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Chronic Myeloid Leukaemia

Chronic myeloid leukaemia (CML) is a blood cancer that begins in the bone marrow, where a genetic rearrangement called the Philadelphia chromosome causes abnormal white blood cells to multiply unchecked. It progresses through three phases: chronic (often manageable for years), accelerated, and blast crisis. Most people are diagnosed in the chronic phase, frequently after a routine blood test turns up an unexpectedly high white cell count.

Hydrea

Hydroxycarbamide

500mg

Hydroxycarbamide 500mg hard capsules, used in the management of chronic myeloid leukaemia, polycythaemia vera, thrombocythaemia and sickle cell anaemia.

From$2.17/ tabletView

Tasigna

Nilotinib

150 · 200mg

Nilotinib 150mg and 200mg hard capsules, used in the management of chronic myeloid leukaemia. A selective inhibitor of the Bcr-Abl tyrosine kinase.

From$12.75/ tabletView

Sprycel

Dasatinib

50mg

Dasatinib 50mg film-coated tablets, used in the management of chronic myeloid and acute lymphoblastic leukaemia. A BCR-ABL and SRC kinase inhibitor.

From$144.50/ bottleView

Gleevec

Imatinib

100 · 400mg

Imatinib 100mg and 400mg film-coated tablets, used in the management of chronic myeloid leukaemia and gastrointestinal stromal tumour. A kinase inhibitor.

From$3.89/ tabletView

Key points

  • A genetic rearrangement joining chromosomes 9 and 22 forms the BCR-ABL gene, whose overactive enzyme drives runaway cell growth.
  • The disease is not inherited and has no known lifestyle trigger, with most people diagnosed around their mid-forties.
  • Imatinib, the first BCR-ABL blocker developed, is usually tried first, with dasatinib or nilotinib held in reserve for progression or poor tolerance.
  • Ongoing PCR checks tracking the BCR-ABL gene marker confirm how well treatment is working and flag emerging resistance early.

What drives CML and who it affects

CML arises from a specific chromosomal swap between chromosomes 9 and 22, producing the BCR-ABL fusion gene. This gene encodes a constantly active tyrosine kinase that drives uncontrolled cell growth. It is not inherited and has no established lifestyle trigger. CML accounts for roughly 15% of all adult leukaemias, with incidence comparable to global averages; median age at diagnosis is the mid-forties.

Targeted treatment: tyrosine kinase inhibitors

The arrival of tyrosine kinase inhibitors (TKIs) transformed CML from a disease with poor long-term outcomes into one where sustained remission is realistic for most patients. First-line treatment typically starts with imatinib, the original BCR-ABL inhibitor. When imatinib is not tolerated or the disease progresses, second-generation agents dasatinib and nilotinib are used; both achieve deeper molecular responses in many patients. Hydroxycarbamide is occasionally used to control a very high white cell count while TKI therapy is being initiated.

Regular PCR monitoring of BCR-ABL transcript levels is essential to confirm response and detect early resistance. For broader context on cancer-support medicines, see oncology support.

Any new bone pain, fever, rapid weight loss, or a noticeably enlarging spleen warrants prompt medical review.

Further reading