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Health condition · Clinically reviewed

Chronic myelogenous leukaemia, the Philadelphia chromosome, TKIs and life beyond diagnosis.

Once a fatal illness, CML is now a well-controlled chronic condition for most people. Tyrosine kinase inhibitors have rewritten the story.

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Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against ELN, BSH and peer-reviewed haematology sources you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK practice including newer TKIs, treatment-free remission and asciminib.

Key facts

CML at a glance.

The essentials, in plain English - what it is, how it presents and how it is treated in the UK today.

  • What it is

    A myeloproliferative neoplasm driven by the Philadelphia chromosome t(9;22) and the BCR-ABL1 fusion, which switches on tyrosine kinase activity.

  • Who it affects

    Most often diagnosed in the 60s, though any adult can be affected. Around 85% present in the chronic phase.

  • Phases

    Chronic (indolent, often incidental), accelerated (progressive), and blast crisis (over 20% blasts, behaves like acute leukaemia).

  • How it presents

    Often an incidental leucocytosis on a routine blood test. Some have fatigue, night sweats, weight loss, left upper quadrant pain or early satiety.

  • Foundation therapy

    Tyrosine kinase inhibitors have transformed CML from a fatal illness into a chronic condition with near-normal life expectancy.

  • Monitoring

    BCR-ABL1 quantitative PCR on the International Scale tracks response at 3, 6 and 12 months and beyond.

Why this guide matters

A modern, long-life disease.

CML is one of medicine’s great success stories. The three points below shape everything else on this page.

  • One driver, one target

    The Philadelphia chromosome creates BCR-ABL1. Tyrosine kinase inhibitors block that single driver and control the disease.

  • Molecular response is the currency

    BCR-ABL1 quantitative PCR at 3, 6 and 12 months sets the trajectory - hitting milestones matters.

  • Life on treatment, sometimes off it

    For many people, near-normal life expectancy is realistic. For a well-selected minority, treatment-free remission is possible.

How the diagnosis is made

From incidental blood test to a molecular plan.

The steps a UK haematology team will normally follow, in order - so you know what to expect and why.

  1. 01

    Assessing

    Full blood count and film

    Leucocytosis with a left-shifted myeloid picture, basophilia, eosinophilia and often thrombocytosis. The blood film is the first clue.

  2. 02

    Assessing

    History and examination

    Fatigue, night sweats, weight loss, left upper quadrant discomfort and early satiety. Splenomegaly is common on examination.

  3. 03

    Assessing

    Bone marrow biopsy

    Hypercellular marrow with myeloid predominance. Confirms phase and provides material for cytogenetics.

  4. 04

    Confirming

    Cytogenetics for Philadelphia

    Karyotyping for the pathognomonic t(9;22) translocation and any additional chromosomal abnormalities.

  5. 05

    Confirming

    BCR-ABL1 quantitative PCR

    The molecular signature, reported on the International Scale. This is the baseline for every future monitoring result.

  6. 06

    Confirming

    Risk stratification

    Sokal, Hasford or EUTOS scores at diagnosis help pick the most appropriate first-line TKI.

  7. 07

    Preparing

    Imaging and mutation testing

    Abdominal ultrasound to size the spleen. If treatment fails, TKI resistance mutation testing, including T315I, guides the next step.

Typical timeline: first blood test to a settled treatment plan in a matter of weeks.

Symptoms

What CML actually feels like.

Often nothing at first. When symptoms do appear, they tend to be constitutional or driven by an enlarged spleen.

  • Incidental leucocytosis

    Many people are diagnosed after a routine blood test shows a very high white cell count with no obvious infection.

  • Fatigue and night sweats

    Classic B symptoms - tiredness, drenching night sweats and unintentional weight loss.

  • Left upper quadrant discomfort

    Splenomegaly causes a dragging pain under the left ribs and early satiety with meals.

  • Bone pain

    Aching bones, particularly the sternum, can reflect marrow expansion.

  • Hyperviscosity features

    Very high white cell counts can cause headaches, blurred vision, retinal haemorrhages and, rarely, priapism.

  • Basophilia on the film

    A rise in basophils is a strong pointer to CML and should prompt molecular testing.

  • Chronic phase presentation

    About 85% of people are in chronic phase at diagnosis - stable, treatable and often symptom-light.

  • Red flag - blast crisis

    Bruising, bleeding, infections and rapid decline suggest transformation to blast crisis and need urgent haematology input.

Treatment

How CML is treated in the UK.

A TKI first, matched to the person and their risk profile - with molecular monitoring shaping every decision that follows.

  • Imatinib (Glivec)

    First-generation TKI at 400 mg once daily. Well established, generic and the workhorse first-line option for standard-risk chronic phase disease.

  • Dasatinib (Sprycel)

    Second-generation TKI at 100 mg once daily. Deeper and faster molecular responses, with a risk of pleural effusion and pulmonary hypertension.

  • Nilotinib (Tasigna)

    Second-generation TKI at 300 mg twice daily. Fast responses but a risk of arterial vascular events and metabolic side effects.

  • Bosutinib (Bosulif)

    Second-generation TKI at 400 mg once daily first line. GI side effects are common; hepatic monitoring is required.

  • Ponatinib and asciminib

    Ponatinib covers the T315I mutation; asciminib (Scemblix) is a novel STAMP inhibitor approved in later lines and moving earlier.

  • Molecular monitoring

    Milestones: under 10% BCR-ABL1 IS at 3 months, under 1% at 6 months, under 0.1% at 12 months (major molecular response).

