• Advances in pediatric surgery
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• v.10 no.2
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• pp.145-149
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• 2004

A 12-year-old boy with severe periumbilical pain visited the emergency room. Physical examination, abdominal ultrasonography, colonoscopy and CT, identified a lesion of sigmoid colon. Endoscopic biopsy showed a signet ring cell carcinoma of the sigmoid colon. On explorative laparotomy, cancer invasions of the adjacent structures and metastases on peritoneal wall were noticed. We performed palliative loop-ileostomy. He underwent chemotherapy and radiotherapy for 3 months. The second case was a 16-year-old boy with abdominal pain and hematochezia, transferred to our hospital with the diagnosis of acute appendicitis with periappendiceal abscess. Although he underwent appendectomy, the abdominal pain persisted. Digital rectal examination revealed a lumen-obstructing fungating mass in the rectum. Endoscopic biopsy revealed a adenocarcinoma. Cancer invasion of the adjacent structures and metastases involving the mesentery of the small intestine were found at laparotomy. A palliative procedure, a Hartmann's operation and end-colostomy at the sigmoid colon were performed. The patient died 8 month later due to pneumonia and sepsis. Chemotherapy was not applied.

• Korean Journal of Clinical Laboratory Science
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• v.36 no.2
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• pp.193-198
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• 2004

PET/CT combines the functional information from a positron emission tomography (PET) exam with the anatomical information from a computed tomography (CT) exam into one single exam. A CT scan uses a combination of x-rays and computers to give the radiologist a non-invasive way to see inside your body. One advantage of CT is its ability to rapidly acquire two-dimensional pictures of your anatomy. Using a computer these 2-D images can be presented in 3-D for in-depth clinical evaluation. A PET scan detects changes in the cellular function - how your cells are utilizing nutrients like sugar and oxygen. Since these functional changes take place before physical changes occur, PET can provide information that enables your physician to make an early diagnosis. The PET exam pinpoints metabolic activity in cells and the CT exam provides an anatomical reference. When these two scans are fused together, your physician can view metabolic changes in the proper anatomical context of your body. PET/CT offers significant advantages including more accurate localization of functional abnormalities, and the distinction of pathological from normal physiological uptake, and improvements in monitoring treatment. A PET/CT scan allows physicians to measure the body's abnormal molecular cell activity to detect cancer (such as breast cancer, lung cancer, colorectal cancer, lymphoma, melanoma and other skin cancers), brain disorders (such as Alzheimer's disease, Parkinson's disease, and epilepsy), and heart disease (such as coronary artery disease).

• Archives of Pharmacal Research
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• v.19 no.5
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• pp.342-347
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• 1996

Doxorubicin, one of the clinically most useful anticancer agents, is used alone or in combination with other drugs against a wide variety of tumors, recently. But cancer cells developed resistance to this agent in many ways. This resistance is an important limiting factor of doxorubicin for anticancer drug. We newly established doxorubicin-resistant HCT15/CL02 subline from parental HCT15 human adenocarcinoma colon cancer cells. HCT15/CL02 revealed resistance to doxorubicin about 85-fold of its parental cells, and it also revealed cross-resistance to actinomycin D, etoposide and vinblastine but not to displatin and tamoxifen. And verapamil, a reversal agent of multidrug-resistance (MDR) by P-glycoprotein, elevated the cytotoxicity of doxorubicin against both HCT15 and GCT15/CL02 cells. But the relative resistant rate was not reduced. Verapamil had no effects on the tosicity of cisplatin to the both cell lines. These results indicate that HCT15/CL02 cells have some functionally complex mechanisms for MDR.

• Biomedical Science Letters
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• v.28 no.4
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• pp.312-316
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• 2022

