📋 Key Information Summary
- Leukaemia is a clonal malignancy of haematopoietic cells classified by lineage (myeloid vs lymphoid) and acuity (acute vs chronic)
- Acute leukaemias (AML, ALL) present with rapidly progressive cytopenias due to bone marrow failure; chronic leukaemias (CML, CLL) are often indolent and discovered incidentally
- AML is the most common acute leukaemia in adults (median age 68 years); ALL predominates in children aged 2–5 years
- CML is characterised by the Philadelphia chromosome t(9;22) BCR-ABL1 and responds to tyrosine kinase inhibitors (TKIs)
- CLL is the most common leukaemia in Western adults (median age 72 years) and many patients require observation only at diagnosis
- Full blood count with peripheral blood film is the essential first investigation — blast cells suggest acute leukaemia; left shift and basophilia suggest CML
- Bone marrow aspirate and trephine biopsy with immunophenotyping, cytogenetics, and molecular studies are required for definitive diagnosis and risk stratification
- Acute leukaemia presenting with hyperleukocytosis (>100 × 10⁹/L) is an oncological emergency requiring urgent leukapheresis and rasburicase
- Treatment of AML centres on intensive induction chemotherapy (7+3 regimen) in fit patients; hypomethylating agents for those unfit for intensive therapy
- ALL treatment involves multi-agent induction, CNS prophylaxis, consolidation, and maintenance; paediatric-inspired regimens improve outcomes in adults up to age 40
- CML treatment is with TKIs (imatinib first-line on PBS); deep molecular response may allow treatment-free remission trials
- CLL management ranges from watch-and-wait for early-stage disease to targeted agents (BTK inhibitors, venetoclax combinations) for symptomatic disease
- Allogeneic haematopoietic stem cell transplant remains curative for high-risk AML, relapsed ALL, and accelerated/blast-phase CML
- Aboriginal and Torres Strait Islander Australians experience higher leukaemia incidence and poorer outcomes; culturally safe care and equitable access to transplant are critical
Introduction & Australian Epidemiology
Leukaemia encompasses a heterogeneous group of haematological malignancies arising from the clonal proliferation of haematopoietic cells in the bone marrow. Classification is determined by both the cell lineage affected (myeloid or lymphoid) and the tempo of disease (acute or chronic). The four principal subtypes — acute myeloid leukaemia (AML), acute lymphoblastic leukaemia (ALL), chronic myeloid leukaemia (CML), and chronic lymphocytic leukaemia (CLL) — differ markedly in their epidemiology, clinical presentation, molecular pathogenesis, and therapeutic approach.
In Australia, leukaemia accounts for approximately 4,500 new cancer diagnoses annually, representing roughly 3% of all cancers. AML is the most common acute leukaemia in adults with an age-standardised incidence of approximately 3.5 per 100,000, predominantly affecting individuals over 60 years of age. ALL has a bimodal distribution with a peak incidence in children aged 2–5 years (approximately 3.8 per 100,000) and a second smaller peak in adults over 60 years. CML has an incidence of approximately 1.6 per 100,000 with a median age at diagnosis of 55–60 years. CLL is the most prevalent leukaemia in Western countries, with an Australian incidence of approximately 5.5 per 100,000 in individuals over 70 years and a male predominance of approximately 1.7:1.
Australian Data (AIHW 2023): Five-year relative survival for all leukaemias combined has improved from 42% (1990–1994) to approximately 62% (2015–2019), driven largely by TKI therapy in CML and improved ALL outcomes in paediatric patients. AML survival remains lower at 27–30% due to the predominance of elderly patients with adverse-risk disease.
Risk factors include ionising radiation, benzene exposure, prior chemotherapy (particularly alkylating agents and topoisomerase II inhibitors), myelodysplastic syndromes, Down syndrome (increased AML/ALL risk), and certain hereditary conditions (Li-Fraumeni syndrome, Fanconi anaemia). Unlike many solid tumours, leukaemia rarely forms a discrete mass; instead, the malignant clone infiltrates the bone marrow, displaces normal haematopoiesis, and often spills into the peripheral blood.