  • Treatment-free remission

    Carefully selected patients with sustained deep molecular response over two years can trial stopping TKI, with close monitoring.

  • Allogeneic stem cell transplant

    Reserved for TKI failure, blast crisis or younger patients where other options are exhausted. Specialist decision.

Supportive care

Hydroxycarbamide can be used at diagnosis to bring the white cell count down while awaiting molecular confirmation. Leukapheresis is reserved for symptomatic hyperleukocytosis. Allopurinol reduces the risk of tumour lysis when treatment starts. Blast crisis is managed with TKI plus intensive AML-type or ALL-type chemotherapy and allogeneic stem cell transplant where suitable. Care is coordinated by a haematology MDT with a clinical nurse specialist, and Blood Cancer UK and Leukaemia Care offer excellent patient support.

What this guide is based on

The sources behind every claim on this page.

European and UK haematology guidance and specialist charity information, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your haematology team knows your bloods, your history and your goals. They can tell you which parts of this guide apply to you.

  • European LeukemiaNet (ELN). Recommendations for treating chronic myeloid leukaemia.

  • British Society for Haematology (BSH). Guidelines on the management of chronic myeloid leukaemia.

  • NICE. Technology appraisals on imatinib, dasatinib, nilotinib, bosutinib, ponatinib and asciminib.

  • Blood Cancer UK and Leukaemia Care. Patient information on CML and living with a TKI.

Red flags

When CML needs urgent attention.

Most CML is managed calmly and slowly. These are the situations that aren’t - and where the haematology team needs to know today.

  • Blast crisis

    Rapid rise in blasts, cytopenias, bruising or infection - behaves like acute leukaemia and needs urgent inpatient haematology care.

  • Hyperviscosity

    Priapism, visual loss, focal neurology or breathlessness with very high white cell counts is an emergency needing leukapheresis.

  • Tumour lysis syndrome

    Metabolic derangement at the start of treatment - needs hydration, allopurinol or rasburicase and biochemical monitoring.

  • Pleural effusion (dasatinib)

    Progressive breathlessness or cough on dasatinib should trigger a chest review and dose reassessment.

  • Arterial events (nilotinib, ponatinib)

    Chest pain, stroke symptoms or claudication need urgent assessment and cardiovascular risk review.

  • Hepatotoxicity and pancreatitis

    Abdominal pain, jaundice or deranged liver enzymes on any TKI should prompt review and possible switch.

  • Suspected pregnancy on TKI

    Most TKIs are teratogenic - contact the haematology team immediately for planning and specialist counselling.

  • Missed doses and loss of response

    Adherence drives outcome. Rising BCR-ABL1 or missed milestones warrants a mutation screen and TKI switch.

  • Severe cytopenias

    Symptomatic anaemia, bleeding or febrile neutropenia needs same-day haematology input and TKI dose review.

Living with it

A long-term partnership with a specialist team.

Four things make the biggest difference day to day - adherence, monitoring, support and planning for the life you want alongside treatment.

A quiet reminder

Consistency beats intensity, every time.

A daily tablet, taken faithfully, is doing quiet, powerful work. Missed doses undo it.

  1. 01 Adherence

    Take it, every day

    TKI response depends on consistent daily dosing. Even short breaks can undo months of progress.

  2. 02 Monitor

    Know your PCR number

    Ask for your BCR-ABL1 IS at each visit. It is the single most useful number in CML.

  3. 03 Support

    Lean on the specialist team

    Your clinical nurse specialist, Blood Cancer UK and Leukaemia Care are there for practical and emotional support.

  4. 04 Life plan

    Fertility, pregnancy and TFR

    Family planning, work, travel and stopping treatment are all worth discussing early - not just at the end.

Frequently asked

Everything we get asked about CML.

Quick answers on diagnosis, TKIs, monitoring and treatment-free remission.

  • What is chronic myelogenous leukaemia?

    Also called chronic myeloid leukaemia, it is a myeloproliferative neoplasm caused by the Philadelphia chromosome, a translocation between chromosomes 9 and 22 that creates the BCR-ABL1 fusion gene. The abnormal protein switches on tyrosine kinase activity and drives uncontrolled production of mature and maturing myeloid cells.

  • How is CML diagnosed?

    Usually starting with a full blood count showing a very high white cell count with a left-shifted myeloid picture, basophilia and often thrombocytosis. Diagnosis is confirmed by bone marrow biopsy, cytogenetics for the Philadelphia chromosome and BCR-ABL1 quantitative PCR on the International Scale.

  • What are the phases of CML?

    Chronic phase (about 85% at diagnosis, often asymptomatic), accelerated phase (progressive with rising counts and additional cytogenetic changes) and blast crisis (over 20% blasts, behaving like acute leukaemia with a poorer prognosis).

  • How is CML treated?

    Tyrosine kinase inhibitors, or TKIs, are the foundation. First-line options include imatinib and the second-generation drugs dasatinib, nilotinib and bosutinib. Ponatinib covers the T315I mutation and asciminib is a newer STAMP inhibitor approved in later lines and moving earlier.

  • Can I ever stop treatment?

    Yes, for carefully selected people. Treatment-free remission is offered when someone has been in a sustained deep molecular response for at least two years, with the STIM and EURO-SKI trials showing that around 40 to 60% remain treatment-free after stopping, with close molecular monitoring.

  • Is CML curable?

    For most people TKIs turn CML into a well-controlled long-term condition with a near-normal life expectancy rather than a curable illness. Allogeneic stem cell transplant is the only established curative option and is reserved for TKI failure, blast crisis or selected younger patients.

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