We have previously reported that genetically modified tumor cells with 4-1BBL have anti-cancer effects in a CT26 mouse colorectal tumor model. In this study, genetically modified tumor cells with 4-1BBL were evaluated for their potential as candidates for preventive and therapeutic cancer vaccine. To identify the effect of preventive and therapeutic vaccine of genetically modified tumor cells with 4-1BBL, tumor growth pattern of CT26-4-1BBL as a cancer vaccine was examined compared to CT26-beta-gal. In therapeutic vaccination, CT26-WT was inoculated into mice and then vaccinated mice with doxorubicin (Dox)-treated CT26-beta-gal and CT26-4-1BBL (single or three times). Triple vaccination with Dox-treated tumor cell inhibited tumor growth compared to single vaccination. Vaccination with CT26-4-1BBL showed an efficient tumor growth inhibition compared to vaccination with CT26-beta-gal. For preventive vaccination, Dox-treated CT26-beta-gal and CT26-4-1BBL was vaccinated into mice with three times and then administered mice with CT26-WT. Preventive vaccination with CT26-4-1BBL showed no tumor growth. Preventive vaccination with CT26-beta-gal also led to tumor-free mice. These results suggest that genetically modified tumor cells with 4-1BBL can be used as therapeutic or preventive cancer vaccine.

• Journal of Digestive Cancer Research
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• v.4 no.2
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• pp.64-76
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• 2016

The step-wise process of colorectal carcinogenesis from aberrant crypt foci, adenoma to adenocarcinoma, is relatively suitable for chemopreventive intervention. Accumulated evidences have revealed that maintaining an undifferentiated state (stemness), inflammation, and oxidative stress play important roles in this colon carcinogenesis process. However, appropriate molecular targets that are applicable to chemopreventive intervention regarding those three factors are still unclear. In this review, we summarized appropriate molecular targets by identification and validation of the prospective targets from a comprehensive overview of data that showed colon cancer preventive effects in clinical trials, epidemiological studies and basic research. We first selected a study that used aspirin, statins and metformin from FDA approved drugs, and epigallocatechin-gallate and curcumin from natural compounds as potential chemopreventive agents against colon cancer because these agents are considered to be promising chemopreventive agents. Experimental and observational data revealed that there are common target molecules in these potential chemopreventive agents: T-cell factor/lymphoid enhancer factor (TCF/LEF), nuclear factor-&B (NF-κB) and nuclear factor-erythroid 2-related factor 2(NRF2). Moreover, these targets, TCF/LEF, NF-κB and NRF2, have been also indicated to suppress maintenance of the undifferentiated state, inflammation and oxidative stress, respectively. In the near future, novel promising candidate agents for colon cancer chemoprevention could be identified by integral evaluation of their effects on these three transcriptional activities.

• IMMUNE NETWORK
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• v.12 no.2
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• pp.66-69
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• 2012

The immunological death induction by EY-6 on the human tumor cell lines was screened. Human colon carcinoma (HCT15, HCT116), gastric carcinoma (MKN74, SNU668), and myeloma (KMS20, KMS26, KMS34) cells were died by EY-6 treatment with dose-dependent manner. CRT expression, a typical marker for the immunological death, was increased on the EY-6-treated colorectal and gastric cancer cells. Interestingly, the effects on the myeloma cell lines were complicated showing cell line dependent differential modulation. Cytokine secretion from the EY-6 treated tumor cells were dose and cell-dependent. IFN-${\gamma}$ and IL-12 secretion was increased in the treated cells (200% to over 1000% of non-treated control), except HCT116, SNU668 and KMS26 cells which their secretion was declined by EY-6. Data suggest the potential of EY-6 as a new type of immuno-chemotherapeutics inducing tumor-specific cell death. Further studies are planned to confirm the efficacy of EY-6 including in vivo study.

• Journal of Nutrition and Health
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• v.27 no.6
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• pp.552-562
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• 1994

The study was designed to observe the effect of different dietary fats on the incidence of colorectal tumor and in vivo cell proliferation in colon carcinogenesis. Male Sprague Dawley rats were intrarectally infused with chemical carcinogen(methylnitrosourea, MNU) and fed 16%(w/w) fat diet containing one of dietary fats(beef tallow, corn oil, perilla oil) for 30 weeks. To measure in vivo cell proliferation, the incorporation of 5-bromo-2-deoxyuridine(BrdU) into DNA was localized using the monoclonal anti-BrdU antibody. Large number of tumors were found in the distal colon and tumor incidence was increased in the order of perilla oil(57.7%)$\alpha$-linolenic acid rich in perilla oil could have a protective effect against colon cancer compared to saturated fatty acid or n-6 linoleic acid.

