• Title/Summary/Keyword: Chronic myelogenous leukemia

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Clinical Experience of Leukemia with Extradural Chloroma during Treatment of Lower Back Pain -A case report- (요통 치료 도중 발견된 경막외강 녹색종을 동반한 백혈병 환자 경험 -증례 보고-)

  • Lim, Kyung-Joon;Oh, Kyoung-Hee;Moon, Hyun-Seok
    • The Korean Journal of Pain
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    • v.13 no.1
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    • pp.119-122
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    • 2000
  • Granulocytic sarcoma (chloroma) is a rare, solid tumor of myelogenous stem cells, shows usually in patients with acute myelogenous leukemia and less commonly in patients with chronic myelogenous leukemia or myeloproliferative disorders. We report here a patient presenting acute paraparesis due to spinal epidural granulocytic sarcoma causing spinal cord compression in acute myelogenous leukemia with a brief review of literature.

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Ferrokinetics on Chronic Myelogenous Leukemia (만성골수성(慢性骨髓性) 백혈병(白血病)의 Ferrokinetics)

  • Whang, Kee-Suk;Chung, Chang-Keun;Lee, Jae-Chang
    • The Korean Journal of Nuclear Medicine
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    • v.1 no.2
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    • pp.35-39
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    • 1967
  • Ferrokinetcs by Pollycove's method on 2 cases of Chronic myelogenous leukemia were presented in order to study the erythropoietic function and pathogenesis of anemia. The results are as follows. (1) The daily hemoglobin syntheses were slightly elevated. Both the mean effective hemoglobinization time and mean erythron life span were shortened. The maximum net ROC incorporations of $^{59}Fe$ weere decreased. The in vivo surface measurements of radioactivity over liver, spleen, and sacral bone marrow revealed findings consistant with hemolysis and extramedullary hematopoies. (2) Based upon those findings it is assumed that anemia in chronic myelogenous leukemia may result from hemolysis and inadequate compensation to the developing anemia.

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Identification of Differentially Expressed Proteins in Imatinib Mesylate-resistant Chronic Myelogenous Cells

  • Park, Jung-Eun;Kim, Sang-Mi;Oh, Jong-K.;Kim, Jin-Y.;Yoon, Sung-Soo;Lee, Dong-Soon;Kim, Young-Soo
    • BMB Reports
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    • v.38 no.6
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    • pp.725-738
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    • 2005
  • Resistance to imatinib mesylate (also known as Gleevec, Glivec, and STI571) often becomes a barrier to the treatment of chronic myelogenous leukemia (CML). In order to identify markers of the action of imatinib mesylate, we used a mass spectrometry approach to compare protein expression profiles in human leukemia cells (K562) and in imatinib mesylate-resistant human leukemia cells (K562-R) in the presence and absence of imatinib mesylate. We identified 118 differentially regulated proteins in these two leukemia cell-lines, with and without a $1\;{\mu}M$ imatinib mesylate challenge. Nine proteins of unknown function were discovered. This is the first comprehensive report regarding differential protein expression in imatinib mesylate-treated CML cells.

Arsenic Trioxide Induces Apoptosis in Chronic Myelogenous Leukemia K562 Cells:Possible Involvement of p38 MAP Kinase

  • Shim, Moon-Jeong;Kim, Hyun-Jeong;Yang, Seung-Ju;Lee, In-Soo;Choi, Hyun-Il;Kim, Tae-Ue
    • BMB Reports
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    • v.35 no.4
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    • pp.377-383
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    • 2002
  • Arsenic trioxide ($As_O_3$) was recently demonstrated to be an effective inducer of apoptosis in patients with relapsed acute promyelocytic leukemia (APL) as well as patients with APL in whom all-trans-retinoic acid and conventional chemotherapy failed. Chronic myelogenous leukemia cells are highly resistant to chemotherapeutic drugs. To determine if $As_O_3$ might be useful for the treatment of chronic myelogenous leukemia, we examined the ability of $As_O_3$ to induce apoptosis in K562 cells. In vitro cytotoxicity of $As_O_3$ was evaluated in K562 cells by a MTT assay: the $IC_50$ value for $As_O_3$ was determined to be $10\;{\mu}m$. When analyzed by agarose gel electorphoresis, the DNA fragments became evident after incubation of the cells with $20\;{\mu}m$ $As_O_3$ for 24 h. We also found morphological changes and chromatin condensation of the cells undergoing apoptosis. Activation of caspase-3 was observed 6 h after treatment with $20\;{\mu}m$ $As_O_3$ by a Western blot analysis. Next, we examined the MAP kinase-signaling pathway of $As_O_3$-induced apoptosis in K562 cells. $As_O_3$ at $10\;{\mu}m$ strongly induced the activation of p38, inhibited $As_O_3$ induced apoptotic cell death. These results suggest that $As_O_3$ is able to induce the apoptotic activity in K562 cells, and its apoptotic mechanism may be associated with the activation of p38.

