Response to Imatinib Mesylate in Patients with Chronic Myeloproliferative Diseases with Rearrangements of the Platelet-Derived Growth Factor Receptor Beta
2002; Massachusetts Medical Society; Volume: 347; Issue: 7 Linguagem: Inglês
10.1056/nejmoa020150
ISSN1533-4406
AutoresJane F. Apperley, Martine Gardembas, Junia V. Melo, R. Russell‐Jones, Barbara J. Bain, E. Joanna Baxter, Andrew Chase, Judith M. Chessells, Marie Colombat, Claire Dearden, Saša Dimitrijević, François-X. Mahon, David Marin, Zariana Nikolova, Eduardo Olavarría, Sandra Silberman, Beate Schultheis, Nicholas C.P. Cross, John M. Goldman,
Tópico(s)Myeloproliferative Neoplasms: Diagnosis and Treatment
ResumoA small proportion of patients with chronic myeloproliferative diseases have constitutive activation of the gene for platelet-derived growth factor receptor beta (PDGFRB), which encodes a receptor tyrosine kinase. The gene is located on chromosome 5q33, and the activation is usually caused by a t(5;12)(q33;p13) translocation associated with an ETV6-PDGFRB fusion gene. The tyrosine kinase inhibitor imatinib mesylate specifically inhibits ABL, PDGFR, and KIT kinases and has impressive clinical efficacy in BCR-ABL–positive chronic myeloid leukemia.
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