Classification & Comparison
The World Health Organization (WHO) 5th edition classification (2022) and the International Consensus Classification (ICC) 2022 provide the current frameworks for leukaemia subtyping. Both systems integrate morphology, immunophenotyping, cytogenetics, and molecular genetics to define biologically and clinically meaningful entities.
| Feature | AML | ALL | CML | CLL |
|---|---|---|---|---|
| Lineage | Myeloid | B-lymphoid (75%) or T-lymphoid (25%) | Myeloid (multipotent stem cell) | B-lymphoid |
| Acuity | Acute — rapid progression | Acute — rapid progression | Chronic (can transform) | Chronic — indolent |
| Median age at diagnosis | 68 years | 17 years (bimodal) | 55–60 years | 72 years |
| Australian incidence | ~1,100/year | ~400/year | ~330/year | ~1,500/year |
| Key molecular hallmark | Heterogeneous (FLT3, NPM1, TP53, RUNX1) | Philadelphia chromosome (25% adults), hyperdiploidy, ETV6-RUNX1 | BCR-ABL1 t(9;22) | del(13q), del(11q), del(17p), TP53 mutation |
| Blast threshold | ≥20% BM blasts (WHO); ≥10% with defining genetic abnormality | ≥20% BM or peripheral blood lymphoblasts | <10% in chronic phase | Small mature lymphocytes; blasts not increased |
| Philadelphia chromosome | ~2–3% of cases (treated as Ph+ AML) | ~25% adults, ~3% paediatric | ~95% — defining feature | Rare |
| Curative potential | Yes (intensive chemo ± HSCT) | Yes (85–90% paediatric; 40–50% adult) | Functional cure (TKI ± TFR) | Generally no (exception: allo-HSCT) |
WHO 5th Edition Classification of AML (Selected Entities)
The WHO 2022 classification separates AML into defined genetic entities and an "NOS" category. The following are clinically significant groupings relevant to Australian practice:
| Category | Key Abnormalities | Prognosis |
|---|---|---|
| AML with t(8;21) RUNX1-RUNX1T1 | Core-binding factor | Favourable |
| AML with inv(16) CBFB-MYH11 | Core-binding factor | Favourable |
| APL with PML-RARA | t(15;17) | Favourable (with ATRA + ATO) |
| AML with NPM1 mutation | NPM1 | Favourable (if no FLT3-ITD high ratio) |
| AML with FLT3-ITD | FLT3 internal tandem duplication | Adverse (improved with midostaurin/gilteritinib) |
| AML with TP53 mutation / complex karyotype | TP53, ≥3 cytogenetic abnormalities | Adverse |
| AML with KMT2A rearrangement | 11q23 rearrangements | Adverse |
| AML, NOS (≥20% blasts) | No defining genetic abnormality | Variable by cytogenetics |
Acute vs Chronic Leukaemia Features
The distinction between acute and chronic leukaemia is fundamental to clinical assessment, urgency of investigation, and therapeutic decision-making. Acute leukaemias are characterised by the rapid accumulation of immature blast cells in the bone marrow, leading to marrow failure, while chronic leukaemias involve the accumulation of more mature-appearing cells with an indolent clinical course, though transformation to an aggressive phase is possible.
Acute
AML / ALL
Blast cells ≥20% in bone marrow. Rapid onset over weeks. Bone marrow failure causing anaemia, thrombocytopenia, neutropenia. Circulating blasts often visible on peripheral film. Tumour lysis risk. Presents with fatigue, bleeding, infection, bone pain (paediatric ALL). Untreated survival measured in weeks to months.
Setting: Urgent haematology referral, often same-day admission
Chronic
CML / CLL
Mature-appearing cells accumulate. Insidious onset over months to years. Often asymptomatic at diagnosis. Incidental finding on routine FBC. CML: elevated WCC with basophilia and left shift. CLL: lymphocytosis with smudge cells. May remain stable without treatment for prolonged periods.
