Leukaemia
A group of cancers of blood-forming cells — acute (AML/ALL) and chronic (CML/CLL) types with very different prognoses.
Overview
Leukaemias arise from malignant proliferation of haematopoietic precursors. Acute leukaemias (AML, ALL) progress over weeks and need urgent treatment. Chronic leukaemias (CML, CLL) often progress over years. Modern targeted therapies (TKIs in CML; BTK and BCL2 inhibitors in CLL; FLT3, IDH inhibitors in AML) have transformed survival.
Symptoms
- • Fatigue and pallor from anaemia
- • Recurrent infection from neutropenia
- • Easy bruising, petechiae, mucosal bleeding
- • Bone pain (especially in children with ALL)
- • Lymphadenopathy, hepatosplenomegaly (CLL, CML)
- • B-symptoms: weight loss, night sweats, fever
Risk factors
- • Age (AML, CLL increase with age; ALL peaks in children)
- • Family history
- • Previous cancer treatment
- • Myelodysplastic syndromes
Causes
- • Acquired somatic mutations in haematopoietic stem cells
- • Prior chemotherapy/radiotherapy (therapy-related AML)
- • Inherited syndromes: Down syndrome, Fanconi anaemia, Li-Fraumeni
- • Benzene, ionising radiation, smoking (AML)
🚨 Red flags — seek urgent care
- • New petechiae, bleeding gums or epistaxis with low platelets
- • Febrile neutropenia — emergency, start antibiotics within 1 hour
- • Tumour lysis: AKI, hyperkalaemia, hyperphosphataemia
- • Hyperleukocytosis with neurological or pulmonary symptoms — leukostasis emergency
When to seek care
- • Unexplained bruising, persistent fever, drenching night sweats
- • Suspected leukaemia is a same-day haematology referral
- • Any fever in a known patient on chemotherapy — A&E immediately
Diagnosis
- • FBC and blood film — blasts, lymphocytosis, anaemia, thrombocytopenia
- • Bone marrow aspirate, trephine biopsy and flow cytometry
- • Cytogenetics and molecular: BCR-ABL (CML), FLT3/NPM1/IDH (AML), IGHV/TP53 (CLL), Philadelphia (ALL)
- • Lumbar puncture in ALL for CNS staging
- • Imaging for nodal/organ involvement
Treatment
- • CML: tyrosine kinase inhibitor (imatinib, dasatinib, nilotinib) — most achieve normal life expectancy
- • CLL: watch-and-wait if asymptomatic; BTK inhibitor (ibrutinib, acalabrutinib), venetoclax + obinutuzumab when treatment indicated
- • AML: intensive induction (7+3) ± targeted agents; allogeneic stem-cell transplant for high-risk disease
- • ALL: multi-phase chemotherapy with CNS prophylaxis; immunotherapy (blinatumomab, inotuzumab) and CAR-T for relapse
- • Supportive: blood products, antimicrobials, growth factors, tumour lysis prophylaxis
Prevention
- • Avoid benzene and unnecessary radiation
- • Stop smoking
- • No effective screening — early symptom recognition is key
Complications
- • Febrile neutropenia and sepsis
- • Tumour lysis syndrome
- • Disseminated intravascular coagulation (especially APL)
- • Treatment toxicity: cardiotoxicity, infertility, secondary malignancy
- • Graft-versus-host disease after transplant
Prognosis
Highly variable: CML on TKI — near-normal life expectancy; childhood ALL — ~90% cure; AML — 5-year survival ~30% (much higher in younger patients with favourable genetics).
Education & self-care
Leukaemias vary enormously. Specialist haematology assessment classifies the subtype and tailors a treatment plan with very different goals.
Frequently asked questions
Is leukaemia inherited?
Most cases are sporadic. A small number occur within familial cancer syndromes.
Will I need a bone marrow transplant?
Only for selected high-risk acute leukaemias or relapsed disease — not most CML or CLL.
Can leukaemia be cured?
Many can — especially childhood ALL, CML on TKIs, and selected AML/lymphoid cancers after transplant.