• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.14-21
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• 2001

Many epidemiological studies have revealed that the use of aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs) can reduce the risk of colon cancer. Since the well-documented pharmacological action of aspirin and other NSAIDs is the inhibition of cyclooxygenase [COX, the rate-limiting enzyme in prostaglandin (PG) biosynthesis], it has been inferred that the beneficial effect of NSAIDs may be mediated through the inhibition of PG biosynthesis.(omitted)

• Korean Journal of Clinical Pharmacy
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• v.25 no.4
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• pp.246-253
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• 2015

Background & Object: Ankylosing spondylitis (AS) is a chronic inflammatory disease that causes ankylosis and deformation of axial joints. Since current medicine cannot cure the disease yet, alleviating pain and preventing deformation with medications are the main therapy for patients with AS. The key medications for these purposes include nonsteroidal anti-inflammatory drugs (NSAIDs), and tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) inhibitors. This study aims to analyze prescribing patterns of AS patients in South Korea. Method: National Patients Sample data compiled by the Health Insurance Review and Assessment Service from 2013 was analyzed. Patients with AS were identified with Korean Standard Classification of Diseases code-6, which was M45. The rates of prescription, discontinuation, and switching ingredients were calculated for each medication during 2013. Results: Total number of patients was 655, and most of them were male (n = 514, 78.5%). Of all age groups, the proportion of 30-40 year old patients was the greatest (35.1%). The most utilized drug class was NSAIDs (82.4%). Less than half of patients were prescribed $TNF-{\alpha}$ inhibitors (n = 212, 32.4%). Meloxicam, aceclofenac, and celecoxib were the most frequently prescribed NSAIDs. In case of $TNF-{\alpha}$ inhibitors, adalimumab, etanercept and infliximab were the top three most prescribed drugs. Although not recommended by the current practice guideline, significant proportions of patients were identified using disease modifying anti-rheumatic drugs (DMARDs). Conclusion: Considering the current practice guideline and previous studies about the efficacy, the use of DMARDs should be reduced and medical insurance term in South Korea should be re-examined.

• Archives of Pharmacal Research
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• v.26 no.11
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• pp.892-897
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• 2003

Anticancer drugs have serious side effects arising from their poor malignant cells selectivity, Since insulin receptors highly express on the cytomembrane of some kind of tumor cells, using insulin as the vector was expected to reduce serious side effects of the drugs. The objective of this study was to evaluate the tumor targeting effect of the newly synthesized mitoxantrone-insulin conjugate (MIT-INS) with the drug loading of 11.68%. In vitro stability trials showed MIT-INS were stable in buffers with different pH (2-8) at $37^{\circ}C$ within 120 h (less than 3% of free MIT released), and were also stable in mouse plasma within 48 h (less than 1 % of free MIT released). In vivo study on tumor-bearing mice showed that, compared with MIT [75.92 $\mu g \cdot$ h/g of the area under the concentration-time curve (AUC) and 86.85 h of mean residence time (MRT)], the conjugates had better tumor-targeting efficiency with enhanced tumor AUC of 126.53 1l9 h/g and MTR of 151.95 h. The conjugate had much lower toxicity to most other tissues with targeting indexes ($TI^c$) no larger than 0.3 besides good tumor targeting efficiency with $TI^c$ of 1.67. The results suggest the feasibility to promote the curative effect in ca.ncer chemotherapy by using insulin as the vector of anti-cancer drugs.

• Biomedical Science Letters
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• v.29 no.3
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• pp.178-183
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• 2023

Natural killer (NK) cells are innate cytotoxic lymphoid cells that actively prevent neoplastic development, growth, and metastatic dissemination in a process called cancer immunosurveillance. Regulation of the cytotoxic activity of NK cells relies on integrated interactions between inhibitory receptors and numerous activating receptors that act in tandem to eliminate tumor cells efficiently. Conventional chemotherapy is designed to produce an anti-proliferative or cytotoxic effect on early tumor cell division. Therapies designed to kill cancer cells and simultaneously maintain host anti-tumor immunity are attractive strategies for controlling tumor growth. Depending on the drug and dose used, several chemotherapeutic agents cause DNA damage and cancer cell death through apoptosis, immunogenic cell death, or other forms of non-killing (i.e., mitotic catastrophe, senescence, autophagy). Among stress-induced immunostimulatory proteins, changes in the expression levels of NK cell activating and inhibitory ligands and tumor cell death receptors play an important role in the detection and elimination by innate immune effectors including NK cells. Therefore, we will address how these cytotoxic lymphocytes sense and respond to high and low concentrations of drug-induced stress to the drug cisplatin, among the various types of drugs that contribute to their anticancer activity.