Setting: Outpatient haematology assessment within 1–2 weeks
Clinical Presentation Comparison
| Feature | Acute (AML/ALL) | Chronic (CML/CLL) |
|---|---|---|
| Onset | Days to weeks | Weeks to years |
| Symptoms at diagnosis | Usually symptomatic | Often asymptomatic |
| WCC at presentation | Variable — low, normal, or very high | Usually elevated |
| Blast cells on film | Present (≥20% in marrow) | Absent (chronic phase) |
| Cytopenias | Prominent (anaemia, thrombocytopenia, neutropenia) | Mild or absent initially |
| Hepatosplenomegaly | Variable | Common (CML splenomegaly; CLL lymphadenopathy) |
| Gum hypertrophy | AML with monocytic differentiation | Not typical |
| Skin infiltration | AML (leukaemia cutis) | Rare |
| CNS involvement | ALL more common (cranial nerve palsies) | Rare |
| Transformation risk | N/A — already acute | CML → blast crisis; CLL → Richter transformation |
Emergency presentations in acute leukaemia: Hyperleukocytosis (>100 × 10⁹/L) can cause leucostasis — a medical emergency presenting with respiratory distress, altered consciousness, or priapism. Acute promyelocytic leukaemia (APL) presents with life-threatening disseminated intravascular coagulation (DIC). Tumour lysis syndrome can occur spontaneously or after initiating treatment. These presentations require immediate haematology consultation.
Investigations (FBC, Bone Marrow Biopsy)
Initial Investigation Pathway
1
Full Blood Count & Peripheral Blood Film
Essential first-line investigation. Quantifies cytopenias, identifies circulating blast cells, and assesses morphological features (Auer rods in AML, smudge cells in CLL). MBS Item 65070.
2
Biochemistry Panel
U&E, LFTs, LDH, urate, phosphate, calcium, coagulation (PT/APTT/fibrinogen — critical in suspected APL). Tumour lysis assessment. MBS Item 66512.
3
Urgent Haematology Referral
Same-day referral if blasts seen on peripheral film, WCC >50 × 10⁹/L, or pancytopenia with clinical concern for acute leukaemia.
4
Bone Marrow Aspirate & Trephine Biopsy
Definitive diagnostic test. Performed under procedural sedation or local anaesthesia at the posterior iliac crest. Aspirate for morphology, cytochemistry, immunophenotyping, cytogenetics (FISH/karyotype), and molecular studies (NGS panel). Trephine for architecture assessment. MBS Item 30445.
Investigation Details by Leukaemia Type
Essential
Full Blood Count with Differential
Available at all Australian laboratories. MBS Item 65070. Anaemia, thrombocytopenia, elevated WCC with or without circulating blasts. In CLL, absolute lymphocyte count >5 × 10⁹/L sustained is diagnostic.
Essential
Peripheral Blood Film Morphology
Blast cells with fine chromatin and nucleoli in acute leukaemia. Auer rods (AML-specific). Smudge cells (CLL). Basophilia and left shift (CML). Atypical lymphocytes.
Essential
Bone Marrow Aspirate & Trephine
Blast percentage, cellularity, dysplastic features, fibrosis grading. MBS Item 30445. Core diagnostic test for all acute leukaemias and uncertain chronic cases.
Available
Flow Cytometry (Immunophenotyping)
Available at major metropolitan centres. Distinguishes myeloid (CD13+, CD33+, CD117+, MPO+) from lymphoid (B-ALL: CD19+, CD10+, CD22+; T-ALL: CD3+, CD7+). CLL immunophenotype: CD5+, CD19+, CD23+, CD200+, dim CD20, dim surface immunoglobulin. Results within 24–48 hours.
Available
Cytogenetics (Conventional Karyotyping)
Metaphase cytogenetics from bone marrow. Critical for risk stratification. Requires viable dividing cells. Turnaround 7–14 days. Identifies t(8;21), inv(16), t(9;22), del(17p), complex karyotype.
Available
FISH (Fluorescence In Situ Hybridisation)
Targeted probe-based testing. Results within 48–72 hours. Used when rapid identification of key translocations is needed (e.g., PML-RARA in suspected APL, BCR-ABL1 in CML, MLL rearrangement).
Available
Molecular Genetics — NGS Panel
Available at reference laboratories (e.g., SA Pathology, Royal Melbourne Hospital). Detects mutations in NPM1, FLT3 (ITD and TKD), IDH1, IDH2, TP53, RUNX1, ASXL1, CEBPA, DNMT3A, KIT. Essential for ELN 2022 risk stratification in AML. Turnaround 7–21 days.
