• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6523-6526
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• 2012

Objective: This study was designed to investigate treatment efficacy and side effects of concomitant Aisu$^{(R)}$ (docetaxel) with three-dimensional conformal external beam radiotherapy for the treatment of inoperable patients with esophageal cancer. Methods: Inoperable patients were treated with three-dimensional conformal external beam radiotherapy (5/week, 2 GY/day, and total dose 60GY) plus docetaxel ($30-45mg/m^2$, iv, d1, 8). Results: Twenty eight patients met the study eligibility criteria and the response rate was evaluated according to RICIST guidelines. Among 28 patients, 2 achieved CR, 22 PR, 3 SD and 1 patient was documented PD. Mild gastrointestinal reaction and bone marrow suppression were also documented. All treatment related side effects were tolerable. Conclusion: Three-dimensional conformal external beam radiotherapy combined with docetaxel is an active and safe regimen for inoperable patients with esophageal cancer.

• Tuberculosis and Respiratory Diseases
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• v.53 no.6
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• pp.656-661
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• 2002

Amidarone is one of the most commonly prescribed anti-arrythmic agents for almost all arrythmias, whether atrial or ventricular in origin. There are several side effects associated with amiodarone therapy. These include corneal deposits, abnormal liver function tests, hyper and hypothyroidism, bluish discolorations of the skin, bone marrow suppression, coagulopathies, peripheral neuropathies, and pulmonary toxicity. Amiodarone-induced pulmonary toxicity(APT), which was first described in 1980, is potentially serious side effects that are believed to develop in 5% of patients. Doctors often assume that APT occurs only when high amiodarone doses are used for a long time, but in practice a low maintenance dose of amiodarone may also be toxic. In this report, a case of amiodarone-induced pulmonary toxicity after a long course of a low dose therapy for refractory supraventricular arrythmia is described.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4801-4804
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• 2013

Purpose: To investigate short-term response rate, quality of life and toxicities of mannan peptide combined with TP regimen in treating patients with non-small cell lung cancer (NSCLC). Patients and Methods: Forty one patients with NSCLC were divided into an experimental group treated with TP regimen combined with mannan peptide (21 patients) and a control group treated with TP alone (20 patients). Results: Response rates were 61.9% (13/21) for the experimental and 60% (12/20) for the control group (p>0.05). Regarding toxicity, white blood cell decreased more frequently in the control group (65%, 13/20) than in the experimental group (33.3%, 7/21) (p<0.05); nausea and vomiting also occurred more frequently in the control group (55%, 11/20 vs 23.8%, 5/21) (p<0.05). In terms of quality of life, this index was improved by 57.1% (12/21) and 25% (5/20) in experimental and control groups, respectively (p<0.05). Conclusions: Response rate of TP after combined with mannan peptide is mildly increased, while this combination alleviates bone marrow suppression as well as nausea and vomiting of TP, and improves quality of life when treating patients with NSCLC. However, this conclusion should be confirmed by randomized clinical trails.

• Journal of Medicine and Life Science
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• v.16 no.2
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• pp.46-51
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• 2019

Inflammatory bowel disease (IBD) is an immune-mediated chronic inflammatory intestinal condition. With development of various treatment options for IBD, 5-aminosalicylic acid (5-ASA) agents became the drugs of choice due to high efficacy and low risk of complication, specifically effective at inducing and maintaining remission in ulcerative colitis(UC). Pancytopenia caused by 5-ASA agents, especially by mesalazine, has been rarely reported compared with azathioprine, which is commonly used for glucocorticoid-dependent IBD and known to have risk of bone marrow suppression. In the present report, we describe the case of a 57-year-old woman diagnosed with UC, who developed pancytopenia due to adverse effect of mesalazine after recovery from azathioprine-induced pancytopenia. After withdrawal of mesalazine, the laboratory values consistent with myelosuppression continued for 3 months while pancytopenia from azathioprine remained only for 2 weeks. Since pancytopenia can be fatal due to its risk of severe bleeding and infection, close monitoring of clinical presentation is important when starting mesalazine and laboratory data should be evaluated whenever the patients present related symptoms. Furthermore, we suggest that complete blood cell counts should be considered when resuming mesalazine following the development of pancytopenia from any cause, as routinely recommended for azathioprine use.

