TY - JOUR
T1 - Chronic eosinophilic leukemia with the FIP1L1-PDGFRα fusion gene in a patient with a history of combination chemotherapy
AU - Tanaka, Yasuhiro
AU - Kurata, Masayuki
AU - Togami, Katsuhiro
AU - Fujita, Haruyuki
AU - Watanabe, Naoko
AU - Matsushita, Akiko
AU - Maeda, Akinori
AU - Nagai, Kenichi
AU - Sada, Akiko
AU - Matsui, Toshimitsu
AU - Takahashi, Takayuki
PY - 2006/2
Y1 - 2006/2
N2 - Hypereosinophilic syndrome (HES) was diagnosed in December 2000 in a 43-year-old man on the basis of persistent eosinophilia (11.7 × 10 9/L) and a normal karyotype of the bone marrow cells. He had developed intra-abdominal non-Hodgkin's lymphoma and in 1992 had received 3 courses of combination chemotherapy with doxorubicin (Adriamycin), cyclophosphamide, vincristine, methotrexate, bleomycin, and prednisolone. The patient was orally given prednisolone (10 mg/day) and cyclophosphamide (50 mg/day) as HES treatment without a subsequent improvement of the eosinophilia. In May 2003, anemia (hemoglobin, 7.9 g/dL) and thrombocytopenia (65 × 109/L) manifested with progressive eosinophilia (21.0 × 10 9/L) and a small number of blasts. The patient became febrile and was admitted in July 2003. Cytogenetic reexamination of the bone marrow cells disclosed the deletion of 4q12, indicating the presence of a fusion of the Fip1-like 1 (FIP1L1) gene to the platelet-derived growth factor receptor α (PDGFRα) gene and consequently the clonal nature of his hematopoietic cells. DNA sequence analysis demonstrated that the breakpoints of the FIP1L1 and PDGFRα genes were present in exon 9 and exon 12, respectively. Treatment with imatinib mesylate (300 mg/day) promptly brought about complete remission. Although a number of similar eosinophilic cases have been reported, our patient may be the first such patient with a history of chemotherapy.
AB - Hypereosinophilic syndrome (HES) was diagnosed in December 2000 in a 43-year-old man on the basis of persistent eosinophilia (11.7 × 10 9/L) and a normal karyotype of the bone marrow cells. He had developed intra-abdominal non-Hodgkin's lymphoma and in 1992 had received 3 courses of combination chemotherapy with doxorubicin (Adriamycin), cyclophosphamide, vincristine, methotrexate, bleomycin, and prednisolone. The patient was orally given prednisolone (10 mg/day) and cyclophosphamide (50 mg/day) as HES treatment without a subsequent improvement of the eosinophilia. In May 2003, anemia (hemoglobin, 7.9 g/dL) and thrombocytopenia (65 × 109/L) manifested with progressive eosinophilia (21.0 × 10 9/L) and a small number of blasts. The patient became febrile and was admitted in July 2003. Cytogenetic reexamination of the bone marrow cells disclosed the deletion of 4q12, indicating the presence of a fusion of the Fip1-like 1 (FIP1L1) gene to the platelet-derived growth factor receptor α (PDGFRα) gene and consequently the clonal nature of his hematopoietic cells. DNA sequence analysis demonstrated that the breakpoints of the FIP1L1 and PDGFRα genes were present in exon 9 and exon 12, respectively. Treatment with imatinib mesylate (300 mg/day) promptly brought about complete remission. Although a number of similar eosinophilic cases have been reported, our patient may be the first such patient with a history of chemotherapy.
KW - Chronic eosinophilic leukemia
KW - FIP1L1-PDGFRα fusion gene
KW - Hypereosinophilic syndrome
KW - Imatinib mesylate
KW - Secondary leukemia
UR - http://www.scopus.com/inward/record.url?scp=33646840877&partnerID=8YFLogxK
U2 - 10.1532/IJH97.05048
DO - 10.1532/IJH97.05048
M3 - Article
C2 - 16513534
AN - SCOPUS:33646840877
SN - 0925-5710
VL - 83
SP - 152
EP - 155
JO - International Journal of Hematology
JF - International Journal of Hematology
IS - 2
ER -