Available
BCR-ABL1 Quantitative PCR
Gold standard for CML diagnosis (qualitative) and monitoring (quantitative). MBS rebate available when performed at approved laboratories. Monitored every 3 months on TKI therapy using International Scale.
Available
Lumbar Puncture with CSF Cytology
Mandatory in ALL (CNS involvement present in 5–10% at diagnosis). Consider in AML with neurological symptoms. Intrathecal chemotherapy administered concurrently if CNS disease confirmed.
Available
CT Chest/Abdomen/Pelvis
Assesses organomegaly, lymphadenopathy (particularly in CLL and ALL), and baseline organ assessment prior to chemotherapy. MBS Item 56807.
Available
Echocardiography
Baseline cardiac assessment (LVEF) prior to anthracycline-containing induction regimens (standard in AML and ALL). MBS Item 55114.
Referral
HLA Typing & Donor Search
Australian Bone Marrow Donor Registry (ABMDR) and international registries. Indicated for AML in first complete remission with intermediate or adverse risk, relapsed ALL, and CML in accelerated/blast phase. Results 2–6 weeks for unrelated donor search.
Diagnostic Criteria Summary
| Leukaemia | WHO Diagnostic Criteria (Simplified) |
|---|---|
| AML | ≥20% myeloid blasts in bone marrow or peripheral blood (exception: APL and AML with defining genetic abnormalities are diagnosed irrespective of blast count) |
| ALL | ≥20% lymphoblasts in bone marrow or peripheral blood with immunophenotypic confirmation of B- or T-lymphoid lineage |
| CML | Philadelphia chromosome t(9;22) BCR-ABL1 by cytogenetics, FISH, or PCR. Chronic phase: <10% blasts. Accelerated phase: 10–19% blasts or specific features. Blast phase: ≥20% blasts or extramedullary blast proliferation |
| CLL | Monoclonal B-lymphocyte count ≥5 × 10⁹/L sustained for ≥3 months with characteristic immunophenotype (CD5+, CD19+, CD23+, CD200+). Small lymphocytic lymphoma (SLL) is the tissue-based equivalent. |
Treatment Principles & Prognosis
Treatment of leukaemia is highly subtype-specific and increasingly guided by molecular risk stratification. General principles apply across all subtypes: confirm diagnosis with adequate tissue, perform comprehensive risk assessment before commencing therapy, and ensure treatment occurs at centres with specialist haematology, blood bank, and supportive care infrastructure.
Acute Myeloid Leukaemia (AML)
Intensive Induction — "7+3" Regimen
Cytarabine (Ara-C)
Cytosar® · Generic · Antimetabolite
Adult dose
100 mg/m²/day continuous IV infusion for 7 days (induction)
High-dose consolidation
3 g/m² IV BD on days 1, 3, 5 (for 3–4 cycles in favourable-risk AML)
Renal adjustment
No specific dose reduction required; monitor closely if CrCl <30 mL/min
PBS status
✔ PBS General Benefit
Daunorubicin
Generic · Anthracycline
Adult dose
60–90 mg/m² IV on days 1–3 (with cytarabine for 7+3 induction)
Key toxicity
Cardiotoxicity — cumulative lifetime dose limit ~550 mg/m². Baseline echo required.
PBS status
✔ PBS General Benefit
Midostaurin addition for FLT3-mutated AML: Patients aged 18–70 with FLT3-mutated AML should receive midostaurin 50 mg PO BD on days 8–21 of each induction and consolidation cycle. Midostaurin is available on PBS via the Life Saving Drugs Programme (LSDP) for this indication.