• IMMUNE NETWORK
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• v.5 no.3
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• pp.150-156
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• 2005

Background: Dendritic cells (DCs) playa critical role not only in the initiation of immune responses, but also in the induction of immune tolerance. In an effort to regulate immune responses through the modulation of antigen presenting cell (APC) function of DCs, we searched for and characterized APC function modulators from natural products. Methods: DCs were cultured in the presence of propolis components, WP and CP, and then examined for their ability to present exogenous antigen in association with major histocompatibility complexes (MHC). Results: WP and CP inhibited class I MHC-restricted presentation of exogenous antigen (cross-presentation) in a DC cell line, DC2.4 cells, and DCs generated from bone marrow cells with GM-CSF and IL-4. The inhibitory activity of WP and CP appeared to be due not only to inhibition of phagocytic activity of DCs, but also to suppression of expression of MHC molecules on DCs. We also examined the effects of WP and CP on T cells. Interestingly, WP and CP increased IL-2 production from T cells. Conclusion: These results demonstrate that WP and CP inhibit MHC-restricted presentation of exogenous antigen through down-regulation of phagocytic activity and suppression of expression of MHC molecules on DCs.

• Archives of Pharmacal Research
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• v.25 no.3
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• pp.364-369
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• 2002

Hepatitis C virus (HCV) is remarkably efficient at establishing chronic infection. One of the reasons for this appears to be the suppression of the accessory cell function of professional antigen presenting cells. In the present study, the immunosuppressive activity of HCV protein was examined on dendritic cells (DCs) generated from mouse bone marrow progenitor cells in vitro. We found that the DCs forced to express HCV protein have defective allostimulatory ability. DCs expressing HCV protein were phenotypically indistinguishable from normal DCs. However, they were unable to produce IL-12 effectively when stimulated with lipopolysaccharide. The functional domain of the HCV protein essential for immunosuppression was determined using a series of ${NH_2}-and$ C-terminal deletion mutants of HCV core protein. We found that amino acid residues residing between the 21 st and the 40th residues from the ${NH_2}-terminus$ of HCV core protein are required for immunosuppression. These findings suggest that HCV core protein suppresses the elicitation of protective Th1 responses by the inhibition of IL-12 production by DCs.

• Toxicological Research
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• v.31 no.1
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• pp.11-16
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• 2015

Our body's immune system has defense mechanisms against pathogens such as viruses and bacteria. Immune responses are primarily initiated by the activation of toll-like receptors (TLRs). In particular, TLR4 is well-characterized and is known to be activated by gram-negative bacteria and tissue damage signals. TLR4 requires myeloid differentiation factor 2 (MD2) as a co-receptor to recognize its ligand, lipopolysaccharides (LPS), which is an extracellular membrane component of gram-negative bacteria. Gambogic acid is a xanthonoid isolated from brownish or orange resin extracted from Garcinia hanburyi. Its primary effect is tumor suppression. Since inflammatory responses are related to the development of cancer, we hypothesized that gambogic acid may regulate TLR4 activation. Our results demonstrated that gambogic acid decreased the expression of pro-inflammatory cytokines ($TNF-{\alpha}$, IL-6, IL-12, and $IL-1{\beta}$) in both mRNA and protein levels in bone marrow-derived primary macrophages after stimulation with LPS. Gambogic acid did not inhibit the activation of Interferon regulatory factor 3 (IRF3) induced by TBK1 overexpression in a luciferase reporter gene assay using IFN-${\beta}$-PRD III-I-luc. An in vitro kinase assay using recombinant TBK1 revealed that gambogic acid did not directly inhibit TBK1 kinase activity, and instead suppressed the binding of LPS to MD2, as determined by an in vitro binding assay and confocal microscopy analysis. Together, our results demonstrate that gambogic acid disrupts LPS interaction with the TLR4/MD2 complex, the novel mechanism by which it suppresses TLR4 activation.

