• 한국환경보건학회지
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• 제21권3호
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• pp.67-76
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• 1995

The frequencies of chromosome aberrations and sister chromatid-exchanges in peripheral blood lymphocyte of 44 nurses handling anticancer drugs were compared with those in 44 age-match controls. The frequencies of dicentric chrdmosome were $2.4\times 10^{-3}$ in the exposed and $0.5\times 10^{-3}$ in the control. The frequencies of sister cromatid exchanges in the exposed were slightly higher (5.68 SCEs/cell) than those in the control (5.04 SCEs/cell). The frequencies of chromosome aberrations and sister cromatid exchanges were not associated with duration of drug handling and types of anticancer drugs, but associated with use of safety cover.

• Toxicological Research
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• 제30권1호
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• pp.1-5
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• 2014

Xenograft models of human cancer play an important role in the screening and evaluation of candidates for new anticancer agents. The models, which are derived from human tumor cell lines and are classified according to the transplant site, such as ectopic xenograft and orthotopic xenograft, are still utilized to evaluate therapeutic efficacy and toxicity. The metastasis model is modified for the evaluation and prediction of cancer progression. Recently, animal models are made from patient-derived tumor tissue. The patient-derived tumor xenograft models with physiological characters similar to those of patients have been established for personalized medicine. In the discovery of anticancer drugs, standard animal models save time and money and provide evidence to support clinical trials. The current strategy for using xenograft models as an informative tool is introduced.

• Asian Pacific Journal of Cancer Prevention
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• 제17권4호
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• pp.1739-1744
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• 2016

We report herein an in vitro anticancer evaluation of a series of seven curcumin analogues (3a-g). The National Cancer Institute (NCI US) Protocol was followed and all the compounds were evaluated for their anticancer activity on nine different panels (leukemia, non small cell lung cancer, colon cancer, CNS cancer, melanoma, ovarian cancer, renal cancer, prostate cancer and breast cancer) represented by 60 NCI human cancer cell lines. All the compounds showed significant anticancer activity in one dose assay (drug concentration $10{\mu}M$) and hence were evaluated further in five dose assays (0.01, 0.1, 1, 10 and $100{\mu}M$) and three dose related parameters $GI_{50}$, TGI and $LC_{50}$ were calculated for each (3a-g) in micro molar drug concentrations (${\mu}M$). The compound 3d (NSC 757927) showed maximum mean percent growth inhibition (PGI) of 112.2%, while compound 3g (NSC 763374) showed less mean PGI of 40.1% in the one dose assay. The maximum anticancer activity was observed with the SR (leukemia) cell line with a $GI_{50}$ of $0.03{\mu}M$. The calculated average sensitivity of all cell lines of a particular subpanel toward the test agent showed that all the curcumin analogues showed maximum activity on leukemia cell lines with $GI_{50}$ values between 0.23 and $2.67{\mu}M$.

• Advances in nano research
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• 제7권4호
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• pp.241-248
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• 2019

Recent researches demonstrated well promising anticancer activities for antibiotics. Such effects would be significantly increased while nanoparticle based delivery systems were applied. In this study, the goal was aim to improve anticancer and antitoxic effects of Streptomycin by loading on special kind of dendrimer (anionic-linear-globular second generation). In the current study, Size and zeta potential as well as AFM techniques have been used to prove the fact that the loading was performed correctly. The Minimum Inhibitory Concentration (MIC) and Minimum Bactericidal Concentration (MBC) of the drug loaded on dendrimer nanoparticle were determined and compared with both of dendrimer alone and free drug with respect to staphylococcus aureus as the test microorganism. The anticancer activity among three groups including Streptomycin, Streptomycin -G2 dendrimer, and control was measured in vitro. In vitro studies showed that G2 anionic linear-globular polyethylene-glycol-based dendrimer, which loaded on Streptomycin was able to significantly improve the treatment efficacy over clinical Streptomycin alone with respect to proliferation assay. Maximal inhibitory concentration (IC50) was calculated to be $257{\mu}g/mL$ for streptomycin alone and $55{\mu}g/mL$ for Streptomycin -G2 dendrimer. In addition, Streptomycin -G2 dendrimer conjugate prevented the growth of MCF-7 cancerous cells in addition to enhance the number of apoptotic and necrotic cells as demonstrated by an annexin V-fluorescein isothiocyanate assay. Streptomycin -G2 dendrimer conjugate was able to increase Bcl-2/Bax ratio in a large scale compared with the control group and Streptomycin alone. Based on results a new drug formulation based nano-particulate was improved against S. aureus with sustained release and enhanced antibacterial activity as well as anticancer activity shown for functional cancer treatment with low side effects.

