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Efficacy of imatinib mesylate (STI571) in chronic neutrophilic leukemia with t(15;19): Case report
Author(s) -
Choi In Keun,
Kim ByungSoo,
Lee KyungA,
Ryu Sookwon,
Seo Hee Yun,
Sul Hyeryoung,
Choi Jong Gwon,
Sung Hwa Jung,
Park Kyong Hwa,
Yoon So Young,
Oh Sang Cheul,
Seo Jae Hong,
Choi Chul Won,
Shin Sang Won,
Yoon SooYoung,
Cho Yunjung,
Kim YoungKee,
Kim Yeul Hong,
Kim Jun Suk
Publication year - 2004
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.20197
Subject(s) - imatinib , imatinib mesylate , chromosomal translocation , medicine , philadelphia chromosome , tyrosine kinase inhibitor , leukemia , tyrosine kinase , breakpoint cluster region , oncology , immunology , cancer research , biology , gene , genetics , receptor , cancer , myeloid leukemia
Chronic neutrophilic leukemia (CNL) is a rare hematologic disorder, for which there is no standard therapy. Recently, STI (imatinib mesylate) has been shown to be effective in treating patients with chronic myeloproliferative disorder (CMPD) displaying the translocation of the PDGFβR gene. Here, we present a case of a patient with CNL carrying t(15;19)(q13;p13.3) who achieved a cytogenetic remission following treatment with imatinib, 400 mg daily. After failure of alpha interferon and hydroxyurea therapy, a durable and complete clinical and cytogenic remission was induced by imatinib. To our knowledge, this is the first case with CNL who showed complete response with cytogenic remission after treatment of imatinib. The mechanism of response to this molecule is unknown in our case (other oncogenes than c‐kit, tyrosine kinase, or PDGFR may be involved). The patient remains in complete remission with an excellent performance status after 7 months of therapy. We demonstrate here that imatinib can induce a clinical and cytogenetic response in a case of CNL associated with a novel translocation other than a 5q33 rearrangement. Further studies including the molecular cloning of the t(15;19)(q13;p13.3) will be important in understanding the pathophysiology of CNL with a heterogeneous clinical course and the exploitation of the basic mechanisms of imatinib treatment. Am. J. Hematol. 77:366–369, 2004. © 2004 Wiley‐Liss, Inc.