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CML
The "molecular era" in cancer treatment was ushered in with the discovery of the Philadelphia chromosome in 1960, the first chromosomal abnormality linked to a specific type of leukaemia. It would take researchers the next 3 decades to elucidate the connections on a molecular level between genetic abnormalities and pathogenesis in cancers such as chronic myeloid leukaemia (CML). By the end of the millennium, new breakthroughs in our understanding of cancer biology had led to the development of Glivec® (imatinib), the first molecularly targeted cancer treatment1.
CML Outlook Before Glivec
Before the molecular era, the outlook for patients with CML was bleak. Diagnosis was poor and tended to occur at later disease stages2. Prognosis was poor. Available treatment options promised only limited efficacy and were often associated with difficult side effects.
Before cytogenetic analysis was available, diagnosis of CML relied primarily on microscopic examination of blood and marrow. The focus of treatment was symptom relief, including blood transfusion to treat anaemia and iron supplementation to improve the haemoglobin level. Irradiation, usually of the spleen, was the main option for controlling the leukaemic process. Chemotherapeutic agents including hydroxyurea and busulfan induced haematological remissions, but did not inhibit progression of CML, and therefore are considered palliative therapy for the symptoms of CML3. Bone marrow transplantation is potentially curative, but access is limited by several factors, including donor suitability and patient age; therefore, it is only an option for 15%-20% of patients, and procedure-related morbidity and mortality are high. A minority of patients treated with interferon alfa (IFN-α) in early chronic-phase CML achieved complete cytogenetic remission (CCyR); however, the doses required to induce CCyR have been associated with issues of tolerability and side effects.
Targeting CML With Glivec
Glivec is confirmed as the standard first-line therapy for all CML patients by clinical studies with 5-year follow-up4-7.
- An 89% overall survival at 5 years with Glivec exceeds that of all other CML therapies, with <5% of deaths related to CML.
- An estimated 98% of patients in chronic-phase CML have had a best response of CHR, and an estimated 92% of patients have had a best response of major cytogenetic response with Glivec.
- Late responses to Glivec occur and responses are durable.
- Annual risk of progression is decreasing with time.
- The annual rate of progression to advanced phases of CML (accelerated phase/blast crisis) at year 5 declined to 0.6% (from 1.5% in year 1).
- Increasing the daily dose of Glivec to 600 or 800 mg may be considered for patients in the absence of severe adverse drug reaction and severe non-leukaemia-related neutropaenia or thrombocytopaenia in certain circumstances, including disease progression, failure to achieve response within prespecified time points, or loss of response (refer to SmPC for further details)4.
- Overall risk of progression to advanced phases of CML is low and is associated with the degree of response, regardless of when achieved.
The remarkable success achieved with Glivec as therapy for CML has established Glivec as the standard of care for Philadelphia chromosome-positive (Ph+) CML8.
In this section of the site, you will get the information you need to make a diagnosis of CML and will explore the benefits of prescribing Glivec as a first-line treatment.
First, find out About CML development, epidemiology, clinical presentation and natural history.
