• Journal of Preventive Medicine and Public Health
• /
• v.36 no.3
• /
• pp.279-288
• /
• 2003

Objectives : Evidence for an effect of rerroductive factors on colorectal carcinogenesis is not yet consistent. Little research has been conducted to investigate whether reproductive factors were associated with colorectal adenomas that are the precursors of colorecta1 cancer, We evaluated the relationships between reproductive factors and the degree of dysplasia of the colorectal adenoma and cancer as colorectal adenoma-carcinoma sequence. Methods : For this study, 241 adenoma cases with histopathologically confirmed incident colorectal adenoma, 76 cancer cases with colorectal cancer and 1677 controls were collected from Our Lady of Mercy Hospital, The Catholic University of Korea, during 1994-1999. Before colonoscopy, information on demographic characteristics, reproductive factors, life style habits and dietary intake were obtained by interviewed questionnaire. Adjusted OR and 95% CI were estimated by using polytomous logistic regression model, Potential confounders that were selected based on the goodness of fit Statistics and interaction between risk factors were considered in this adjustment. The Wald statistic was calculated to test the heterogeneity of the odds ratios for each case. Results .: Postmenopausal women with natural menopause were found to be positively associated with the risk of mild dysplasia adenoma (multivariate-adjusted OR : 2.59, 95% CI=1.1-0.2). Parity was found to be negatively associated with the risk of colorectal lancer (age-adjusted OR : 0.40, 95% CI=0.2-0.9), but did not significantly decrease the risk of colorectal cancer (multivariate-adjusted OR : 0.95, 95% CI=0.3-2.9). Me associations were seen between a9e at menarche, breast feeding, induced abortion, oral contraceptive use, menopausal types, menopausal age or hormone replacement therapy (HRT and the degree of dysplasia of the colorectal adenoma and cancer. However, none of these associations differed' significantly between the degree of dysplasia of the colorectal adenoma and cancer. Conclusions : These findings suggest that postmenopausal women with natural menopause may experience increased risk of mild dysplasia adenorna among colorectal adenoma-carcinoma sequence.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.38 no.2
• /
• pp.142-145
• /
• 2009

The cytotoxic activity against human cancer cells and anti-tumor effect in Balb/c mice of a 70% ethanol extract from masou salmon (MSE) was investigated. The cancer cell lines including human breast adenocarcinoma (MCF-7), human lung carcinoma (A549), human hepatoblastoma (HepG2), human gastric carcinoma (AGS), human cervical adenocarcinoma (HeLa) and transformed primary human embryonal kidney (293) exposed to MSE decreased cell viability as indicated by the MTT assay. The MSE shows significant cytotoxicity on MCF-7, A549, HepG2, AGS and HeLa cells, and are more active than 293 cells. The treatment with 1 mg/mL MSE resulted in 9.2%, 12.7%, 16.6%, and 16.9% cell survival against A549, MCF-7, HepG2, and AGS cells, respectively. Moreover, anticancer effect in vivo of MSE was tested in the animal system using Balb/c mice transplanted sarcoma-180 cells. MSE showed inhibition of tumor growth and the rate of inhibition was 44.7% and 55.7% at the 25 mg/kg body weight and 250 mg/kg body weight, respectively. Thus, we suggest that MSE could be a beneficial material for human cancer prevention.

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

• Korean Journal of Medicinal Crop Science
• /
• v.10 no.2
• /
• pp.139-143
• /
• 2002

Ixeris dentate was used to extract the natural compounds with methanol and then the extracts were further fractionated using n-hexane, ethyl acetate, butanol and aqueous fraction. The methanol extract of Ixeris dentate had strong antimutagenic effect in Ames mutagenicity test. Among the extracts fractioned from the methanol extract, the butanol fraction exhibited the greatest antimutagenic effect suppressing the mutagenicity of Salmonella typhimurium TA100 with inhibition rate of 88.93%. Cancer cell lines include human lung carcinoma(A549), human breast adenocarcinoma(MCF-7) and human hepatocellular carcinoma(Hep3B). Hexane fraction showed the strongest effect against A549, MCF-7 and Hep3B at the same concentration compared to those of other fractions.

• Food Science and Preservation
• /
• v.11 no.2
• /
• pp.214-220
• /
• 2004

This study was carried out to determine the antioxidative, antimutagenic, and anticancer effects of functional food manufactured from fermented soybean(FFMFS) using DPPH free radical donating method, Ames test and cytotoxicity, respectively. FFMFS extracted with ethanol and then further fractionated to n-hexane, chloroform, ethyl acetate(EtOAc), butanol and water, stepwise. Among five fractions, the EtOAc fractions showed highest electron donating activities (31.6 $\mu\textrm{g}$/mL). The inhibition rate of ethanol extract(200 $\mu\textrm{g}$/plate) of FFMFS in the S. typhimurium TA100 strain showed 84.8% against the mutagenesis induced by MNNG. In addition, the suppression of EtOAc fractions with same concentration of FFMFS the S. typhimurium TA98 and TA100 strains showed 88.7% and 92.8% inhibition against Trp-P-l, respectively. The cytotoxic effects of FFMFS against the cell lines with human lung carcinoma(A549), human gastric carcinoma(AGS) and human breast adenocarcinoma(MCF-7) were inhibited with the increase of the extract concentration. The treatment of 1.0 mg/mL FFMFS of EtOAc fraction showed strong cytotoxicities of 84.5%, 88.7% and 85.6% against A549, AGS and MCF-7, respectively.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.36 no.2
• /
• pp.143-148
• /
• 2007

