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Low Frequency and Variability of FLT3 Mutations in Korean Patients with Acute Myeloid Leukemia
방수미,안정열,박지윤,박세훈,박진희,조은경,신동복,이재훈,유수진,전인상,김여경,김형준,김희남,이일권,강형진,신희영,안효섭 대한의학회 2008 Journal of Korean medical science Vol.23 No.5
FLT3 mutations are common genetic changes, and are reported to have prognostic significance in acute myeloid leukemia (AML). The FLT3 internal tandem duplication (ITD) and the D835 activating mutation in the tyrosine kinase domain (TKD) were analyzed by polymerase chain reaction (PCR) in the genomic DNA of Korean patients with AML at diagnosis and during follow-up. There were 226 patients with AML enrolled between March 1996 and August 2005. The incidence of ITD and TKD at diagnosis was 13% (29/226) and 3% (6/226). When compared to Western and other Asian patients with AML, Korean patients had a lower frequency by about two-thirds of ITD and TKD. Among the non-M3 cases (N=203), the patients with an ITD had a significantly shorter event-free survival when compared with those without an ITD (p=0.0079). Among 54 relapsed patients, 9 patients had the FLT3 ITD at diagnosis. Six patients demonstrated a reappearance of the ITD and 3 patients remained negative at relapse. One patient, among 45 patients who relapsed, had a negative baseline ITD but acquired a de novo ITD at relapse. There were 101 samples from 93 patients in remission; they were all negative for an ITD. Among 34 patients who failed to achieve a remission, five patients had a persistent ITD and one patient had a de novo ITD. These results support the concept of resistance of FLT3 ITD leukemic clones to chemotherapy. Therefore, effective therapy with FLT3 targeting agents may improve the prognosis of non-M3 AML patients with the FLT3 mutation.
방수미,EunKyungCho,CheolwonSuh,Sung-SooYoon,ChuMyungSeong,KyungSamCho,YoonGooKang,SeonyangPark,Myung-JuAhn,YoungSukPark,DoyeunOh,정철원,SamyongKim 대한의학회 2003 Journal of Korean medical science Vol.18 No.5
We conducted a phase II multicenter trial to estimate the response and survival of patients with newly diagnosed multiple myeloma to high dose melphalan therapy followed by autologous peripheral blood stem cell transplantation. Eligible patients who had undergone induction with vincristine, adriamycin and dexamethasone (VAD) should have adequate cardiac, pulmonary and renal function (creatinine <2 mg/dL). Melphalan at 200 mg/m2 was used as a conditioning regimen. Eighty patients were enrolled from 13 centers. The median age of the patients was 53 yr (range; 20 to 68 yr). The initial stage was IA/IIA/IIB/IIIA/IIIB in 3/8/1/54/14 patients, respectively. Beta2-microglobulin, CRP and LDH were increased in 74, 42 and 34% of the patients examined. Cytogenetic data were available in 30 patients, and 6 patients showed numeric or structural abnormalities. Two therapy-related mortalities occurred from infection. Among the 78 evaluable patients, CR/PR/MR/NC/PD were achieved in 48/26/2/1/1patients, respectively. After a median follow-up of 30 months, the median overall and event-free survivals were 66 months (95% CI: 20-112) and 24 months (95% CI: 18-29), respectively. This study verifies the efficacy and feasibility of high dose melphalan therapy with autologous stem cell transplantation in newly diagnosed multiple myeloma.
방수미,김호영,김효정,김희진,원종호,김봉석,정철원,지현숙 대한의사협회 2011 대한의사협회지 Vol.54 No.1
The myeloproliferative neoplasm (MPN), polycythemia vera (PV), essential thrombocytosis (ET), and primary myelofibrosis (PMF) are clonal hematopoietic stem cell diseases that share in common overproduction of one or more of the formed elements of the blood with overlapping clinical features but exhibit different natural histories and different therapeutic requirements. Therefore, accuracy of diagnosis is the cornerstone of therapy. The World Health Organization diagnostic criteria for both the classic BCR-ABL-negative MPNs (that is PV, ET, and PMF) and chronic eosinophilic leukemia/hypereosinophilic syndrome have been revised in the 2008 edition, by incorporating new information on their V617F mutation in the Janus kinase 2 (JAK2) tyrosine kinase. The JAK2 V617F point mutation makes the normal hematopoietic progenitor cells hypersensitive to thrombopoietin, erythropoietin, and myeloid progenitor cells, leading to trilinear hematopoietic myeloproliferation. JAK2 V617F is found in most patients with PV, ET, or PMF and is, therefore, useful as a clonal marker when present. However their absence does not exclude the diagnosis of an MPN. The major complications of the MPN are thrombosis, hemorrhage and extramedullary hematopoiesis with massive splenomegaly and bone marrow failure. Myelofibrosis is classically listed as a complication of the MPN. Current treatment options are low dose aspirin, phlebotomy and cytoreductive therapy with hydroxyurea, anagrelide, and interferon for PV and ET but the most effective therapy is still bone marrow transplantation for PMF for the relief of symptoms and the prevention of complications. Drugs targeting JAK2 V617F are promising. This article reviews the changes in diagnostic criteria and algorithms, and also provides treatment guidelines that are tailored to routine clinical practice.