• 대한의생명과학회지
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• 제7권3호
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• pp.133-138
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• 2001

The recently proposed Bethesda system for cervical/vaginal cytology has made a standardization related to "atypia". In cellular change due to inflammation or repair, the word "benign cellular change" has been suggested as a substitute for atypia. Terminology related to atypia cells may become standardized, but the cytologic criteria has not been well defined yet Among 8113 cases screened, we evaluated 182 cases as atypia squamous cells undetermined significance (ASCUS) by the Bethesda system (TBS): 52 cases of ASCUS were cytologically diagnosed and 33 cases were histologically verified. ASCUS was diagnosed based on nuclear enlargement and nonclassical signs of condyloma. The results are as follows; Six cases (16.6%) turned out to have benign cellular change. Twenty five cases (69.1%) demonstrated squamous intraepthelial lesion, condyloma was 2 cases (6.0%) and mild dysplasia was not revealed. Moderate and severe dysplasia were 1 case (3.0%) and 16 cases (48.4%), squamous cell carcinoma and adenocarcinoma were 4 (12.1%) and 1 cases (3.0%), respectively. Our data suggested that patients with ASCUS are highly recommended to be examined colposcopic biosy to cornfim.

• International Journal of Oral Biology
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• 제41권4호
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• pp.183-190
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• 2016

Anthricin (Deoxypodophyllotoxin), a naturally occurring flavolignan, has well known anti-cancer properties in several cancer cells, such as prostate cancer, cervical carcinoma and pancreatic cancer. However, the effects of Anthricin are currently unknown in oral cancer. We examined the anticancer effect and mechanism of action of Anthricin in human FaDu hypopharyngeal squamous carcinoma cells. Our data showed that Anthricin inhibits cell viability in a dose- and time-dependent manner ($IC_{50}$ 50 nM) in the MTT assay and Live & Dead assay. In addition, Anthricin treated FaDu cells showed marked apoptosis by DAPI stain and FACS. Furthermore, Anthricin activates anti-apoptotic factors such as caspase-3, -9 and poly (ADP-ribose) polymerase (PARP), suggesting that caspase-mediated pathways are involved in Anthricin- induced apoptosis. Anthricin treatment also leads to accumulation of the pro-apoptotic factor Bax, followed by inhibition of cell growth. Taken together, these results indicate that Anthricn-induced cell death of human FaDu hypopharyngeal squamous carcinoma cells is mediated by mitochondrial-dependent apoptotic pathway. In summary, our findings provide a framework for further exploration on Anthricin as a novel chemotherapeutic drug for human oral cancer.

• Asian Pacific Journal of Cancer Prevention
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• 제16권14호
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• pp.5749-5754
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• 2015

Cervical carcinoma is the main cause of cancer-related mortality in women and is correlated with more than 15 risk cofactors, including infection of cervical cells with high-risk types of HPV (hrHPV). Indeed, both aberrant methylation of the RASSF1A promoter and hrHPV infection are often observed in cervical carcinomas. The purpose of our meta-analysis was to evaluate the role of RASSF1A promoter methylation and hrHPV infection in cervical cancer. Our meta-analysis involved 895 cervical cancer patients and 454 control patients from 15 studies. Our results suggested that RASSF1A promoter hypermethylation increased the risk of cervical cancer (OR=9.77, 95%CI=[3.06, 31.26], P=0.0001, $I^2=78%$). By grouping cases according to cancer subtypes, we found that HPV infection was higher in cervical squamous cell carcinomas (SCCs) than in cervical adenocarcinomas/adenosquamous cancers (ACs/ASCs) (OR=4.00, 95%CI=[1.41, 11.30], P=0.009, $I^2=55%$). Interestingly, HPV infection tended to occur in cervical cancers with relatively low levels of RASSF1A promoter methylation (OR=0.59, 95%CI=[0.36, 0.99], P=0.05, I2=0%). Our study provides evidence of a possible interaction between HPV infection and RASSF1A promoter methylation in the development of cervical cancers.