• Journal of Microbiology and Biotechnology
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• v.25 no.7
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• pp.1036-1046
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• 2015

Extracts from Asian medicinal herbs are known to be successful therapeutic agents against cancer. In this study, the effects of three types of herbal extracts on anti-tumor growth were examined. Among the three types of herbal extracts, H9 showed stronger anti-tumor growth effects than H5 and H11 in vivo. To find the molecular mechanism by which H9 inhibited the proliferation of breast cancer cell lines, the levels of apoptotic markers were examined. Proapoptotic markers, including cleaved PARP and cleaved caspases 3 and 9, were increased, whereas the anti-apoptotic marker Bcl-2 was decreased by H9 treatment. Next, the combined effect of H9 with the chemotherapeutic drugs doxorubicin/cyclophosphamide (AC) on tumor growth was examined using 4T1-tumor-bearing mice. The combined treatment of H9 with AC did not show additive or synergetic anti-tumor growth effects. However, when tumor-bearing mice were co-treated with H9 and the targeted anti-tumor drug trastuzumab, a delay in tumor growth was observed. The combined treatment of H9 and trastuzumab caused an increase of natural killer (NK) cells and a decrease of myeloid-derived suppressor cells (MDSC). Taken together, H9 induces the apoptotic death of tumor cells while increasing anti-tumor immune activity through the enhancement of NK activity and diminishment of MDSC.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.1
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• pp.489-494
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• 2014

Background: Psychiatric patients appear to be at lower risk of cancer. Some antipsychotic drugs might have inhibitory effects on tumor growth, including penfluridol, a strong agent. To test this, we conducted a study to determine whether penfluridol exerts cytotoxic effects on tumor cells and, if so, to explore its anti-tumor mechanisms. Methods: Growth inhibition of mouse cancer cell lines by penfluridol was determined using the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Cytotoxic activity was determined by clonogenic cell survival and trypan blue assays. Animal tumor models of these cancer cells were established and to evaluate penfluridol for its anti-tumor efficacy in vivo. Unesterified cholesterol in cancer cells was examined by filipin staining. Serum total cholesterol and tumor total cholesterol were detected using the cholesterol oxidase/p-aminophenazone (CHOD-PAP) method. Results: Penfluridol inhibited the proliferation of B16 melanoma (B16/F10), LL/2 lung carcinoma (LL/2), CT26 colon carcinoma (CT26) and 4T1 breast cancer (4T1) cells in vitro. In vivo penfluridol was particularly effective at inhibiting LL/2 lung tumor growth, and obviously prolonged the survival time of mice bearing LL/2 lung tumors implanted subcutaneously. Accumulated unesterified cholesterol was found in all of the cancer cells treated with penfluridol, and this effect was most evident in LL/2, 4T1 and CT26 cells. No significant difference in serum cholesterol levels was found between the normal saline-treated mice and the penfluridol-treated mice. However, a dose-dependent decrease of total cholesterol in tumor tissues was observed in penfluridol-treated mice, which was most evident in B16/F10-, LL/2-, and 4T1-tumor-bearing mice. Conclusion: Our results suggested that penfluridol is not only cytotoxic to cancer cells in vitro but can also inhibit tumor growth in vivo. Dysregulation of cholesterol homeostasis by penfluridol may be involved in its anti-tumor mechanisms.

