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BCR-ABL IS (International Scale) Transcript fusion Quantification by Real Time PCR - Blood
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Molecular test quantifying BCR-ABL fusion gene transcript.
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BCR-ABL IS (International Scale) Transcript Fusion Quantification by Real Time PCR - Blood
- Why is it done?
- Detects and quantifies the BCR-ABL fusion gene transcript, which results from the Philadelphia chromosome translocation characteristic of chronic myeloid leukemia (CML)
- Used for initial diagnosis of CML to confirm the presence of the BCR-ABL fusion transcript
- Monitors treatment response and disease progression in patients undergoing tyrosine kinase inhibitor (TKI) therapy
- Assesses minimal residual disease (MRD) and helps guide treatment decisions and dosage adjustments
- Detects BCR-ABL transcripts in patients with acute lymphoblastic leukemia (ALL) with Philadelphia chromosome positivity
- Performed at baseline for newly diagnosed CML and regularly during follow-up (typically every 3 months during treatment)
- Normal Range
- Normal/Negative Result: BCR-ABL transcript not detected or <0.001% on International Scale (IS). This represents a negative or undetectable result.
- Units of Measurement: Percentage (%) on International Scale (IS); also expressed as log reduction from baseline (log10 reduction) or copies per microliter
- Interpretation Guide: BCR-ABL IS <0.1% represents major molecular response (MMR); <0.0032% represents deep molecular response (DMR); undetectable BCR-ABL represents complete molecular response (CMR) or major molecular response (MMR) depending on assay sensitivity
- Reference Standard: The International Scale (IS) standardizes BCR-ABL expression to a common baseline (usually set at 100%) for comparison across laboratories and reporting systems; helps define molecular milestones in CML treatment response
- Interpretation
- Detectable BCR-ABL (>0.1% IS): Indicates active disease burden; in newly diagnosed CML, confirms diagnosis; in treated patients, suggests inadequate disease control or possible treatment resistance; requires evaluation for treatment failure and consideration of alternative or escalated therapy
- BCR-ABL 0.01% to 0.1% IS: Represents partial or suboptimal molecular response; falls between MMR and threshold for optimal response; warrants close monitoring and possible therapeutic intervention depending on timeline and trend
- BCR-ABL <0.1% IS (Major Molecular Response): Indicates significant disease reduction and favorable prognosis; represents at least 3-log reduction from baseline; associated with improved long-term outcomes and survival; generally considered optimal response to treatment
- BCR-ABL <0.0032% IS (Deep Molecular Response): Represents profound disease suppression; may be associated with treatment-free remission (TFR) eligibility; requires sustained achievement and is considered excellent treatment response
- Undetectable BCR-ABL (Complete Molecular Response): BCR-ABL transcript not detected; represents best achievable response; associated with extended survival; assay sensitivity determines interpretation (e.g., CMR4 indicates 4-log reduction below baseline)
- Rising BCR-ABL Levels: Increase of ≥0.5-log (3-fold) from nadir or confirmed increase suggests treatment failure, development of resistance mutations, or non-compliance; requires urgent investigation and possible therapy modification
- Factors Affecting Results: BCR-ABL type (p210, p190, p230) affects transcript detection; BCR-ABL kinase domain mutations may confer TKI resistance; assay sensitivity and specimen quality impact detection; time on therapy and adherence to treatment significantly influence levels
- Associated Organs
- Primary Organ Systems: Bone marrow (site of hematopoietic stem cells affected by BCR-ABL); blood/hematologic system; spleen (prone to enlargement in CML); liver (potential involvement in advanced disease)
- Primary Condition - Chronic Myeloid Leukemia (CML): Myeloproliferative neoplasm characterized by clonal expansion of BCR-ABL-positive hematopoietic stem cells; presents with Philadelphia chromosome translocation (9;22); three phases: chronic, accelerated, and blast crisis
- Associated Conditions: Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL); blast crisis (transformation to acute leukemia); secondary malignancies related to treatment; treatment resistance with acquired BCR-ABL kinase domain mutations
- Potential Complications of Abnormal Results: Disease progression to accelerated phase or blast crisis; development of TKI resistance requiring second or third-line therapy; splenomegaly with pain and splenic infarction; leukostasis causing cerebrovascular or pulmonary complications; infection and sepsis from severe leukopenia; bleeding complications; increased risk of thrombotic events; organ infiltration by leukemic cells
- Clinical Significance: BCR-ABL quantification is the gold standard for assessing disease burden and treatment efficacy in CML; directly impacts prognosis and guides therapeutic decisions; predicts long-term survival and progression-free survival; enables early detection of treatment failure
- Follow-up Tests
- BCR-ABL Kinase Domain Mutation Testing: Performed if BCR-ABL levels rise or remain elevated; identifies resistance mutations that guide selection of alternative TKI therapies
- Cytogenetic Analysis: Fluorescence in situ hybridization (FISH) or conventional cytogenetics at baseline and during follow-up to assess chromosomal response; detects additional cytogenetic abnormalities; performed less frequently with improved molecular monitoring
- Complete Blood Count (CBC): Monitors white blood cell count, hemoglobin, and platelet levels; assesses hematologic response to therapy; performed concurrently or shortly after BCR-ABL testing
- Bone Marrow Biopsy and Aspiration: Performed at baseline for assessment and if molecular relapse or loss of response suspected; evaluates morphology and confirms diagnosis; less frequently used with sensitive molecular monitoring
- Blood Chemistry Panel: Assesses liver and renal function to ensure tolerance of TKI therapy; measures electrolytes and glucose to detect treatment side effects
- Monitoring Frequency: Initial monthly BCR-ABL testing for first 3 months, then every 3 months if stable; more frequent monitoring (every 1-2 months) if levels suboptimal or rising; annual baseline cytogenetics; ongoing CBC and chemistry panels every 3-6 months during treatment
- Imaging Studies: Ultrasound or CT imaging of abdomen to assess splenomegaly and hepatomegaly if clinically indicated; chest imaging if respiratory symptoms present; PET-CT may be considered in advanced disease
- Additional Molecular Tests: BCR-ABL transcript type (p210, p190, p230) determination at baseline; digital PCR for ultra-sensitive detection in deep molecular response; next-generation sequencing (NGS) for comprehensive mutation analysis
- Fasting Required?
- Fasting Requirement: No
- Patient Preparation: No fasting is required for this blood test; patient may eat and drink normally; no specific dietary restrictions necessary
- Medication Considerations: Continue all prescribed tyrosine kinase inhibitors (TKI) and other medications as directed; do not discontinue TKI therapy prior to testing unless specifically instructed by physician; medication timing does not affect BCR-ABL quantification
- Specimen Collection: Peripheral blood collected by venipuncture into EDTA (lavender-top) or PAXgene tube depending on laboratory protocol; timing of collection relative to TKI dose should be consistent if possible; room temperature transport acceptable with most systems
- General Instructions: Arrive as scheduled for blood draw; bring insurance card and identification; inform phlebotomist of any bleeding disorders or anticoagulant use; remain seated or lie down for 5-10 minutes after venipuncture to prevent dizziness; maintain adequate hydration on day of test
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