings together?
- If a sibling donor is being considered, has germline predisposition been excluded first?
At relapse or resistance
The molecular picture at diagnosis is not always the molecular picture later.
- Has the disease been re-profiled at relapse, rather than the diagnostic result being carried forward?
- Have surface markers been reassessed, since target loss is a recognised resistance mechanism to immune-based treatment?
- Has measurable residual disease been used to detect relapse earlier than morphology would?
Where it fits
The result feeds Blueprint Care in the same way as a solid-tumour Signature test: a ranked decision, contraindications, matched trials, access mapping and a resistance plan, all signed by KPCIRC.
It also establishes the molecular baseline that Sentinel Blood and Clear Blood track over time.
The other Signature B panel
Being clear about our limits
What we do and do not do
What we DO
- Profile the drivers, fusions and cytogenetic risk markers of the leukaemia
- Support risk stratification alongside morphology, flow cytometry and cytogenetics
- Feed a tumour-board-signed Blueprint Care decision
- Establish a baseline that later monitoring can be measured against
- State turnaround explicitly, because in acute leukaemia timing is part of the result
What we DON’T do
- Diagnose leukaemia on its own, morphology and flow cytometry remain essential
- Replace your haematologist’s assessment or scheduled testing
- Detect changes in genes outside the panel
- Guarantee a drug, its approval, cover, or that it will work
Plain-language glossary (10 terms)
| Term | What it means |
|---|---|
| Blast | An immature blood cell. Leukaemia is driven by blasts that fail to mature. |
| ALL | Acute lymphoblastic leukaemia, arising from lymphoid precursor cells. |
| AML | Acute myeloid leukaemia, arising from myeloid precursor cells. |
| Lineage | Whether the leukaemia arises from the myeloid or the lymphoid line. The first question asked. |
| Karyotype | The chromosome picture of the leukaemia, long used to assign risk. |
| Fusion transcript | Two genes joined abnormally, a common and highly informative driver in leukaemia. |
| MRD | Measurable residual disease, the small amount left after treatment that predicts relapse. |
| Risk stratification | Sorting patients into risk groups so treatment intensity matches need. |
| Mixed phenotype | A leukaemia carrying features of both lineages. It needs a panel that reads both. |
| Clonality | Whether a population of cells descends from one ancestor. Used to confirm and to track disease. |
Important information and regulatory status
Signature BLL+ is a genomic (DNA-based) test for use by qualified healthcare professionals. It supports clinical judgement, it does not replace it, and it must be read alongside your full clinical history and applicable guidelines.
- A result is not a diagnosis and does not by itself decide treatment.
- A “not detected” result does not rule out cancer or a genetic change.
- Not all cancers release enough DNA into blood to be detected.
- We cannot guarantee that a medicine will be available, approved, covered or effective.
- Collection kits are for qualified phlebotomists. They are not for self-testing.
- Confirmatory testing may be required.
Regulatory status (India). Registration of our genomic tests as in-vitro diagnostic (IVD) medical devices with CDSCO is in progress, with the IVD class pending. Sequencing and variant calling are done by an accredited laboratory partner holding NABL (ISO 15189), CAP and CLIA accreditation, following ACMG/AMP/ASCO/CAP guidelines and a CE-IVD certified variant database. The OnKommon interpretation engine is provided for research and decision-support use. Marketing follows the Drugs and Magic Remedies (Objectionable Advertisements) Act, 1954.
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