Leukemia

What leukemia actually is

Your bone marrow — the spongy tissue inside your bones — is a factory. Every day, it produces billions of new blood cells: red cells to carry oxygen, white cells to fight infection, and platelets to stop bleeding. In leukemia, one type of these cells starts to multiply abnormally and crowds out the rest. The crowded-out cells can no longer do their job, and that's where most of the symptoms come from.

Leukemias are grouped by two questions: how quickly they grow (acute vs chronic) and which cell line is affected (myeloid vs lymphoid). That gives us four main types.

The four main types — at a glance

How leukemia tends to present

Acute leukemias come on over weeks; chronic ones may simmer quietly for years. The symptoms reflect what's failing in the bone marrow:

• Tiredness, breathlessness, pale skin — from low red cells (anaemia).
• Frequent or unusually severe infections — from low or dysfunctional white cells.
• Easy bruising, nosebleeds, gum bleeding, tiny red spots on the skin — from low platelets.
• Bone or joint aches — especially in children with ALL.
• Swollen lymph nodes, enlarged spleen, fullness in the belly — more typical of CLL and CML.
• Fevers, night sweats, weight loss — possible across all types.

None of these symptoms means leukemia by itself. They mean: get a blood test.

"When a patient walks in worried, the first thing I do is reach for the CBC. Most of the time it reassures us. When it doesn't, the next steps are very well mapped out — and we walk them together."

How we diagnose leukemia

The diagnostic path is methodical. Each step answers a specific question.

1. Complete Blood Count (CBC) with differential. The starting point. It tells us how many of each cell type are circulating, and whether abnormal forms are visible.
2. Peripheral blood smear. A drop of blood under the microscope. An experienced eye can often suggest the type within minutes.
3. Bone marrow aspirate and biopsy. A small sample from the back of the hip bone. This confirms the diagnosis, tells us what percentage of the marrow is involved, and provides material for the next tests. Read what the procedure is like →
4. Flow cytometry / immunophenotyping. Identifies the precise lineage of the leukemic cells — myeloid vs lymphoid, B-cell vs T-cell.
5. Cytogenetics and FISH. Looks at the chromosomes of the leukemic cells. Specific changes (like the Philadelphia chromosome in CML, or 17p deletion in CLL) change both prognosis and treatment.
6. Molecular tests (PCR, next-generation sequencing). Hunts for specific gene mutations — FLT3, NPM1, IDH1/2 in AML; BCR-ABL in CML; IGHV status in CLL — that increasingly guide targeted therapy.
7. Lumbar puncture, in ALL and some AML, to check whether leukemic cells have reached the fluid around the brain.

Treatment — different for every type

AML

For fit adults, treatment classically follows two phases: induction (a week of intensive intravenous chemotherapy in hospital, designed to clear the marrow of leukemic cells) followed by consolidation (further cycles, sometimes a stem cell transplant, to keep it gone). For older or less fit patients, gentler outpatient regimens — venetoclax with azacitidine, for example — have transformed outcomes. Targeted drugs against FLT3 and IDH mutations are now part of routine care.

ALL

Treatment is longer than AML — typically two to three years — and given in phases: induction, consolidation, CNS-directed therapy (to protect the brain), and a long maintenance phase. For Philadelphia-positive ALL, a TKI is added. Children with ALL have cure rates above 85%; adults below 40 often do very well too; older adults are treated with carefully adapted regimens.

CML

CML is the textbook success story of modern oncology. A class of drugs called tyrosine kinase inhibitors (TKIs) — imatinib, nilotinib, dasatinib, bosutinib — taken as one tablet a day, shuts down the abnormal protein driving the disease. Most patients reach deep, durable remission and live a normal lifespan. We monitor with periodic PCR tests on the blood. Some patients who reach a sustained deep response may even attempt stopping the drug under supervision.

CLL

Many CLL patients need no treatment at all — a strategy called watch and wait, which feels strange but is genuinely the right answer when the disease is stable. Treating too early shortens neither survival nor symptoms. When treatment is needed, the modern menu is excellent: BTK inhibitors (ibrutinib, acalabrutinib, zanubrutinib), the BCL2 inhibitor venetoclax with obinutuzumab, and selective use of chemo-immunotherapy. Chemotherapy alone is rarely the first choice now.

What outcomes can realistically look like

Outlook in leukemia varies more by subtype than perhaps any other cancer. Honest examples:

Daily life during and after treatment

Acute leukemia treatment is demanding — there are weeks of being more vulnerable to infection, days of feeling unwell, and a need for someone trustworthy at home. Chronic leukemia treatment, by contrast, is often a single daily tablet with periodic blood tests; most patients work, travel and live fully. We'll be honest with you upfront about which path you're on, and we'll plan together — work, family, fasting during Ramadan, travel, fertility if relevant — so that life doesn't simply pause for treatment.

What to bring to your first visit

• Every blood test you have, even old ones — trends over time tell a story.
• Any bone marrow, flow cytometry, cytogenetic or molecular reports.
• A list of current medications and any allergies.
• A family member or close friend — two pairs of ears are better than one.