• Journal of Korean Dental Science
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• v.11 no.2
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• pp.82-85
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• 2018

Leukemia is a hematological malignant disease with various clinical symptoms. Due to the fatal nature of the disease, early detection is important. Oral manifestations include ulcers and gingival enlargement with bleeding. Moreover, myeloid sarcoma or opportunistic infections may also occur. This report introduces a 31-year-old male presenting with generalized gingival enlargement with bleeding and another 81-year-old female with neoplasm on the left retromolar area. Both were diagnosed as acute monocytic leukemia. These cases implicate that gingival enlargement or mucosal lesion in the oral cavity may represent underlying systemic diseases. Related to this, it has to be reminded that making timely diagnosis and referral according to the clinical findings is crucial.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.130.1-130.1
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• 2003

As a potent antigen presenting cells and a powerful inducer of antigen specific immunity including cytotoxic T cell activity, dendritic cells(DCs) are being considered as a promising anti-tumor therapeutic module. Unlike solid tumors, leukemia is the hematologic malignancy involving immune effector cells. The expected usage of DCs in leukemia is the treatment of minimal residual disease(MRD) after the remission or stem cell transplantation. In this study, syngeneic leukemia cells were inoculated intra-venously into the mouse (WEHI-3 into the Balb/c), and the autologous tumor cell lysate pulsed DCs were injected as a therapeutic module twice in two weeks. (omitted)

• Biomedical Science Letters
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• v.24 no.2
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• pp.134-137
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• 2018

S100A8 and S100A9 are involved in pathogenesis of cancer by induction or inhibition of cancer as well as inflammation. In this study, we investigated the association of S100A8 and S100A9 with pathogenesis of leukemia using human monocytic leukemia cells, THP-1. The expression of TLR4, which is a known receptor of S100A8 and S100A9, was examined by using flow cytometry and Western blotting. THP-1 cells have high surface and cytosol expression of TLR4. S100A8 and S100A9 suppressed the cell survival, and this suppression was found to be associated with apoptosis because they increased the number of apoptotic cells in a dose- and a time-dependent manners. However, S100A8 and S100A9 had no effect on the survival and apoptosis of monocytes isolated from the peripheral blood. We next examined the apoptotic effect of lipopolysaccharide (LPS) and monophosphoryl lipid A (MPLA), which are other ligands of TLR4, in THP-1 cells. Lipopolysaccharide had no effect on cell survival, but MPLA is effective on the cell apoptosis. These results suggest that S100A8 and S100A9 may regulate leukemia cell survival via TLR4, which is an essential receptor in the pro-apoptotic mechanism induced by S100A8 and S100A9. These findings may shed light on development of a possible therapeutic drug for leukemia treatment.

• Genomics & Informatics
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• v.8 no.4
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• pp.185-193
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• 2010

Histone deacetylation and demethylation are epigenetic mechanisms implicated in cancer. Studies regarding the role of modulation of gene expression utilizing the histone deacetylase inhibitor scriptaid and the demethylating agent 5-azacytidine in HL-60 leukemia cells have been limited. We studied the possibility of recovering epigenetically silenced genes by scriptaid and 5-azacytidine in human leukemia cells by DNA microarray analysis. The first group was leukemia cells that were cultured with 5-azacytidine. The second group was cultured with scriptaid. The other group was cultured with both agents. Two hundred seventy newly developed genes were expressed after the combination of 5-azacytidine and scriptaid. Twenty-nine genes were unchanged after the combination treatment of 5-azacytidine and scriptaid. Among the 270 genes, 13 genes were differed significantly from the control. HPGD, CPA3, CEACAM6, LOC653907, ETS1, RAB37, PMP22, FST, FOXC1, and CCL2 were up-regulated, and IGLL3, IGLL1, and ASS1 were down-regulated. Eleven genes associated with oncogenesis were found among the differentially expressed genes: ETS1, ASCL2, BTG2, BTG1, SLAMF6, CDKN2D, RRAS, RET, GIPC1, MAGEB, and RGL4. We report the results of our leukemia cell microarray profiles after epigenetic combination therapy with the hope that they are the starting point of selectively targeted epigenetic therapy.