• The Journal of Korean Medicine
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• v.24 no.3
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• pp.138-144
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• 2003

Objective : Though modern medicine has made various studies in cancer treatment, the results of the treatments are not satisfactory. Considering this, Oriental medicine can be a breakthrough in treatment of cancer, and therefore, its constant research eagerly needed. According to preceding studies, Hangamjedoktang (Kangaizhidu-tang) with Hagocho appeared to be statistically significant against cancer, and therefore to seek a better medication for cancer, Holotrichia which seemed to be effective against cancer was added to the formula, and herbs which showed an anti-tumor effect in preceding studies composed Hangamyagjaebang. The efficacy of both Hangamjedoktang with Holotrichia (HJJ) and Hangamyagjaebang (Kangaiyaocaijang) (HM) was compared. Methods : To examine the anti-cancer effect of HJJ and HM, inhibitory effect on solid tumor growth in mice induced by Sarcoma-180 (s-180), change of body and organ weight in tumor bearing mice and the activity of machrophages and lymphocytes in the spleen were examined. Results : 1. In the HJJ and HM treated groups, tumor growth was markedly decreased. 2. HJJ and HM increased the activity of ALP which is produced from the splenocytes transplanted with S-180. 3. HJJ and HM increased the ACP activity of the macrophages of the mice transplanted with S-180. Conclusion : These results suggest that HJJ and HM are good candidates for new drugs for cancer therapy.

• Biomolecules & Therapeutics
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• v.28 no.6
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• pp.503-511
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• 2020

Autophagy is a major catabolic process that maintains cell metabolism by degrading damaged organelles and other dysfunctional proteins via the lysosome. Abnormal regulation of this process has been known to be involved in the progression of pathophysiological diseases, such as cancer and neurodegenerative disorders. Although the mechanisms for the regulation of autophagic pathways are relatively well known, the precise regulation of this pathway in the treatment of cancer remains largely unknown. It is still complicated whether the regulation of autophagy is beneficial in improving cancer. Many studies have demonstrated that autophagy plays a dual role in cancer by suppressing the growth of tumors or the progression of cancer development, which seems to be dependent on unknown characteristics of various cancer types. This review summarizes the key targets involved in autophagy and malignant transformation. In addition, the opposing tumor-suppressive and oncogenic roles of autophagy in cancer, as well as potential clinical therapeutics utilizing either regulators of autophagy or combinatorial therapeutics with anti-cancer drugs have been discussed.

• Microbiology and Biotechnology Letters
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• v.44 no.4
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• pp.420-431
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• 2016

The complement system comprises a set of essential molecules that bridge the innate and adaptive immune responses. Research has focused on how the complement system's destructive mechanism could potentially be harnessed for cancer treatment. However, cancer subverts the complement system to avoid immunosurveillance. In addition, a complement-triggered biological mechanism that contributes to cancer growth has been identified. Thus, drugs should be designed to homeostatically maintain a normal concentration of complement. This review explores three types of complement-related anti-cancer drugs: therapeutic antibodies, complement inhibitory drugs, and anti-complement regulatory drugs.

• Biomedical Science Letters
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• v.17 no.3
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• pp.253-260
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• 2011

Chaga mushroom (Inonotus obliquus) extract has been known to have therapeutic effects, such as anti-inflammatory, hepato-protective, anti-oxidant and anti-tumor effect. In this study, we evaluated the effects of Chaga extract on the cytotoxic actions of cisplatin in HepG2 hepatoma cells. The viability of the HepG2 cells was decreased to 10% at 3 ${\mu}M$ cisplatin and to 20% at 500 ${\mu}g$/ml Chaga extract as measured by the MTT assay. The viability of HepG2 cells co-treated with cisplatin (3 ${\mu}M$) and Chaga extract (500 ${\mu}g$/ml) was decreased to 50% in compared with the control cells. The cytotoxicity of two drugs was revealed as apoptosis characterized by the chromatic condensation, nuclear fragmentation and the cleavage of pro caspase-3 in HepG2 cells. Also, the cells treated with combination of two drugs showed synergistically the loss of mitochondrial membrane potential and increase of intracellular ROS levels. Therefore, these results suggest that the combination treatment of cisplatin and Chaga extract induces apoptotic cell death in HepG2 cells and has more potential anti-tumor effect than cisplatin alone.