• Advances in Traditional Medicine
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• v.4 no.4
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• pp.275-277
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• 2004

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.

• Oncology Letters
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• v.41 no.5
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• pp.2625-2635
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• 2019

The majority of natural killer (NK) cells serve an important role in eliminating malignant cells. The cytotoxic effects of NK cells were first identified against leukemia cells, and it is now hypothesized that they may have a critical role in leukemia therapy. The cellular functions of NK cells are mediated by their cell surface receptors, which recognize ligands on cancer cells. The role of NK cells is specifically regulated by the activating or inhibitory killer cell immunoglobulin-like receptors (KIRs) on their surface, which bind to the human leukocyte antigen (HLA) class I ligands present on the target cells. The association between KIR and HLA is derived from the diversity of KIR/HLA gene profiles present in different individuals, and this determines the cytotoxic effect of NK cells on cancer cells. Chronic myeloid leukemia (CML) is a hematological leukemia characterized by the hyper-proliferation of myeloid cells, with the majority of patients with CML presenting with abnormal immune cells. Tyrosine kinase inhibitors are the present standard therapy for CML, but are associated with numerous adverse side effects. Various studies have proposed CML therapy by immunotherapeutic approaches targeting the immune cells. This review summarizes the contents of NK cells and the association between KIR/HLA and leukemia, especially CML. This is followed by a discussion on the development of NK cell immunotherapy in hematological malignancies and research into strategies to enhance NK cell function for CML treatment.

• The Journal of Internal Korean Medicine
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• v.37 no.2
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• pp.202-211
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• 2016

Objective: This clinical study reports on a case of generalized edema with hypoalbuminemia and pleural effusion improved by combined traditional Korean and Western medical treatments in a patient with chronic myeloid leukemia medicated with dasatinib.Method: Combined traditional Korean and Western medical treatment was carried out, including herbal medicine, acupuncture, moxibustion, and albumin injection. We examined the serum albumin, measured the circumference of both thighs and ankles to estimate the volume of the edema, and evaluated the pleural effusion symptoms.Results: The serum albumin increased, and generalized edema and pleural effusion improved significantly after the administration of Bojungchiseub-tang-gami.Conclusion: These results showed that complications of generalized edema and pleural effusion associated with dasatinib medication have the potential to be improved via combined traditional Korean and Western medical treatments.

• Korean Journal of Clinical Pharmacy
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• v.26 no.1
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• pp.53-58
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• 2016

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.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.17
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• pp.7415-7423
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• 2015

Chronic myeloid leukemia (CML) is a stem cell disorder characterized by unrestricted proliferation of the myeloid series that occurs due to the BCR-ABL fusion oncogene as a result of reciprocal translocation t(9;22) (q34;q11). This discovery has made this particular domain a target for future efforts to cure CML. Imatinib revolutionized the treatment options for CML and gave encouraging results both in case of safety as well as tolerability profile as compared to agents such as hydroxyurea or busulfan given before Imatinib. However, about 2-4% of patients show resistance and mutations have been found to be one of the reasons for its development. European Leukemianet gives recommendations for BCR-ABL mutational analysis along with other tyrosine kinase inhibitors (TKIs) that should be administered according to the mutations harbored in a patient. The following overview gives recommendations for monitoring patients on the basis of their mutational status.

• Biomedical Science Letters
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• v.24 no.4
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• pp.426-429
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• 2018

Chronic eosinophilic leukemia (CEL) is characterized by eosinophilia and organ damage. Imatinib is widely used for treating CEL, chronic myeloid leukemia (CML) and acute myeloid leukemia (AML). Unfortunately, the cancer cells gain resistance against the drug after prolonged molecular-targeted therapies. Imatinib-resistant EoL-1 (EoL-1-IR) cells were produced from chronic eosinophilic leukemia cells (EoL-1) after treatment with imatinib for a long duration. Two-dimensional electrophoresis (2-DE) analysis revealed numerous protein variations in the EoL-1 and EoL-1-IR sub-types. Compared to the EoL-1 cells, expression levels of TIP49, RBBP7, ${\alpha}$-enolase, adenosine deaminase, C protein, galactokinase, eukaryotic translation initiation factor, $IFN-{\gamma}$, and human protein homologous to DROER were increased, whereas core I protein, proteasome subunit p42, heterogeneous ribonuclear particle protein, chain B, and nucleoside diphosphate were decreased in the EoL-1-IR cells. Taken together, these results contribute to understanding the pathogenic mechanism of drug-resistant diseases.

