By Timothy P Hughes, David M Ross, Junia V Melo
This concise, clinically centred pocket guide assembles and synthesizes the most recent advancements and developments within the analysis and remedy of CML and gives an authoritative and handy precis of the newest development in TKI trials, the molecular tracking of CML responses, and the advance of recent treatments to beat resistance and increase sufferer care. persistent myeloid leukemia (CML) is an extraordinary kind of leukemia (1–2 in step with 100,000 humans) yet is the commonest power myeloproliferative neoplasm. CML continues to be a key version for the enhanced realizing of the pathophysiology of a malignancy at a molecular point; CML was once the 1st melanoma to be linked to a ordinary chromosome abnormality, which generates the Philadelphia (Ph) chromosome and its linked fusion gene BCR-ABL1. The scientific end result for sufferers with CML has replaced dramatically long ago 15 years and this has been as a result of improvement of tyrosine kinase inhibitors (TKIs), compounds that inhibit the task of the oncogenic BCR-ABL1 protein. a few first-, moment- and third-generation TKIs are actually to be had for the therapy of CML, even though a few remedy demanding situations stay, no longer least the advance of treatment-resistant CML. Parallel to the advance of particular medications for treating CML, significant advances were made within the box of ailment tracking and standardization of reaction standards.
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This concise, clinically centred pocket guide assembles and synthesizes the most recent advancements and tendencies within the prognosis and remedy of CML and offers an authoritative and handy precis of the newest development in TKI trials, the molecular tracking of CML responses, and the advance of latest remedies to beat resistance and enhance sufferer care.
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Extra resources for Handbook of Chronic Myeloid Leukemia
Br J Haematol. 1999;107:587-599. Lange T, Bumm T, Otto S, et al. Quantitative reverse transcription polymerase chain reaction should not replace conventional cytogenetics for monitoring patients with chronic myeloid leukemia during early phase of imatinib therapy. Haematologica. 2004;89:49-57. Cuneo A, Bigoni R, Emmanuel B, et al. Fluorescence in situ hybridization for the detection and monitoring of the Ph-positive clone in chronic myelogenous leukemia: comparison with metaphase banding analysis.
While it would be tempting to use the TKI that is most familiar to the clinician it is probably not optimal management to select the same drug in every case. There is emerging evidence that in specific circumstances one TKI may be a better choice for a particular patient. Detailed knowledge of the efficacy and safety profile of each TKI, the susceptibility of the patient to toxicities, and clarity about the therapeutic goals should all be weighed carefully when choosing the frontline TKI. Here, we review the strengths and weaknesses of the three currently available frontline TKIs.
Nilotinib Nilotinib is structurally similar to imatinib although its affinity for BCR–ABL and off-target effects are different. Nilotinib binds to the kinase domain of BCR–ABL, with greater affinity than imatinib and is less vulnerable to kinase domain mutations. Only five mutations are of major concern in the context of nilotinib treatment (T315I, F359V, E255K, E255V, and Y253H); these mutations emerge most frequently on frontline or second-line nilotinib therapy, and their presence is a contraindication to the use of nilotinib after failure of another TKI [16,17].