• Journal of Life Science
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• v.31 no.10
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• pp.929-936
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• 2021

In the present study, we screened candidate natural compounds which possess the strong anti-proliferative effects on human colorectal HCT116 cells using the commercial natural product library (Selleckchem, L1400) based on cell viability assay. Human colorectal cancer HCT116 cells were incubated with 50 μM of each compound from the natural product library, and then cell viability was measured by MTT assay. From the first screening, five different kinds of natural products (chrysin, diosmetin, emodin, piperlongumine, and tanshinone I) were selected based on cell viability assay in HCT116 cells and commercial availability. All selected natural products significantly decreased cell viabilities in HCT116 cells, whereas pro-apoptotic protein NAG-1 is strongly induced by chrysin or emodin treatment. Chrysin and emodin decreased cell viability in a dose-dependent manner. Moreover, chrysin and emodin increased the expression of pro-apoptotic NAG-1 protein in a dose- and time-dependent manner. In addition, PARP cleavage induced by chrysin or emodin was recovered in part by the transfection of NAG-1 siRNA indicating that NAG-1 may be one of the genes responsible for apoptosis induced by chrysin or emodin. Overall, our findings may provide basic screening data on natural products which possess anti-proliferative activities and may help to understand the molecular mechanisms of anti-proliferative and pro-apoptotic activities mediated by chrysin and emodin.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.11
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• pp.6761-6767
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• 2013

The nuclear receptor, peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$), is expressed in various cancer cells including breast, prostate, colorectal and cervical examples. An endogenous ligand of $PPAR{\gamma}$, 15-deoxy-${\Delta}^{12,14}$ prostaglandin $J_2$ (PGJ2), is emerging as a potent anticancer agent but the exact mechanism has not been fully elucidated, especially in breast cancer. The present study compared the anticancer effects of PGJ2 on estrogen receptor alpha ($ER{\alpha}$)-positive (MCF-7) and $ER{\alpha}$-negative (MDA-MB-231) human breast cancer cells. Based on the reported signalling cross-talk between $ER{\alpha}$ and $ER{\alpha}$, the effect of the $ER{\alpha}$ ligand, $17{\beta}$-estradiol (E2) on the anticancer activities of PGJ2 in both types of cells was also explored. Here we report that PGJ2 inhibited proliferation of both MCF-7 and MDA-MB-231 cells by inducing apoptotic cell death with active involvement of mitochondria. The presence of E2 potentiated PGJ2-induced apoptosis in MCF-7, but not in MDA-MB-231 cells. The $ER{\alpha}$ antagonist, GW9662, failed to block PGJ2-induced activities but potentiated its effects in MCF-7 cells, instead. Interestingly, GW9662 also proved capable of inducing apoptotic cell death. It can be concluded that E2 enhances $ER{\alpha}$-independent anticancer effects of PGJ2 in the presence of its receptor.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.1
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• pp.73-80
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• 2016

Colorectal cancer is a very prevalent diagnosed cancer. The current study was performed in order to examine the role of BRAE (Basella rubra aqueous extract) in regulating aberrant crypt foci (ACF) formation, cell proliferation and inhibition of apoptosis in a colon carcinogenesis model in male Wistar rats. Rats were randomly allocated into six groups. Group I served as control, and group II acted as a drug control administered BRAE (250mg/kg b.w.) orally for 30 weeks. Rats in group III-VI were given subcutaneous injections of DMH (25mg/kg b.w. weekly) for 15 weeks to initiate colon carcinogenesis. Those in group IV and VI were administered BRAE along with DMH injections. Rats in group V were administered with BRAE after cessation of DMH injection. After 30 weeks of experimental period colons were obtained from experimental groups and analyzed for ACF incidence, argyrophilic nucleolar organizing region-associated proteins (AgNOR) count, histopathological and immunohistochemical changes. Only in DMH exposed groups were ACF and AgNOR numbers increased. Administration of BRAE appreciably decreased the numbers of ACF and AgNOR in BRAE treated groups. Histopathological findings revealed a high level of dysplastic changes with decreased number of goblet cells found only in only DMH injected rats. Administration of BRAE in treated group rats reversed these changes. Expression markers for cell proliferation (PCNA and Ki67) were elevated in DMH treated rats, but reduced with BRAE treatement. This expression was reversed with apoptosis markers (p53 and Caspase-3). Thus the results results of the present study were found to be significant and confirmed the potential efficacy of BRAE against colon carcinogenesis.