• Asian Pacific Journal of Cancer Prevention
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• 제15권6호
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• pp.2803-2807
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• 2014

Bioassay-guided chemical investigation of the roots of Anthriscus sylvestris (L.) Hoffm. resulted in the isolation of nine compounds, whose structures were determined by spectroscopic methods. Compound 1 was isolated from this plant for the first time and compounds 3 and 9 were first found from this genus. Different polar fractions of A. sylvestris extract and compounds 1, 6-8 and 9 were evaluated for antitumor activities against HepG2 (human hepatocellular carcinoma), MG-63 (human osteosarcoma cells), B16 (melanoma cells) and HeLa (human cervical carcinoma cells) lines by the MTT method. The petroleum ether fraction of A. sylvestris extract exhibited excellent inhibitory activity with an $IC_{50}$ value of $18.3{\mu}g/ml$. Among the isolates from the petroleum ether fraction, compound 7 showed significant inhibition against the growth of the four tumor cells with $IC_{50}$ values ranging from $12.2-43.3{\mu}g/ml$.

• Preventive Nutrition and Food Science
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• 제11권1호
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• pp.17-24
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• 2006

Methanolic and aqueous extracts from 37 seaweed species (10 green and 27 brown seaweeds) collected from Jeju Island coast were prepared at high ($70^{\circ}C$) and room ($20^{\circ}C$) temperatures and examined for cytotoxic activity against 4 tumor cell lines: U937 (human monoblastoid leukemia cell line), HL60 (human promyelocytic leukemia cell line), HeLa (woman cervical carcinoma cell line) and CT26 (mouse colon carcinoma line). Both MeOH extracts of Desmarestia tabacoides and Dictyota dichotoma possessed strong cytotoxic activities against all the tumor cell lines tested, but the aqueous extract exhibited no activity. On the other hand Ecklonia cava showed strong cytotoxic activities for the $20^{\circ}C$ aqueous extract against the three tumor cells except HeLa cell. Sagassum coreanum and Sagassum siliquastrum $20^{\circ}C$ aqueous extracts also exhibited strong cytotoxic activities against U937, HL60, HeLa cells. Even though green seaweeds showed less activity than brown seaweeds, $20^{\circ}C$ aqueous extracts of Codium contractum and Codium fragile exhibited strong cytotoxic activities against HL60 or CT26 cells, respectively.

• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2002년도 생물공학의 동향 (X)
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• pp.581-584
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• 2002

Individual surface(hydrophilic/hydrophobic) were prepared and mammalian cells were cultured on the hydrophilic region. For drug test, cancer and normal cells were treated with Taxol, as an example. Our system was compared with MTT assay. CHO cells were resistant to Taxol up to 100 nM in both Methods. However, A549 cells was sensitive at 100 nM Taxol in the 2 day-treatment. Cervical carcinoma cell, HeLa, was very sensitive to Taxol. In our system, the cells were not shown from above 20 nM Taxol treatment. Our system was competitive to MTT assay in animal cells for drug test.

• The Korean Journal of Physiology and Pharmacology
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• 제13권2호
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• pp.115-121
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• 2009

Functional defects in mitochondria are involved in the induction of cell death in cancer cells. We assessed the toxic effect of camptothecin against the human cervical and uterine tumor cell line SiHa with respect to the mitochondria-mediated cell death process, and examined the combined effect of camptothecin and anticancer drugs. Camptothecin caused apoptosis in SiHa cells by inducing mitochondrial membrane permeability changes that lead to the loss of mitochondrial membrane potential, decreased Bcl-2 levels, cytochrome c release, caspase-3 activation, formation of reactive oxygen species and depletion of GSH. Combination of camptothecin with other anticancer drugs (carboplatin, paclitaxel, doxorubicin and mitomycin c) or signaling inhibitors (farnesyltransferase inhibitor and ERK inhibitor) did not enhance the camptothecin-induced cell death and caspase-3 activation. These results suggest that camptothecin may cause cell death in SiHa cells by inducing changes in mitochondrial membrane permeability, which leads to cytochrome c release and activation of caspase-3. This effect is also associated with increased formation of reactive oxygen species and depletion of GSH. Combination with other anticancer drugs (or signaling inhibitors) does not appear to increase the anti-tumor effect of camptothecin against SiHa cells, but rather may reduce it. Combination of camptothecin with other anticancer drugs does not seem to provide a benefit in the treatment of cervical and uterine cancer compared with camptothecin monotherapy.

