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.
Medicines used to treat Chronic Myeloid Leukaemia
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 and occurs across Asia, with registries in India, South Korea, and Japan reporting incidence comparable to global averages; median age at diagnosis is the mid-forties, slightly younger than in Western cohorts.
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.