The majority of patients with chronic phase chronic myeloid leukaemia (CP-CML) treated with imatinib achieves cytogenetic disease remission. Molecular monitoring for residual disease has prognostic significance: rising BCR-ABL levels may provide earliest indication that a patient has become resistant to treatment. The emergence of resistance to imatinib has dampened the enthusiasm for this drug. The most common cause of resistance is the selection of leukemic clones mutated in ABL kinase domain due to amino acid substitutions with prevention of appropriate binding of the drug. Amplification and over-expression of BCR-ABL, acquired cytogenetic aberrations and modulation of drug efflux or influx transporters have been reported. These observations have established the rationale for the creation of new compounds that have been explored in clinical trials. This review will discuss the underlying mechanisms of imatinib-resistance and new strategies to avoid and overcome this phenomenon.
Scheda prodotto non validato
Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo
|Titolo:||Resistance to imatimib in chronic myeloid leukemia and therapeutic approaches to circumvent the problem.|
|Data di pubblicazione:||2009|
|Citazione:||Resistance to imatimib in chronic myeloid leukemia and therapeutic approaches to circumvent the problem. / Breccia, M; Alimena, Giuliana. - In: CARDIOVASCULAR & HAEMATOLOGICAL DISORDERS - DRUG TARGETS. - ISSN 1871-529X. - STAMPA. - 9(2009), pp. 21-28.|
|Appare nella tipologia:||01a Articolo in rivista|