Venetoclax Combinations for Unfit/Unsuitable Patients
Venetoclax + Azacitidine
Venclexta® · BCL-2 inhibitor + Vidaza® · Hypomethylating agent
Dose
Venetoclax 400 mg PO daily (ramped up over 3–5 days) + azacitidine 75 mg/m² SC/IV days 1–7 of each 28-day cycle
Indication
Newly diagnosed AML in adults unfit for intensive chemotherapy
PBS status
Authority Required — venetoclax PBS-listed for AML in combination
Acute Lymphoblastic Leukaemia (ALL)
ALL treatment is among the most complex of all cancer regimens, comprising induction, consolidation/intensification, CNS prophylaxis, and maintenance phases over 2–3 years. Paediatric-inspired regimens (e.g., COG-based protocols) have demonstrated superior outcomes compared to adult-type regimens in adolescents and young adults (AYA) aged 15–40 years.
Dasatinib / Imatinib (Ph+ ALL)
Sprycel® / Glivec® · Tyrosine kinase inhibitors
Ph+ ALL dose
Dasatinib 100 mg PO daily or imatinib 600 mg PO daily in combination with ALL chemotherapy backbone
PBS status
✔ PBS General Benefit (imatinib); PBS Restricted Benefit (dasatinib)
Inotuzumab Ozogamicin
Besponsa® · Anti-CD22 antibody-drug conjugate
Indication
Relapsed/refractory B-ALL with CD22 expression
Dose
0.8 mg/m² IV day 1 (cycle 1); 0.5 mg/m² IV days 1 and 8 (subsequent cycles), 21-day cycles
PBS status
Authority Required (LSDP)
Chronic Myeloid Leukaemia (CML)
CML management has been revolutionised by tyrosine kinase inhibitors targeting BCR-ABL1. Imatinib (Glivec®) is the standard first-line agent, available as a PBS General Benefit. Second-generation TKIs (dasatinib, nilotinib) are used for suboptimal response or intolerance. Treatment-free remission (TFR) is a goal for patients achieving deep molecular response (DMR) sustained for ≥2 years.
Imatinib
Glivec® · BCR-ABL1 TKI (1st generation)
Adult dose (chronic phase)
400 mg PO once daily, with food
Monitoring
qPCR for BCR-ABL1 on International Scale every 3 months. MMR target: BCR-ABL1 <0.1% IS by 12 months.
Renal adjustment
Max 400 mg/day if CrCl 20–40 mL/min; avoid if CrCl <20 mL/min
PBS status
✔ PBS General Benefit
Chronic Lymphocytic Leukaemia (CLL)
CLL management has shifted from chemoimmunotherapy to targeted agents. The approach is determined by disease stage (Rai/Binet), molecular risk factors (IGHV mutation status, TP53/del17p), comorbidities, and patient preference. Watchful wait is appropriate for asymptomatic early-stage disease.
Venetoclax + Obinutuzumab
Venclexta® + Gazyva® · First-line CLL (fixed duration)
Dose
Venetoclax ramp-up over 5 weeks to 400 mg PO daily + obinutuzumab IV. Total treatment: 12 months (fixed duration)
Key risk
Tumour lysis syndrome — mandatory prophylaxis, dose ramp-up, hospital monitoring for first dose increase
PBS status
Authority Required
Ibrutinib
Imbruvica® · BTK inhibitor (continuous therapy)
Dose
420 mg PO once daily, continuous until progression or intolerance
Key toxicity
Atrial fibrillation, bleeding, hypertension. Avoid with concurrent anticoagulation where possible.
PBS status
Authority Required
Prognosis Summary
Favourable
Best outcomes
CML chronic phase on TKI (10-year OS ~80–85%). Paediatric ALL (5-year EFS 85–90%). AML with t(8;21) or inv(16) (5-year OS 60–70%). APL treated with ATRA + ATO (cure rate >90%). CLL with IGHV-mutated, no TP53 abnormality, Binet A.
Standard treatment protocols; cure achievable
Intermediate
Variable outcomes
AML with normal karyotype (risk depends on NPM1/FLT3 status). Adult ALL without Ph chromosome (5-year OS 40–50%). CML with suboptimal molecular response. CLL intermediate Rai/Binet stage.
Intensive treatment ± allogeneic HSCT consideration
Adverse
Poor prognosis
AML with complex karyotype, TP53 mutation, monosomal karyotype (5-year OS <15%). Ph+ ALL historically adverse (improved with TKI addition). CML in blast crisis. CLL with del(17p)/TP53 mutation.
