Some recent papers have focused on the activity of imatinib-mesylate, a selective inhibitor of tyrosine kinase, in idiopathic hypereosinophilic syndrome (HES) [1], [2], [3] and [4]. In this setting, a possible therapeutic target was identified by Cools et al. [2], who described the fusion tyrosine-kinase gene FIP1L1/PDGFRA as the result of an interstitial deletion within chromosome 4 in nine out of sixteen (56%) patients affected by HES. Of interest, although in this study the response to imatinib was strictly correlated with the presence of FIP1L1/PDGFRA rearrangement (all patients with such a molecular lesion treated with imatinib responded), only five out of nine responding patients evidenced the abnormal transcript [2]. Among the possible alternative mechanisms for the activation of the PDGFRA tyrosine-kinase domain, these authors suggested there may be a different fusion gene.
Musto, P., Perla, G., Minervini, M., Carella, A., LO COCO, F., Catalano, G. (2004). Imatinib-mesylate for all patients with hypereosinophilic syndrome?. LEUKEMIA RESEARCH, 28(7), 773-774 [10.1016/j.leukres.2003.11.014].
Imatinib-mesylate for all patients with hypereosinophilic syndrome?
LO COCO, FRANCESCO;CATALANO, GIANFRANCO
2004-07-01
Abstract
Some recent papers have focused on the activity of imatinib-mesylate, a selective inhibitor of tyrosine kinase, in idiopathic hypereosinophilic syndrome (HES) [1], [2], [3] and [4]. In this setting, a possible therapeutic target was identified by Cools et al. [2], who described the fusion tyrosine-kinase gene FIP1L1/PDGFRA as the result of an interstitial deletion within chromosome 4 in nine out of sixteen (56%) patients affected by HES. Of interest, although in this study the response to imatinib was strictly correlated with the presence of FIP1L1/PDGFRA rearrangement (all patients with such a molecular lesion treated with imatinib responded), only five out of nine responding patients evidenced the abnormal transcript [2]. Among the possible alternative mechanisms for the activation of the PDGFRA tyrosine-kinase domain, these authors suggested there may be a different fusion gene.File | Dimensione | Formato | |
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