• International Journal of Oral Biology
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• v.36 no.4
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• pp.173-178
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• 2011

Tumor necrosis factor alpha ($TNF{\alpha}$) is a multifunctional cytokine that is elevated in inflammatory diseases such as atherosclerosis, diabetes and rheumatoid arthritis. Recent evidence has suggested that ${\beta}2$ adrenergic receptor (${\beta}2AR$) activation in osteoblasts suppresses osteogenic activity. In the present study, we explored whether $TNF{\alpha}$ modulates ${\beta}AR$ expression in osteoblastic cells and whether this regulation is associated with the inhibition of osteoblast differentiation by $TNF{\alpha}$. In the experiments, we used C2C12 cells, MC3T3-E1 cells and primary cultured mouse bone marrow stromal cells. Among the three subtypes of ${\beta}AR$, ${\beta}2$ and ${\beta}3AR$ were found in our analysis to be upregulated by $TNF{\alpha}$. Moreover, isoproterenol-induced cAMP production was observed to be significantly enhanced in $TNF{\alpha}$-primed C2C12 cells, indicating that $TNF{\alpha}$ enhances ${\beta}2AR$ signaling in osteoblasts. $TNF{\alpha}$ was further found in C2C12 cells to suppress bone morphogenetic protein 2-induced alkaline phosphatase (ALP) activity and the expression of osteogenic marker genes including Runx2, ALP and osteocalcin. Propranolol, a ${\beta}2AR$ antagonist, attenuated this $TNF{\alpha}$ suppression of osteogenic differentiation. $TNF{\alpha}$ increased the expression of receptor activator of NF-${\kappa}B$ ligand (RANKL), an essential osteoclastogenic factor, in C2C12 cells which was again blocked by propranolol. In summary, our data show that $TNF{\alpha}$ increases ${\beta}2AR$ expression in osteoblasts and that a blockade of ${\beta}2AR$ attenuates the suppression of osteogenic differentiation and stimulation of RANKL expression by $TNF{\alpha}$. These findings imply that a crosstalk between $TNF{\alpha}$ and ${\beta}2AR$ signaling pathways might occur in osteoblasts to modulate their function.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.4
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• pp.2611-2614
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• 2013

Aims: To explore efficacy and side effects of intrapleural or intraperitoneal lobaplatin for treating patients with malignant pleural or peritoneal effusions. Methods: Patients in Jiangsu Cancer Hospital and Research Institute with cytologically confirmed solid tumors complicated with malignant pleural effusion or ascites were enrolled into this study. Lobaplatin (20-30 $mg/m^2$) was intrapleurally or intraperitoneally infused for patients with malignant pleural effusion or ascites. Results: From 2012 to 2013, intrapleural or intraperitonea lobaplatin was administered for patients with colorectal or uterus cancer who were previous treated for malignant pleural effusion or ascites. Partial response was achieved for them. Main side effects were nausea/vomiting, and bone marrow suppression. No treatment related deaths occurred. Conclusion: Intrapleural or intraperitoneal infusion of lobaplatin is a safe treatment for patients with malignant pleural effusion or ascites, and the treatment efficacy is encouraging.

• Journal of Korean Academy of Nursing Administration
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• v.8 no.1
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• pp.85-95
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• 2002

The purpose of this study was to develope a critical pathway for the chemotherapy of non-small cell lung cancer patients and to identify its effects after implementation. Critical pathway was developed through 5 steps including content and clinical validity tests with collaborative efforts of nurses, clinicians, and other allied healthcare professionals with the aim of improving the quality of patient care, while minimizing cost to the patients. This paper was described an evaluation of the impact of a developed critical pathway on complication rate, length of stay, costs, the interval of treatment and patient satisfaction by nonequivalent control group posttest-only non-synchronized research design.Results were compared between the two groups of patients. There were no significant differences in demographic variables and the occurrence of bone marrow suppression between experimental group and control group(t=-0.01, p=0.992). There were statistically significant decreases in the average length of stay(t=-10.45, p=0.000), in the average cost(t=-2.988, p=0.004), and in the interval of treatment(t=-6.75, p=0.000) after implementation of the critical pathway compared to control group. Also, there was a statistically significant improvement of the patient satisfaction after implementation of the critical pathway compared to control group(t=4.57, p=0.000). This paper concludes that critical pathway in chemotherapy for lung cancer, implemented in the context of an general hospital, is the useful tool to shorten the hospital stay, reduce treatment costs, and improve the quality of life in cancer patients. Further study needs to be conducted to identify other clinical outcomes including job satisfaction, collaboration among health professionals and potential for use in education. Also, it is recommended that nurses should revise continuously the developed critical pathway through clinical implementation and maintain their role of patient advocacy through monitoring pathway compliance.