Imatinib Mesylate Versus Allogeneic Hematopoietic Stem Cell Transplantation for Patients with Chronic Myelogenous Leukemia

  • Zhang, Gui-Fang;Zhou, Min;Bao, Xie-Bing;Qiu, Hui-Ying;Li, Zheng;Xue, Sheng-Li
    • Asian Pacific Journal of Cancer Prevention
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    • v.17 no.9
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    • pp.4477-4481
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    • 2016
  • Purpose: To compare the relative merits of imatinib and allogeneic hematopoietic stem cell transplantation (allo-HSCT) for chronic myelogenous leukemia (CML). Materials and Methods: This cohort study was designed to compare the outcomes of imatinib (n=292) versus allo-HSCT (n=141) for CML, the clinical data of these patients being retrospectively analyzed so as to compare the event free survival (EFS) and overall survival (OS) between these two groups with patients in the chronic phase (CP) and advanced phases, including accelerate (AP) and blast phases (BP). Results: (1) Patients treated with imatinib (278 in the CP) demonstrated superior EFS, OS, 5-year EFS and 5-year OS rates of 88.5% versus 70.0% (P<0.05), 93.2% versus 80.0% (P<0.05), 84% versus 75.0% (P<0.05) and 92% versus 79.0% (P<0.05), respectively, to those treated with allo-HSCT (120 patients in the CP). (2) Both treatments resulted in similar survival, with EFS and OS rates of 42.9% versus 47.6% (P>0.05), 42.9% versus 57.1% (P> 0.05), respectively, for imatinib (14 patients in the AP and BP) and allo-HSCT (21 patients in the AP and BP). Conclusions: Imatinib confers significant survival advantage (EFS and OS) for CML patients with CP compared with allo-HSCT treatment. However, the outcomes are equally good with both treatments in AP and BP patients.

Granulocytic Sarcoma Involving the Pectoralis Muscle in a Patient with Chronic Myelogenous Leukemia (만성골수성백혈병 환자에서 대흉근에 발생한 과립백혈구육종)

  • Baek, Jong-Hyun;Lee, Jung-Cheul;Lee, Jang-Hoon;Kim, Jung-Hee;Kim, Mi-Jin
    • Journal of Chest Surgery
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    • v.43 no.4
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    • pp.466-469
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    • 2010
  • We report here on a very rare case of granulocytic sarcoma of the pectoralis muscle on the left chest wall of a patient with chronic myelogenous leukemia, and this malady presented as a very rapidly growing hematoma-like mass.

Clinical Experience of Management of Lower Leg Pain due to Chloroma of Lumbosacral Bone in Chronic Myelogenous Leukemia (만성골수성 백혈병 환자에서 발생한 요천추부 Chloroma로 인한 좌하지통증의 치료경험 1예 보고)

  • Sung, Choon-Ho;Chung, Woon-Hyok
    • The Korean Journal of Pain
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    • v.2 no.1
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    • pp.61-65
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    • 1989
  • Chloroma is a localized myeloblastic tumor which may develop during the course of myelogenous leukemia or as a presenting sign of the disease. A 47-year-old female diagnosed as chronic myelogenous leukemia in her hematologic remission period complained of left lower leg pain. The lumbar-spine series showed multiple osteolytic changes in the left lateral border of the lumbar spine. An inhomogenous soft tissue mass involving left lateral aspects of lumbar vertebrae was identified by CT-scanning. At the first pain attack, lumbar epidural steroid and local anesthetic injection could abolish her pain and the patient could go a few days without pain. The following radiation therapy could also improve the symptom and retain the pain free interval. One month later, a second pain attack occurred and lumbar and caudal epidural steroid and local anesthetic injections could result only in an incidental relief of pain. Radiation and chemotherapy were started but failed to relieve pain. A neurolytic block was considered but the patient's general condition was aggravated and even verbal communication with her became impossible.