• The Journal of the Korea Contents Association
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• v.17 no.10
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• pp.289-299
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• 2017

To verify the association between susceptibility to chronic myeloid leukemia (CML) and GSTM1, GSTT1 gene polymorphisms in Asian populations, 9 papers published until July 2017 were cited in a meta-analysis. The null present types of the GSTM1, GSTT1 gene were analyzed individually. The significant association was found between CML and GST polymorphism (GSTM1; OR=1.306, 95% CI=1.091-1.563, p=0.004, GSTT1; OR=1.987, 95% CI=1.438-2.746, p=0.000). In addition, there was association between CML and the null type of the combination GSTM1-GSTT1 polymorphisms (OR=4.191, 95% CI=2.833-6.201, p=0.000). Thus, genetic polymorphisms of the GSTM1, GSTT1 and combination GSTM1-GSTT1 polymorphism in Asian populations may be risk factors for CML.

• YAKHAK HOEJI
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• v.60 no.3
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• pp.118-127
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• 2016

A growing number of studies have demonstrated that ABCB1 gene polymorphisms are associated with the variability of responses to imatinib. However, the effects of ABCB1 polymorphisms on imatinib response in chronic myeloid leukemia (CML) are inconsistent. The aim of the present study was to clarify the associations between ABCB1 polymorphisms and imatinib response in CML. A systematic literature review was performed. The databases of PubMed, Embase, 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', 'ABCB1', 'MDR1', 'polymorphism', 'SNP', and 'imatinib'. Using the Review Manager 5, odds ratios (ORs) were pooled to estimate the effect of ABCB1 polymorphisms on imatinib response in CML. The pooled analysis showed that ABCB1 2677 G allele was significantly associated with poor response to imatinib in African and Asian patients (GG vs TT, OR: 0.32, p<0.0001; GG+GT vs TT, OR: 0.44, p=0.0005). In subgroup analyses, African patients carrying ABCB1 1236 C allele exhibited higher risk for worse response, whereas Asian patients with 1236 C allele showed better response (CC+CT vs TT, OR: 0.41, p=0.008 for African; OR: 1.65, p=0.03 for Asian). There was no association between C3435T polymorphisms and imatinib response in African, Asian, and Caucasian CML patients.

• Journal of the Korean Society of Radiology
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• v.83 no.4
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• pp.918-923
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• 2022

Large vessel vasculitis is characterized by chronic inflammation within the aortic wall and its major branches. The inflammation is considered to occur as a result of immune dysregulation. Hematologic malignancy is one of the rare causes of secondary vasculitis. Herein, we report a rare case of large vessel vasculitis associated with acute myeloid leukemia mimicking primary vasculitis.

• Korean journal of aerospace and environmental medicine
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• v.31 no.3
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• pp.82-83
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• 2021

Chronic myeloid leukemia (CML) is myeloproliferative neoplasm associated with a characteristic chromosomal translocation (bcr-abl) called Philadelphia chromosome which plays a key role in the pathogenesis. Approximately 85% of patients with CML are in the chronic phase at the time of diagnosis. During this phase, patients are well tolerated and have few symptoms. But untreated, over the course of several years progresses to an accelerated phase and ultimately to a blast crisis, the terminal phase. CML is largely treated with targeted drug therapy called tyrosine-kinase inhibitors (TKIs) which have led to dramatically improved long-term survival rates since 2001. These drugs became standard treatment of this disease and allow most patients to have much better quality of life when compared to the former chemotherapy drugs and the bone marrow transplantation. Imatinib (Gleevec or Glivec, Norvatis) was the first of these TKIs and found to inhibit the progression of CML in the majority of patients (65%-75%) sufficiently to achieve remission. Since the advent of imatinib, CML has become the first neoplasm in which a medical treatment can give to the patient a normal life expectancy.