A Case of Leukemia Cutis in Myelodysplastic Syndrome Evolving into An Atypical Chronic Myeloid Leukemia

Ryu, Hwa Jung,Kye, Young Chul,Kim, Soo-Nam 대한피부과학회 2003 Annals of Dermatology Vol.15 No.2

We report a patient who had been initially diagnosed as a myelodysplastic syndrome in 1998 presenting purpuric patches on the left arm that started to develop about a year prior. The purpuric lesions were diagnosed as leukemia cutis by skin biopsy. Her subsequent bone marrow biopsy showed progression into an atypical chronic myeloid leukemia with increased numbers of leukocytes in the peripheral blood. Leukemia cutis typically is regarded as a sign of progression of disease or a manifestation of recurrent disease in treated patients with an established diagnosis of leukemia. We suggest that the skin lesion in this patient could have been a sign of conversion into atypical chronic myeloid leukemia.

만성 골수성 백혈병 경과 중에 발생한 말초 T 세포림프종 1 예

임충현(Chung Hyun Lim),김지현(Ji Hyun Kim),김선임(Sun Im Kim),정은주(Eun Ju Chung),윤범(Beom Yun),김응주(Eung Joo Kim),조혜제(Hye Jae Cho),유영진(Young Jin Yuh),김성록(Sung Rok Kim) 대한내과학회 2001 대한내과학회지 Vol.61 No.4

Lymphoid malignancies have been reported in association with chronic myelogenous leukemia, but the development of chronic myelogenous leukemia and T-cell lymphoma in the same patients is rare. We experienced a case of peripheral T-cell lymphoma developed in the course of chronic myelogenous leukemia. In December 1993, a diagnosis of chronic myelogenous leukemia was made. The patient was treated with hydroxyurea and busulphan. In June 1999, the patient was admitted because of a swelling in right submandibular area and throat pain. He underwent right tonsilectomy. The histologic and immunologic examination of tonsil revealed a peripheral T-cell lymphoma. This case is additional one to a few previously reported cases of concurrence of chronic myelogenous leukemia and T-cell lymphoma. (Korean J Med 61:444-448, 2001)

ABCG2 C421A Polymorphism and Imatinib Response in Chronic Myeloid Leukemia: A Systematic Review and Meta-Analysis

오다현,천부순 한국임상약학회 2016 한국임상약학회지 Vol.26 No.1

Objective: To estimate the association between ABCG2 C421A polymorphism and response to imatinib in chronic myeloid leukemia. Methods: A systematic review was conducted to evaluate the effect of ABCG2 C421A polymorphism on imatinib response. The databases of PubMed, Embase, Web of science, CINAHL with FullText, and Cochrane Library were searched for all published studies from inception to December 2015. The following terms were used with functions of ‘AND’ and ‘OR’: ‘chronic myeloid leukemia’, ‘CML’, ‘drug transporter’, ‘ABCG2’, ‘BCRP’, ‘polymorphisms’, ‘SNPs’, and ‘imatinib’. The studies reporting the association between ABCG2 polymorphism and imatinib response were evaluated. Results: A total of 7 studies were included in the present meta-analysis. The pooled analysis showed that ABCG2 c.421CC genotype was significantly associated with poor response to imatinib under the dominant model (CC vs CA+AA; OR: 0.56; 95% CI: 0.41, 0.77; p = 0.0004). The subgroup analysis of Asian studies demonstrated a significantly lower response in c.421CC genotype than in c.421CA or c.421AA genotype (OR: 0.52; 95% CI: 0.37, 0.73; p = 0.0002). In subgroup analyses of 5 studies, the patients with the c.421CC genotype exhibited higher risk for worse response than the patients with c.421CA or c.421AA genotype (heterozygote codominant model: CC vs. AC; OR: 0.49, 95% CI: 0.33, 0.73; p = 0.0006; homozygote codominant model: CC vs AA; OR: 0.43; 95% CI: 0.25, 0.75, p = 0.003). Conclusion: The ABCG2 c.421CC genotype was significantly associated with poor response to imatinib compared to the c.421CA and c.421AA genotypes in chronic myeloid leukemia, especially in Asian patients.

만성 골수성 백혈병과 연관하여 발생한 양안의 중심망막정맥폐쇄 1예

김미리내(Mirinae Kim),신정아(Jeong Ah Shin),박영훈(Young Hoon Park) 대한검안학회 2016 Annals of optometry and contact lens Vol.15 No.1

Purpose: To report a rare case of a simultaneous bilateral central retinal vein occlusion, as the initial presentation of chronic myeloid leukemia. Case summary: A 22-year-old man presented with conjunctival injection of both eye, decreased visual acuity of left eye, nausea and dizziness. Ophthalmic examination was consistent with non-ischemic central retinal vein occlusion of both eye. After a systemic evaluation including laboratory examinations, bone marrow biopsy, and abdomen computed tomography, he was diagnosed as chronic myeloid leukemia. The patient received massive hydration and chemotherapy with hydroxyurea, allopurinol, and torsemide. On follow-up at 2 months, his visual acuity recovered to 0.8 in right eye, and 0.63 in left eye. The ocular status has remained stable at 2 year of follow-up. Conclusions: All ocular structures have been found to be involved in patients with leukemia, but visual impairment as the initial symptom of leukemia is rare. A prompt search for the underlying systemic disease should be performed in young patients presenting with central retinal vein occlusion.

LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21

Zhou, Xiangyu,Yuan, Ping,Liu, Qi,Liu, Zhiqiang The Korean Society of Applied Pharmacology 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.5

Imatinib resistance has become a major clinical problem for chronic myeloid leukemia. The aim of the present study was to investigate the involvement of MEG3, a lncRNA, in imatinib resistance and demonstrate its underlying mechanisms. RNAs were extracted from CML patients' peripheral blood cells and human leukemic K562 cells, and the expression of MEG3 was measured by RT-qPCR. Cell proliferation and cell apoptosis were evaluated. Western blotting was used to measure the protein expression of several multidrug resistant transporters. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. In addition, miR-21 mimics reversed the phenotype of MEG3-overexpression in imatinib-resistant K562 cells. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.

LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21

( Xiangyu Zhou ),( Ping Yuan ),( Qi Liu ),( Zhiqiang Liu ) 한국응용약물학회 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.5

Imatinib resistance has become a major clinical problem for chronic myeloid leukemia. The aim of the present study was to investigate the involvement of MEG3, a lncRNA, in imatinib resistance and demonstrate its underlying mechanisms. RNAs were extracted from CML patients` peripheral blood cells and human leukemic K562 cells, and the expression of MEG3 was measured by RT-qPCR. Cell proliferation and cell apoptosis were evaluated. Western blotting was used to measure the protein expression of several multidrug resistant transporters. Luciferase reporter assay was performed to determine the binding between MEG3 and miR-21. Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells. Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. In addition, miR-21 mimics reversed the phenotype of MEG3-overexpression in imatinib-resistant K562 cells. Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.

A case of chronic myeloid leukemia in a diagnostic radiographer

Chulyong Park,Sungyeul Choi,Dohyung Kim,Jaechan Park,Saerom Lee 대한직업환경의학회 2014 대한직업환경의학회지 Vol.26 No.-

Background: Occupational radiation exposure causes certain types of cancer, specifically hematopoietic diseases like leukemia. In Korea, radiation exposure is monitored and recorded by law, and guidelines for compensation of radiation-related diseases were implemented in 2001. However, thus far, no occupation-related disease was approved for compensation under these guidelines. Here, we report the first case of radiation-related disease approved by the compensation committee of the Korea Workers’ Compensation and Welfare Service, based on the probability of causation. Case presentation: A 45-year-old man complained of chronic fatigue and myalgia for several days. He was diagnosed with chronic myeloid leukemia. The patient was a diagnostic radiographer at a diagnostic radiation department and was exposed to ionizing radiation for 21 years before chronic myeloid leukemia was diagnosed. His job involved taking simple radiographs, computed tomography scans, and measuring bone marrow density. Conclusion: To our knowledge, this is the first approved case report using quantitative assessment of radiation. More approved cases are expected based on objective radiation exposure data and the probability of causation. We need to find a resolution to the ongoing demands for appropriate compensation and improvements to the environment at radiation workplaces.

Granulocytic and Monocytic Myeloid-Derived Suppressor Cells are Functionally and Prognostically Different in Patients with Chronic Myeloid Leukemia

Ahn Ari,Park Chan-Jeoung,Kim Min-sun,Cho Young-Uk,Jang Seongsoo,Bae Mi Hyun,Lee Jung-Hee,Lee Je-Hwan,Koh Kyung-Nam,Im Ho Joon 대한진단검사의학회 2021 Annals of Laboratory Medicine Vol.41 No.5

Myeloid-derived suppressor cells (MDSCs) represent phenotypically heterogeneous populations that suppress tumor-specific T-cell responses. MDSCs are produced from myeloid precursors in emergent states and are increased in several hematologic malignancies. We evaluated the differences in the levels and prognostic significance of MDSCs according to the clinical status of chronic myeloid leukemia (CML). The percentages and numbers of granulocytic (g)MDSCs and monocytic (m)MDSCs in peripheral blood (PB) and bone marrow (BM) aspirates were determined by five-color flow cytometry (HLA-DR/CD11b/CD15/CD33/CD14). The median BM-gMDSC% and PB-gMDSC% of the CML group were lower than those of the complete hematologic response (CHR) and control groups (P<0.001). In the CHR group, patients with major molecular response (MMR) showed higher median BM-gMDSC% than those without MMR (P=0.039). Conversely, the PB-mMDSC number of the CML group was higher than those of the CHR and control groups (P<0.001). Patients with high PB-gMDSC number exhibited superior survival to those with low PB-gMDSC number (P=0.021), and patients with high PB-mMDSC% showed inferior survival to those with low PB-mMDSC%, but there was no statistical significance (P=0.182). Increased gMDSCs at CHR may reflect non-leukemic granulopoiesis, and a high number of PB-gMDSCs suggests better prognosis in CML. However, mMDSCs may be associated with malignant conditions and poor prognosis.

급성백혈병 및 만성골수성백혈병에서의 Telomerase 활성도 변화 양상

김명유,이정녀 大韓血液學會 2001 大韓血液學會誌 Vol.36 No.3

Qi therapy as a complementary therapy in chronic myeloid leukemia

Lee, Myeong-Soo Kyung Hee Oriental Medicine Research Center 2004 Oriental pharmacy and experimental medicine Vol.4 No.4

We describe the successful treatment of a case of chronic myeloid leukemia with Qi therapy. The patient's disease was managed with conventional medical treatment and Qi therapy as a complementary therapy. Before Qi therapy, 95% of the patient's bone marrow showed evidence of disease. A second bone marrow sample five months after Qi therapy revealed that 38% of the bone marrow was normal; one year after Qi therapy the bone marrow was no longer producing any cancer cells. Although these results were obtained for a single case only and may not constitute conclusive evidence, the data suggest that Qi therapy given as a complementary therapy during conventional medical treatment may have beneficial effects on chronic myeloid leukemia.