• 대한예방의학회:학술대회논문집
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• 1994.02a
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• pp.651-657
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• 1994

To assess quantitatively the association between benzene exposure and leukemia, we examined the mortality rate of a cohort with occupational exposure to benzene. Cumulative exposure for each cohort member was estimated from historical air-sampling data and, when no sampling data existed, from interpolation on the basis of existing data. The overall standardized mortality ratio (a measure of relative risk multiplied by 100) for leukemia was 337 (95 percent confidence interval, 154 to 641), and that for multiple myeloma was 409 (95 percent confidence interval, 110 to 1047). With stratification according to levels of cumulative exposure, the standardized mortality ratios for leukemia increased from 109 to 322, 1186, and 6637 with increases in cumulative benzene exposure from less than 40 parts per million-years (ppm-years), to 40 to 199, 200 to 399, and 400 or more. respectively. A cumulative benzene exposure of 400 ppm years is equivalent to a mean annual exposure of 10 ppm over a 40-year working lifetime; 10 ppm is the currently enforceable standard in the United States for occupational exposure to benzene. To examine the shape of the exposure-response relation, we performed a conditional logistic-regression analysis, in which 10 controls were matched to each cohort member with leukemia. From this model, it can be calculated that protection from benzene induced leukemia would increase exponentially with any reduction in the permissible exposure limit.

• 대한예방의학회:학술대회논문집
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• 1994.02a
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• pp.681-691
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• 1994

The American Conference of Governmental Industrial Hygienists (ACGIH) has proposed a threshold limit value (TLV) for benzene of 0.1 ppm. Individuals representing the American Petroleum Institute (API)and the Chemical Manufacturers Association (CMA) have argued that 1) the risk assessment by Rinsky .et al. which ACGIH partially relied upon for its proposed TLV overestimates the risk; however, at the exposures levels of interest - (e.g., 0.1 to 1.0 ppm) for establishing a benzene TLV, the Rinsky et al. assessment provides lower estimates of leukemia risk than most others; 2) ACGIH should not use the Dow study for direct observational evidence of leukemia risk associated with low-level benzene exposure because of confounding exposure; however, it is unlikely that confounding exposures played a role in the excess of leukemia demonstrated in the study, and the Dow cohort was exposed to an average benzene concentration of about 5.5 ppm benzene for 7.11 years (31:1.5 ppm-years), while some of the individuals in the study who died from leukemia were exposed to an average of only 1.0 ppm without the opportunity for highpeak exposures; 3) the Occupational Safety and Health Administration (OSHA) established an 8-hour time-weighted average (TWA) of 1.0 ppm in 1987, and there is no new evidence that would justify reducing the TWA below that level; however, the OSHA TWA of 1.0 ppm was based on economic feasibility and the level of excess risk remaining at 1.0 ppm, i.e., 10 excess leukemia deaths per 1000 workers over an occupational lifetime (45 years) according to OSHA's preferred estimate leaves behind I risk considered significant by OSHA. In addition, chromosomal studies among workers and in animals exposed to benzene indicate that low-level exposure, i.e., 1.0 ppm, is associated with elevated Cytogenetic damage. On the basis of adverse health effects data alone, in this author's opinion, it would be poor science and poor public health policy to establish a benzene TLV greater than 0.1 ppm.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.22
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• pp.9915-9919
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• 2014

Lamellarin D (LamD) is a marine alkaloid with a pronounced cytotoxicity against a large panel of cancer cells, affecting cell growth and inducing apoptosis. However, the molecular mechanisms of action of this compound are poorly understood. In this study, the anticancer efficacy of LamD was investigated in human leukemia K562 cells. The results showed suppressed cell proliferation and induction of G0/G1-phase arrest,while expression of CDK1, and activity of smad3 and smad5 were reduced, but that of p27, p53 and STGC3 was increased. LamD induced cell apoptosis through activation of caspases-8/-3, inhibition of survivin and Bcl-2, suggesting that this compound may also act through a caspase-independent pathway. Moreover, LamD inhibited the secretion of TGF-${\beta}$, IL-$1{\beta}$, IL-6, IL-8 and other inflammatory cytokines and the transcriptional activity of transcription factor NF-${\kappa}B$ in human leukemia K562 cells.Taken together, our results suggest that LamD-mediated inhibition of leukemia cell proliferation may be related to the induction of apoptosis and the regulation of cell cycle, tumor-related gene expression and cytokine expression, which may provide a new way of thinking for the treatment leukemia.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.16
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• pp.6923-6928
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• 2014

