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Chronic-phase chronic myeloid leukaemia is the disease that imatinib turned from fatal into manageable: a daily pill blocks the BCR::ABL1 protein that drives it. Blood tests track the leukaemia gene to a millionth, newer pills such as asciminib (ASC4FIRST) reach deeper responses faster, and patients with years of undetectable disease can try stopping.
The Philadelphia chromosome, t(9;22), fuses BCR to ABL1 and produces a constitutively active tyrosine kinase; in chronic phase the marrow overproduces mature granulocytes with fewer than 10 percent blasts (WHO) and the disease is symptomless in half of patients, found on a routine blood count. Response is measured by quantitative PCR for BCR::ABL1 on the International Scale, with ELN milestones of 10 percent or less at three months, 1 percent or less at six months and 0.1 percent or less (major molecular response) at twelve months; failure to reach them prompts kinase domain mutation testing and a switch of drug.
IRIS (2003) randomised 1,106 newly diagnosed patients to imatinib or interferon plus cytarabine: complete cytogenetic response at 18 months in 76 percent versus 14 percent, and at ten years 83 percent of imatinib patients were alive, most without progression. Second-generation inhibitors dasatinib (DASISION), nilotinib (ENESTnd) and bosutinib (BFORE) produce faster and deeper responses without a survival advantage, at the cost of pleural effusions, vascular events and liver toxicity respectively. Asciminib, which binds the myristoyl pocket rather than the ATP site, beat investigator-selected inhibitors in ASC4FIRST (2024): major molecular response at 48 weeks in 67.7 percent against 49.0 percent, and 69.3 percent against 40.2 percent for imatinib, with fewer side effects, earning accelerated approval for newly diagnosed disease in October 2024.
Resistance through kinase domain mutations is handled by switching: ponatinib or asciminib for T315I, and the third-generation olverembatinib in China; allogeneic transplant is reserved for failure of several inhibitors. Treatment-free remission is now a goal: EURO-SKI found about half of patients with at least three years of therapy and a year of deep molecular response stayed in remission two years after stopping. The unsolved problems are the residual stem cell pool that keeps the other half relapsing, cardiovascular toxicity over decades of therapy, and the price and access gap that leaves patients in low-income countries on older drugs or none.
Averages across everyone diagnosed, often years ago. A median is the middle of a group: half the people counted lived longer than the figure shown, and some lived far longer. Your stage, subtype, age, fitness and the treatment you receive matter more than the average, and the numbers are improving quickly.
Averages across everyone diagnosed, often years ago. A median is the middle of a group: half the people counted lived longer than the figure shown, and some lived far longer. Your stage, subtype, age, fitness and the treatment you receive matter more than the average, and the numbers are improving quickly.
Leukaemias, myeloma and MDS live in the marrow and blood; lymphomas grow in lymph nodes and spleen. The node stations are the disease map, not a route of spread, and staging counts them.
In lymphoma the node stations are the disease itself; staging (Ann Arbor / Lugano) counts how many regions and sides of the diaphragm are involved.
Same organ: High-grade B-cell lymphoma with MYC and BCL2 rearrangements (double-hit lymphoma), Mediastinal grey zone lymphoma, Primary effusion lymphoma, Plasmablastic lymphoma, T-cell/histiocyte-rich large B-cell lymphoma, EBV-positive diffuse large B-cell lymphoma, Primary large B-cell lymphoma of the testis, Gastric MALT lymphoma, Ocular adnexal MALT lymphoma, Extranodal NK/T-cell lymphoma, Adult T-cell leukaemia/lymphoma, ALK-positive anaplastic large cell lymphoma, ALK-negative anaplastic large cell lymphoma, Breast implant-associated anaplastic large cell lymphoma, Primary cutaneous anaplastic large cell lymphoma, Lymphomatoid papulosis, Mycosis fungoides, Enteropathy-associated T-cell lymphoma, Monomorphic epitheliotropic intestinal T-cell lymphoma, Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), Splenic marginal zone lymphoma, Nodal marginal zone lymphoma, Primary cutaneous marginal zone lymphoma, Primary cutaneous follicle centre lymphoma, Sezary syndrome, Nodal T-follicular helper cell lymphoma, angioimmunoblastic type (angioimmunoblastic T-cell lymphoma), Hepatosplenic T-cell lymphoma, Intravascular large B-cell lymphoma, Lymphomatoid granulomatosis, T-cell prolymphocytic leukaemia, Splenic B-cell lymphoma/leukaemia with prominent nucleoli (formerly B-cell prolymphocytic leukaemia and hairy cell leukaemia variant), T-cell large granular lymphocytic leukaemia, Mixed-phenotype acute leukaemia, Myeloid leukaemia of Down syndrome, Burkitt leukaemia, Marginal zone lymphoma, Cutaneous T-cell lymphoma (mycosis fungoides and Sezary syndrome), Primary mediastinal (thymic) large B-cell lymphoma, Leukaemia (all types), Acute myeloid leukaemia, Acute lymphoblastic leukaemia, Chronic lymphocytic leukaemia, Chronic myeloid leukaemia (CML), Diffuse large B-cell lymphoma, Follicular lymphoma, Hodgkin lymphoma, Mantle cell lymphoma, Multiple myeloma, Non-Hodgkin lymphoma (all types), Myelodysplastic syndromes / neoplasms (MDS), Myeloproliferative neoplasms (PV, ET, myelofibrosis), Polycythaemia vera (PV), Essential thrombocythaemia (ET), Waldenström macroglobulinaemia, Hairy cell leukaemia, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma), Blastic plasmacytoid dendritic cell neoplasm (BPDCN), Burkitt lymphoma, HIV-associated (AIDS-related) lymphomas, Chronic myelomonocytic leukaemia and MDS/MPN overlap neoplasms, Systemic mastocytosis, Erdheim-Chester disease, Rosai-Dorfman disease and other histiocytic neoplasms, Langerhans cell histiocytosis (LCH), Post-transplant lymphoproliferative disorder (PTLD), FLT3-mutated acute myeloid leukaemia, IDH1- and IDH2-mutated acute myeloid leukaemia, NPM1-mutated and KMT2A-rearranged acute myeloid leukaemia, Secondary and therapy-related acute myeloid leukaemia, Acute promyelocytic leukaemia, Acute myeloid leukaemia in older or unfit patients, Smouldering multiple myeloma, Newly diagnosed multiple myeloma, transplant-eligible, Newly diagnosed multiple myeloma, transplant-ineligible, Relapsed or refractory multiple myeloma, Plasma cell leukaemia, Lower-risk myelodysplastic syndromes, Higher-risk myelodysplastic syndromes, Chronic lymphocytic leukaemia, first treatment, Relapsed or refractory chronic lymphocytic leukaemia, Richter transformation of chronic lymphocytic leukaemia, Chronic myeloid leukaemia, accelerated and blast phase, Primary myelofibrosis, Standard-risk B-cell acute lymphoblastic leukaemia in children, High-risk acute lymphoblastic leukaemia in children (high-risk B-ALL and T-ALL), Philadelphia chromosome-positive acute lymphoblastic leukaemia in children (Ph-positive ALL), Philadelphia chromosome-like acute lymphoblastic leukaemia (Ph-like or BCR::ABL1-like ALL), Infant acute lymphoblastic leukaemia (KMT2A-rearranged, under one year), Relapsed and refractory acute lymphoblastic leukaemia in children, Acute myeloid leukaemia in children, Erdheim-Chester disease, Rosai-Dorfman-Destombes disease, Single-system Langerhans cell histiocytosis (bone, skin or one other organ), Multisystem Langerhans cell histiocytosis (with or without risk-organ involvement), Indolent and smouldering systemic mastocytosis, Advanced systemic mastocytosis (aggressive SM, SM with an associated haematological neoplasm, mast cell leukaemia), Early-stage classical Hodgkin lymphoma (stage I to II), Advanced-stage classical Hodgkin lymphoma (stage III to IV), Nodular lymphocyte-predominant Hodgkin lymphoma (nodular lymphocyte-predominant B-cell lymphoma), Relapsed and refractory classical Hodgkin lymphoma
Imatinib 400 mg daily, a second-generation inhibitor (dasatinib, nilotinib, bosutinib) chosen by comorbidity and treatment goal, or asciminib (ASC4FIRST); PCR at 3, 6 and 12 months against ELN milestones.
Switch inhibitor guided by kinase domain mutation testing; ponatinib or asciminib for T315I; radotinib or olverembatinib where approved; allogeneic transplant after failure of two or more inhibitors.
Attempt treatment-free remission after at least three to five years of therapy and two years of MR4 or better, with monthly PCR for six months; restart on loss of major molecular response.
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IRIS made imatinib the first-line standard for CML worldwide and established the tyrosine kinase inhibitor as a chronic, life-long oral therapy. For most patients CML became a manageable condition with near-normal life expectancy. Later generations of TKIs (dasatinib, nilotinib, asciminib) produce faster, deeper responses but have not shown a survival advantage over imatinib.
Druker's 2001 imatinib paper turned the idea of hitting a cancer's specific molecular engine into a working medicine. For people with CML it began the shift from a fatal disease treated with interferon or transplant to one managed with a daily tablet. It also set expectations, later tempered, that every cancer might have its own imatinib.
Query for this cancer: (TITLE:"Chronic myeloid leukaemia, chronic phase" OR ABSTRACT:"Chronic myeloid leukaemia, chronic phase" OR TITLE:"CML-CP" OR ABSTRACT:"CML-CP" OR TITLE:"Chronic-phase CML" OR ABSTRACT:"Chronic-phase CML" OR TITLE:"Newly diagnosed Ph-positive CML" OR ABSTRACT:"Newly diagnosed Ph-positive CML" OR TITLE:"BCR::ABL1-positive chronic phase" OR ABSTRACT:"BCR::ABL1-positive chronic phase") AND (treatment OR therapy OR trial OR survival OR diagnosis). Results are unfiltered search hits about Chronic myeloid leukaemia, chronic phase, not a curated reading list.
The targets of this cancer's medicines and the ones linked to it directly.
Cases by country, the UK and NHS pathway and other country lenses, the expert centres with trials on record, and the centres named on this cancer's subtypes.
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Fainting, near-fainting, or an irregular or racing heartbeat; several kinase inhibitors prolong the QT interval and the labels require ECG and electrolyte monitoring.
QT: both Dasatinib and Nilotinib prolong the QT interval (known and known risk).. Avoid other QT-prolonging drugs where possible; check ECG and correct potassium and magnesium before and during treatment.
Take on an empty stomach.
Take with food.
Take with a meal and a large glass of water.
Take on an empty stomach (no food 2 hours before or 1 hour after): food raises exposure up to 82% and QT risk.
See all on the product pages:AsciminibBosutinibDasatinibImatinibNilotinibOlverembatinibPonatinibRadotinib·Printable cards in the navigator
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