• 대한의생명과학회지
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• 제29권3호
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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.

• 대한약학회:학술대회논문집
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• 대한약학회 2001년도 Proceedings of International Convention of the Pharmaceutical Society of Korea
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• pp.243.3-244
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• 2001

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.167.2-168
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• 2003

Anticancer drug resistance occasionally occurs in malignant hematologic diseases such as acute myelocytic leukemia (AML) treated with chemotherapy and is a major problem to complete remission. Malignant cells primarily induce intrinsic resistance to treatment of anticancer drug, but gradually obtain acquired resistance to cytotoxic activities of chemotherapy. In this study, we monitored the expression profiles of doxorubicin resistance-related genes in AML-2/DX100, a doxorubicin-resistant human acute myelocytic leukemia cell line. (omitted)

• Journal of Microbiology and Biotechnology
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• 제29권4호
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• pp.571-576
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• 2019

Microenvironmental stress, which is naturally observed in solid tumors, has been implicated in anticancer drug resistance. This tumor-specific stress causes the degradation of topoisomerase $II{\alpha}$, rendering cells resistant to topoisomerase $II{\alpha}$-targeted anticancer agents. In addition, microenvironmental stress can induce the overexpression of 78kDa glucose regulated protein (GRP78), which can subsequently block the activation of apoptosis induced by treatment with anticancer agents. Therefore, inhibition of topoisomerase $II{\alpha}$ degradation and reduction in GRP78 expression may be effective strategies for inhibiting anticancer drug resistance. In this study, we investigated the active compound arctigenin, which inhibited microenvironmental stress-induced etoposide resistance in HT-29 cells. Arctigenin was also highly toxic to etoposide-resistant HT-29 cells, with an $IC_{50}$ value of $10{\mu}M$ for colony formation. We further showed that arctigenin inhibited the degradation of topoisomerase $II{\alpha}$ and reduced the expression of GRP78. Thus, these results suggest that arctigenin is a novel therapeutic agent that inhibits resistance to etoposide associated with microenvironmental stress conditions.

• 대한수의학회지
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• 제62권1호
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• pp.3.1-3.7
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• 2022

Disulfiram (DSF) is a marketed drug to treat patients with alcohol dependence by inhibiting aldehyde dehydrogenase. Over the last few decades, DSF has been shown to have anticancer effects through different mechanisms. Moreover, this effect can be elevated when used with copper (Cu). Subsequent studies have been conducted on various cancers, but few on lymphoma. This study investigated the anticancer effects of DSF on lymphoma and how this effect changed when treated with Cu. DSF synergistically decreased the metabolic activity of EL4 lymphoma cells when combined with Cu. At 1 µM of DSF alone, the metabolic activity of EL4 cells decreased by 49% compared to the control, whereas it decreased by 87% with a DSF + CuCl₂ treatment. Rhodamine 123 and 2',7'-dichlorofluorescein diacetate staining showed that DSF induced the reduction of the mitochondrial membrane potential and promoted the production of reactive oxygen species. In particular, the combined treatment of DSF + Cu induced cell death based on multiple assays, including annexin V-fluorescein isothiocyanate/propidium iodide staining. Overall, DSF has anticancer effects on lymphoma cells and exhibits synergistic effects when combined with Cu. This study provides some valuable information to broaden the use of DSF in clinics and basic research.

• 공업화학
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• 제29권2호
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• pp.147-154
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• 2018

현재 항암제의 낮은 치료 효율과 부작용을 해결하기 위해 고분자 기반의 약물전달체의 연구가 활발하게 진행되고 있다. 기존의 고분자기반의 약물 전달체는 우수한 결과를 보이는 등 상당한 진전이 있었음에도 불구하고, 대부분 혈중에서 안정성이 감소하여 표적 부위에 도달하기 전에 약물이 방출될 뿐만 아니라 오랜 시간 동안에 약물을 방출함으로써 부작용 및 낮은 치료 효율을 초래한다는 문제점을 가지고 있다. 본 총론에서는 이러한 비효율적인 약물 방출의 문제점을 개선하기 위한 방법으로 독성이 없고 생체 적합한 천연 고분자 키토산에 자극 응답성 물질을 도입하여 혈중에서 안정성을 높이고 표적 부위에서 약물을 과다 방출하여 치료 효율을 극대화할 수 있는 방법을 제시하고자 한다.