• Asian Pacific Journal of Cancer Prevention
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• 제13권4호
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• pp.1325-1331
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• 2012

Tumor formation and growth is dictated by a very small number of tumor cells, called cancer stem cells, which are capable of self-renewal. The genesis of cancer stem cells and their resistance to conventional chemotherapy and radiotherapy via mechanisms such as multidrug resistance, quiescence, enhanced DNA repair abilities and anti-apoptotic mechanisms, make it imperative to develop methods to identify and use these cells as diagnostic or therapeutic targets. Aldehyde dehydrogenase 1 (ALDH1) is used as a cancer stem cell marker. In this study, we evaluated ALDH1 expression in CaSki, HeLa and SiHa cervical cancer cells using the Aldefluor method to isolate ALDH1-positive cells. We showed that higher ALDH1 expression correlated with significantly higher rates of cell proliferation, microsphere formation and migration. We also could demonstrate that SiHa-ALDH1-positive cells were significantly more tumorigenic compared to SiHa-ALDH1-negative cells. Similarly, SiHa cells overexpressing ALDH1 were significantly more tumorigenic and showed higher rates of cell proliferation and migration compared to SiHa cells where ALDH1 expression was knocked down using a lentivirus vector. Our data suggested that ALDH1 is a marker of cervical cancer stem cells and expand our understanding of its functional role.

• 대한임상검사과학회지
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• 제39권3호
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• pp.210-216
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• 2007

There is increasing evidence that stromal reaction in cancer has an important diagnostic and prognostic significance. The aim of our study is to analyze the relation between the increase in mast cell number and the expression CD34 and alpha-smooth muscle actin (${\alpha}$-SMA) in the stroma of cervical intraepithelial neoplasia (CIN) and squamous cell carcinoma (SCC). We investigated a total of 29 CIN (1,2,3) and 21 SCC (microinvasive and invasive) specimens and compared the distribution of $CD34^+$ stromal cells, ${\alpha}-SMA^+$ cells, transforming growth factor-${\beta}1$ $(TGF-{\beta}1)^+$ cells, and the density of mast cells using immunohistochemistry with antibodies against CD34, ${\alpha}$-SMA, TGF-${\beta}1$, and c-Kit (CD117) respectively. Computerized image analysis was to evaluate the positive area (%) and density of the respective immunoreactive cells. In CIN $CD34^+$ cells were abundant in the stroma but no ${\alpha}-SMA^+$ cells were identified except the wall of blood vessels. $CD34^+$ cells were progressively decreased along the continuum from CIN 2 to microinvasive SCC and not observed in the stroma of invasive SCC. Whereas ${\alpha}-SMA^+$ cells were only observed in the stroma of microinvasive and invasive SCC. We found more intense TGF-${\beta}1$ expression in the increased mast cells in the stroma of invasive SCCs than that in the stroma of CIN. These results indicate that disappearance of $CD34^+$ stromal cells and appearance of ${\alpha}-SMA^+$ cells are associated with the stromal change of CIN to SCC and the transformation of $CD34^+$ stromal cells into ${\alpha}-SMA^+$ cells is mediated by TGF-${\beta}1$ secretions in the stromal mast cell of SCC.

• 대한수의학회지
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• 제30권4호
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• pp.447-457
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• 1990

In order to observe the distribution of mast cell on the stages of the mammary carcinogenesis, the numerical changes of mast cells in the mammary tumor development in rats treated with DMBA and compound 48/80 have been investigated by the light microscope. The results observed were summarized as follows: The appearance of tumor were not observed during the whole experimental period in the rats of the control group received injection of sterile saline, but tumors appeared in 100% of the animals, the tumor induction time that represented the number of days elapsing between the 3rd DMBA administration until a first tumor became $10{\times}10mm$ in diameter was $42.5{\pm}4.7$ days and the mean number of tumor masses per rat was $3.4{\pm}1.2$ in the DMBA treated group. And the majority of the DMBA-induced mammary neoplasms were appeared cervical mammary gland and thoracic mammary gland. The histological findings of mammary carcinoma were recognized adenocarcinoma in the DMBA treated group. Mast cells were distributed within the adipose tissues and the interglandular connective tissue in the control, but found to be randomly dispersed within the tumor cell masses, in the connective tissues adjacent to the periphery of the tumor, the adipose tissues and the subcutaneous tissues contiguous to the region of tumor development in the DMBA treated group. Numerical alterations of mast cells were observed in the mammary tumors that separated into three major classes of tumors: hyperplasia, atypical hyperplasia and carcinoma. The number of mast cells were distributed in the connective tissues adjacent to the mammary gland was $45.3{\pm}3.4$ cells in the control group, but was $50.2{\pm}4.9$ cells, $126.7{\pm}10.5$ cells and $340.3{\pm}19.2$ cells according to each stages of mammary tumorigenesis in the DMBA treated group.