This study was to investigate the mixed buckwheat flour quality by observing antimutagenic and cytotoxic effects of mixed buckwheat flour extracts using Ames test and SRB (sulforhodamine B) assay. Samples were prepared to the ratio of 100% (B1), 90% (BF1), 80% (BF2), 70% (BF3) and 60% (BF4) (w/w) flour buckwheat based on wheat flour weight. The initial pasting temperature in an amylograph was increased according to the increase of the buckwheat flour. The water absorption in farinograph decreased with the addition of buckwheat flour. The inhibition rates of B1, BF3 and BF4 extract (160 g/plate) were 45%, 37.3% and 42% against the mutagenesis of Salmonella Typhimurium TA100 induced by MNNG $(0.4{\mu}g/plate)$, respectively. In addition, the B1 at the same concentration showed 64% and 44.3% inhibition on the mutagenesis of Salmonella Typhimurium TA98 and TA100 induced by 4NQO $(0.15{\mu}g/plate)$, respectively. In SRB assay, human breast adenocarcinoma (MCF 7), human hepatocellular carcinoma (Hep3B), human stomach adonocarcinoma (AGS), human lung carcinoma (A549) and human cervical adenocarcinoma (HeLa) proliferations were inhibited by the increase in the sample concentration.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.37 no.4
• /
• pp.410-415
• /
• 2008

This study was performed to observe the antimutagenic and cytotoxic activities of methanol extract of kochujang added with sea tangle and deep sea water salts (SDK) and kochujang added with sea tangle (SK) using the Ames test and SRB assay, respectively. The direct antimutagenic effect of SDK and SK methanol extracts were examined by Ames test using Salmonella Typhimurium TA98 and TA100. In the Ames test, methanol extract of SDK and SK alone did not exhibit mutagenicity and most of the samples showed high antimutagenic effects against mutation induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and 4-nitroquinoline-1-oxide (4NQO). Methanol extract of SDK ($200{\mu}g$/plate) showed approximately 71.4% inhibitory effect on the mutagenesis induced by 4NQO against TA98 strain; whereas 56.1% and 83.6% inhibitions were observed on the mutagenensis induced by 4NQO and MNNG against TA100 strain. The cytotoxic effects of SDK and SK increased with increasing sample concentration against human cervical adenocarcinoma (HeLa), human hepatocellular carcinoma (Hep3B), human breast adenocarcinoma (MCF-7), human stomach adenocarcinoma (AGS), and human lung carcinoma (A549). The SDK at the concentration of 1 mg/ml showed cytotoxicities of 61.5%, 61.3%, 51.4%, 57.9% and 77.7% against HeLa, Hep3B, MCF-7, AGS and A549, respectively. In contrast 1 mg/ml treatment of SDK and SK methanol extract had only $2{\sim}38%$ cytotoxicity on human transformed primary embryonal kidney cell (293).

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
• /
• v.27 no.5
• /
• pp.373-384
• /
• 2001