In recent years, mounting evidence has indicated that the CCND1 G870A gene polymorphism, which impacts the mitotic cell cycle, may influence leukemia or non-Hodgkin lymphoma risk. Unfortunately, the previous results were inconsistent. Therefore, a meta-analysis was performed to obtain a more precise estimation of any association. We conducted a search in PubMed, Embase and CNKI covering all published papers up to March, 2014. A total of 9 publications including 10 case-control studies met the inclusion criteria. Odds ratios (ORs) and their 95% confidence intervals (95%CIs) were applied to assess association. The pooled ORs showed significant association in non-Hodgkin lymphoma (comparison A vs G: OR= 1.114, 95%CI=1.053-1.179, p=0.000; homozygote comparison AA vs GG: OR=1.245, 95%CI=1.110-1.396, p=0.000; heterozygote comparison AG vs GG: OR=1.095, 95%CI=1.000-1.199, p=0.05; dominant model AA/GA vs GG: OR=1.137, 95%CI=1.043-1.239, p=0.003; and recessive model AA vs GA/GG: OR=1.177, 95%CI=1.066-1.301, p=0.001). However, there was no association between the CCND1 G870A polymorphism and leukemia risk. In conclusion, the CCND1 G870A polymorphism may increase risk of non-Hodgkin lymphoma, but not leukemia. However, more primary large scale and well-designed studies are still required to evaluate the interaction of CCND1 G870A polymorphism with leukemia and non-Hodgkin lymphoma risk.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.26 no.3
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• pp.310-312
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• 2000

Leukemia is a malignancy caused by precursor cells of white blood cell. It is a malignant tumor of hematopoietic organs, characterized by the disorder of hematopoietic function due to the proliferation of immature bone marrow cells or lymphatic cells and by abnormal tissue infiltration of leukemic cells. The major signs of leukemia are caused by the failure of bone marrow function. As the number of red blood cells decreases, anemia is to appear. The number of white blood cells in leukemia is usually increased but immature white blood cells circulating the body has little defense ability, thus become susceptible to infection. 27 year-old female patient who was treated chemotherapy and bone marrow transplantation after diagnosed as chronic myelogenous leukemia(CML) was diagnosed as osteomyelitis in mandible after clinical and dental radiographic film examination. Because of the result of examination, the involved tooth of the patient was extracted accompanied by sequestrectomy and saucerization under general anesthesia. After the patient had long term medication of antibiotics, the lesion was healed. Therefore. author, et al. report this case with literature review.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.21
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• pp.9283-9289
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• 2014

Background: Acute lymphoblastic leukemia (ALL) is the most common cancer diagnosed in children and represents approximately 25% of cancer diagnoses among those younger than 15 years of age. Materials and Methods: This study investigated alterations in the displacement loop (d-loop) region of mitochondrial DNA (mtDNA) as a risk factor and diagnostic biomarker for early detection and diagnosis of acute lymphoblastic leukemia. Using mtDNA from 23 subjects diagnosed with acute lymphoblastic leukemia, the first 450 bp of the d-loop region were amplified and successfully sequenced. Results: This revealed 132 mutations at 25 positions in this region, with a mean of 6 alterations per subject. The d-loop alterations in mtDNA in subjects were all identified as single nucleotide polymorphisms in a homoplasmic distribution pattern. Mutant alleles were observed in all subjects with individual frequency rates of up to 95%. Thirteen mutant alleles in the d-loop region of mtDNA occurred with a high frequency. Novel alleles and locations were also identified in the d-loop of mtDNA as follows: 89 G insertions (40%), 95 G insertions (13%), 182 C/T substitutions (5%), 308 C insertions (19%), and 311 C insertions (80%). The findings of this study need to be replicated to be confirmed. Conclusions: Further investigation of the relationship between mutations in mitochondrial d-loop genes and incidence of acute lymphoblastic leukemia is recommended.