Allogeneic HSCT if feasible; clinical trial enrolment recommended
Allogeneic Haematopoietic Stem Cell Transplant
Allogeneic HSCT remains a potentially curative option for high-risk and relapsed leukaemia. Indications include:
- AML in first complete remission with intermediate or adverse ELN 2022 risk (in patients medically fit for transplant)
- ALL in first complete remission with high-risk features (Ph+, MLL rearrangement, hypodiploidy, poor MRD response)
- CML in accelerated or blast phase, or with TKI resistance/failure
- Relapsed/refractory acute leukaemias achieving second remission
Australian transplant centres are located in all major capital cities (e.g., Royal Adelaide Hospital, Westmead Hospital Sydney, Royal Melbourne Hospital, Peter MacCallum Cancer Centre). Donor options include matched sibling, matched unrelated (ABMDR/international registry), haploidentical family donor, and cord blood. Transplant-related mortality ranges from 15–30% depending on conditioning intensity, patient age, and comorbidities.
Special Populations
Pregnancy
Acute leukaemia in pregnancy: Requires urgent multidisciplinary team including haematology, obstetrics, neonatology. Chemotherapy is generally safe in the second and third trimesters. ATRA is teratogenic — contraindicated in first trimester.
CML in pregnancy: TKIs are teratogenic. Imatinib classified D; dasatinib/nilotinib classified D. Interferon-alpha is the preferred agent during pregnancy if treatment is required. Hydroxyurea should be avoided.
CLL in pregnancy: Watchful waiting preferred if feasible. If treatment required, rituximab may be used in second/third trimester. Avoid chlorambucil and fludarabine.
Paediatrics
ALL dominates: ALL accounts for ~75% of paediatric leukaemias. Cure rate 85–90% with contemporary multi-agent protocols. Risk stratification uses NCI criteria, cytogenetics, and minimal residual disease (MRD).
Paediatric AML: Less common (~15–20% of paediatric leukaemias). Treated with intensive ADE (ara-c, daunorubicin, etoposide) induction. Allogeneic HSCT for high-risk disease.
Children's Cancer Trials: Australian children with ALL/AML should be enrolled on current ANZCHOG (Australian and New Zealand Children's Haematology/Oncology Group) clinical trials where available.
Elderly (≥70 years)
AML: Intensive chemotherapy associated with high early mortality in elderly patients. Venetoclax + azacitidine is the preferred first-line regimen for patients unfit for intensive induction.
CLL: Predominantly an older-age disease. Ibrutinib or venetoclax-obinutuzumab are well tolerated in elderly patients. Dose adjustment for renal impairment and drug interactions.
Comprehensive geriatric assessment: Should be performed prior to treatment decisions in patients ≥70 years with acute leukaemia.
Renal Impairment
Cytarabine: No dose reduction recommended but monitor for neurotoxicity (cerebellar) at high doses with renal impairment.
Allopurinol: Reduce dose to 100 mg/day if eGFR <20 mL/min. Rasburicase is preferred in tumour lysis prophylaxis with renal impairment (not affected by renal function).
Imatinib: Max 400 mg/day if CrCl 20–40 mL/min; avoid if CrCl <20 mL/min. Venetoclax: no dose adjustment but monitor closely.
Hepatic Impairment
Venetoclax: Avoid if severe hepatic impairment (Child-Pugh C). Dose reduction to 100 mg/day with moderate impairment.
Dasatinib: Increase starting dose with hepatic impairment is not recommended — use standard dose with monitoring.
Monitoring: LFTs at baseline and regularly during treatment. Hepatotoxicity is a known complication of many leukaemia therapies.
Immunocompromised
Infection risk: All patients receiving intensive chemotherapy are profoundly immunocompromised. Antimicrobial prophylaxis with fluoroquinolones, antifungals (posaconazole), and antivirals (aciclovir) is standard.
CLL-specific: Hypogammaglobulinaemia is common — IVIg replacement if recurrent infections with IgG <4 g/L.
Vaccination: Live vaccines contraindicated during treatment. Annual influenza and COVID-19 vaccination recommended. Pneumococcal vaccination (23vPPV) recommended for CLL patients.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
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