Cellular proliferation is an intricately regulated process mediated by the coordinated interactions of critical growth control genes. Two of these factors in mammalian cells are the p53 and mdm-2 genes. A protein product of the mem-2 oncogene has been recently shown to associate with the protein encoded by the tumor suppressor gene p53. The p53 tumor suppressor protein is stabilized in response to DNA damage and other stress signals and causes the cell to undergo growth arrest or apoptosis, thus preventing the establishment of mutations in future cellular generations. Mutation or loss of p53 is a very common event in tumor progression. It occurs in about 50% of all tumors analysed including of colon, lung, breast and liver. The cellular mdm-2 gene, which has potential transforming activity that can be activated by overexpression, is amplified in a significant percentage of human sarcoma and in other mammalian tumors. Proteins encoded by the mdm-2 gene are able to bind to the p53 protein and, when overexpressed, can inhibit p53's transcriptional activation function, thus mdm-2 can act as a negative regulator of p53 function. Experimental study was performed to observe the relationship between p53 gene mutation and mdm-2 protein expression and apply the results to the clinical activity. 36 golden syrian hamster each weighing $60{\sim}80g$ were used and painted with 0.5% DMBA by 3 times weekly on the right buccal cheek(experimental side) for 6, 8, 10, 12, 14 and 16 weeks. Left buccal cheek(control side) was treated with mineral oil as the same manner to the right side. The hamsters were sacrificed on the 6, 8, 10, 12, 14 & 16 weeks. Normal and tumor tissues from paraffin block were examined for histology and immunohistochemistry observation, and were completely dissected by microdissection and DNA from both tissue were isolated by proteins K/phenol/chloroform extraction. Segments of the hamster p53 exons 5, 6, 7 and 8 were amplified by PCR using the oligonucleotide primers, and then confirmational change was observed by SSCP respectively. The results were as follows : 1. Dysplasia at 6 weeks, carcinoma in situ at 8 weeks and invasive carcinoma from 10 weeks could be observed in experimental groups. 2. p53 mutations were detected in 10 of the 36(28%) and the exons 6(6 of the 10 : 60%) was the most hot spot area among the highy conserved region(exons 5, 6, 7 & 8). 3. Immunohistochemical study confirmed 22 of the 36(61%) of p53 expression involving 10 of p53 mutations. 4. mdm-2 expression of was showed in 3 of the 36(8%) involving 1 of the 22 of p53 expression and 2 of the 14 of p53 non-expression. From the above results, mutation of p53 gene or expression of p53 protein may have the influence of the DMBA induced carcinoma of hamster buccal pouch but the expression of mdm-2 protein may not have relationship with tumorigenesis.

• Tuberculosis and Respiratory Diseases
• /
• v.47 no.3
• /
• pp.331-338
• /
• 1999

Background: Nearly 10% of cancer patients will develop a second primary cancer within ten years after surgical removal of the primary tumor. The detection of risk factors for developing multiple primary tumors would be important This study was conducted to evaluate the clinical characteristics and abnormal p53 expression of lung cancer associated with multiple primary cancer(MPC). Method: Clinical characteristics and abnormal p53 expression were compared between 20 cases of lung cancer(NSCLC ; 16 cases, SCLC ; 4 cases) associated with MPC and 26 cases of primary non-small cell lung cancer. Result: MPC associated with lung cancer was gastric cancer(8), lung cancer(2), esophageal cancer(2), colon cancer(2), laryngeal cancer(1), bladder cancer(1), small bowel cancer(l), adrenal cancer(1), hepatocellular carcinoma(1), and breast cancer (1) in order. The clinical stage of primary NSCLC was relatively advanced, but NSCLC associated with MPC was even distribution at each stage. The detected incidences of abnormal p53 expressions were 62.5% in NSCLC associated with MPC and 76.9% in primary NSCLC(p>0.05). Conclusion: There was no difference in abnormal p53 expression between non-small cell carcinoma associated with multiple primary cancer and primary non-small cell carcinoma.

• Korean Journal of Food Science and Technology
• /
• v.32 no.6
• /
• pp.1371-1378
• /
• 2000

This study was performed to determine the antimutagenic and cytotoxic effect of Agaricus blazei Murill methanol extract on Salmonella typhimurium TA98, TA100 and human cancer cell lines using Ames test and cytotoxicity assay, respectively. In Ames test, methanol extract from A. blazei Murill did not exhibit any mutagenicity and most of the samples showed high antimutagenic effects against mutation induced by N-methyl-N'-nitro-N-nitrosoguanidine(MNNG), 4-nitroquinoline-1-oxide(4NQO), 3-amino-1,4-dimethyl-5H-pyrido [4,3-b] indol(Trp-P-1) and $benzo({\alpha})pyrene(B({\alpha})P)$. The methanol extracts of A. blazei Murill$(200\;{\mu}g/plate)$ showed approximately 92.4%, 81.9% and 83.4% inhibitory effect on the mutagenesis induced by 4NQO, Trp-P-1 and $B({\alpha})P$ against TA98 strain, whereas 87.3%, 94.7%. 92.3% and 89.9% inhibitions were observed on the mutagenesis induced by MNNG, 4NQO, Trp-P-1 and $B({\alpha})P$ against TA100 strain. The solvent fractions of methanol extracts from A. blazei Murill except water fraction showed high antimutagenic effects of $70{\sim}90%$ against mutation induced by MNNG, 4NQO. Trp-P-1 and $B({\alpha})P$. In anticancer effects of A. blazei Murill extract and fraction against cancer cell lines including human breast adenocarcinoma(MCF7), human lung carcinoma(A549), human fibrosarcoma(HT1080), human hepatocellular carcinoma(Hep3B), human epitheloid carcinoma(HeLa), human gastric carcinoma(KATO III) and human chronic myelogenous leukemia(K562) were investigated. The treatment of 1 mg/mL A. blazei Murill extracts had the highest cytotoxicity with 91.9% against HeLa, followed by KATO III(88.7%), A549(86.5%) and Hpe3B(84.3%). Whereas 1 mg/mL treatment of A. blazei Murill extracts had only $10{\sim}40%$ cytotoxicity on human normal liver cell (WRL68).