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Efficacy of imatinib mesylate-based front-line therapy in pediatric chronic myelogenous leukemia

  • Oh, Hyun Jin;Cho, Mun Sung;Lee, Jae Wook;Jang, Pil-Sang;Chung, Nack-Gyun;Cho, Bin;Kim, Hack-Ki
    • Clinical and Experimental Pediatrics
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    • v.56 no.8
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    • pp.343-350
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    • 2013
  • Purpose: Despite the established role of imatinib (IM) in chronic myelogenous leukemia (CML) in adults, there are few reports on its efficacy in children. In this study, we compared the outcomes of children with CML before and after the advent of IM-based treatment. Methods: The study cohort consisted of 52 patients treated for CML at the Department of Pediatrics, The Catholic University of Korea from January 1995 to October 2010. Patients were divided and analyzed according to the preImatinib group (pre-IMG) and imatinib group (IMG). Results: Median age at diagnosis for the overall cohort (pre-IMG, n=27; IMG, n=25) was 9 years, with a median follow-up duration of survivors of 84 months. Except for 5 patients in the IMG, all were diagnosed in chronic phase (CP). The overall survival (OS) of patients diagnosed in CP was 45.7% and 89.7% for pre-IMG and IMG, respectively (P=0.025). The OS of hematopoietic stem cell transplantation (HSCT) recipients in the 2 groups was similar, but the OS of patients diagnosed in CP who did not receive HSCT was superior in IMG (91.7% vs. 16.7%, P=0.014). Of the 12 patients in IMG who remained on IM without HSCT, 2 showed disease progression, compared to 11 of 12 in pre-IMG. No difference was observed in the progression free survival (PFS) of matched donor HSCT recipients and IM-based treatment recipients. Conclusion: Similar PFS of patients treated with IM and those who received matched donor HSCT underscore the potential of IM as effective first-line treatment in childhood CML.

The treatment of pediatric chronic myelogenous leukemia in the imatinib era

  • Lee, Jae-Wook;Chung, Nack-Gyun
    • Clinical and Experimental Pediatrics
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    • v.54 no.3
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    • pp.111-116
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    • 2011
  • Childhood chronic myelogenous leukemia (CML) is a rare hematologic disease, with limited literature on the methods of treatment. Previously, allogeneic hematopoietic stem cell transplantation (HSCT) was considered the only curative treatment for this disease. Treatment with imatinib, a selective inhibitor of the BCR-ABL tyrosine kinase (TKI), has resulted in prolonged molecular response with limited drug toxicity. Imatinib is now implemented in the primary treatment regimen for children, but the paucity of evidence on its ability to result in permanent cure and the potential complications that may arise from long-term treatment with TKIs have prevented imatinib from superseding HSCT as the primary means of curative treatment in children. The results of allogeneic HSCT in children with CML are similar to those observed in adults; HSCT-related complications such as transplant-related mortality and graft-versus-host disease remain significant challenges. An overall consensus has been formed with regards to the need for HSCT in patients with imatinib resistance or those with advanced-phase disease. However, issues such as when to undertake HSCT in chronic-phase CML patients or how best to treat patients who have relapsed after HSCT are still controversial. The imatinib era calls for a reevaluation of the role of HSCT in the treatment of CML. Specific guidelines for the treatment of pediatric CML have not yet been formulated, underscoring the importance of prospective studies on issues such as duration of imatinib treatment, optimal timing of HSCT and the type of conditioning utilized, possible treatment pre-and post-HSCT, and the role of second-generation TKIs.