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Na, K.,Kim, E. K.,Jang, W.,Kim, H.-S. Potamitis Press 2017 Anticancer research Vol. No.
<P>Background/Aim: Microcystic stromal tumor (MCST) is a rare stromal tumor of the ovary. In this study, we describe clinicopathological characteristics and results of mutational analyses of the CTNNB1gene in two cases of ovarian MCST and we provide a thorough review of previously published cases alongside our current cases and clarify the clinicopathological characteristics of ovarian MCST. Patients and Methods: Patients' age was 33 and 31 years, respectively. One patient presented with fever and low abdominal pain, whereas a pelvic mass was incidentally detected in another patient. Grossly, the cut surface of the tumors was mixed solid and cystic. Results: Histologically, the tumor characteristically displayed numerous microcysts, solid cellular areas, and intervening hyalinized stroma. Areas of moderate-to-severe nuclear pleomorphism with occasional multinucleated giant cells and bizarre nuclei were noted in one of the two cases. Immunohistochemically, both cases demonstrated diffuse and strong beta-catenin expression in the nuclei and the cytoplasm. The tumor cells were also diffusely positive for CD10, vimentin, Wilms tumor 1, and cyclin D1. The tumor cells were consistently negative for E-cadherin, inhibin-a, calretinin, estrogen receptor, and progesterone receptor. Mutational analyses using direct sequencing and pyrosequencing methods exhibited a single nucleotide mutation in CTNNB1 exon 3 (c.122C>T) in one case. We also found a novel deletion mutation in the same exon (c.88_99delTACCTGGACTCT) in another case. Conclusion: We demonstrated a previously reported CTNNB1 point-mutation using pyrosequencing and a novel deletion mutation in ovarian MCSTs. The review of the literature of previously published cases in combination with our current cases clarifies the clinicopathological characteristics of ovarian MCST and the comprehensive analysis of these cases would expand our knowledge regarding ovarian MCST.</P>
Paik, Woo Hyun,Kim, Hye Ree,Park, Joo Kyung,Song, Byeong Jun,Lee, Sang Hyub,Hwang, Jin-Hyeok Potamitis Press 2013 Anticancer research Vol.33 No.4
<P>Overexpression of microRNA-21 (miR-21) indicates chemoresistance in pancreatic cancer. We evaluated the change of chemosensitivity to gemcitabine through the down-regulation of miR-21 in human pancreatic cancer cells (Panc-1).</P>
Functional polymorphism in the MicroRNA-367 binding site as a prognostic factor for colonic cancer.
Chae, Yee Soo,Kim, Jong Gwang,Kang, Byung Woog,Lee, Soo Jung,Lee, Yoo Jin,Park, Jun Seok,Choi, Gyu Seog,Lee, Won Kee,Jeon, Hyo-Sung Potamitis Press 2013 Anticancer research Vol.33 No.2
<P>As microRNAs play important roles in cancer development and progression by regulating the expressions of oncogenes and tumor suppressor genes though interacting with the 3' untranslated region (UTR) of target genes, we aimed to evaluate the association between genetic variants of miRNAs and their binding sites and prognosis in patients with colorectal cancer (CRC).</P>
Kim, Jin Won,Im, Seock-Ah,Kim, Miso,Cha, Yongjun,Lee, Kyung-Hun,Keam, Bhumsuk,Kim, Min A,Han, Sae-Won,Oh, Do-Youn,Kim, Tae-You,Kim, Woo Ho,Bang, Yung-Jue Potamitis Press 2012 Anticancer research Vol.32 No.4
<P>We aimed to clarify the prognostic significance of HER2 positivity in advanced gastric cancer.</P>
Min, Sun Young,Kim, Hee Sung,Jung, Eun Jung,Jung, Eun Ji,Jee, Chang Do,Kim, Woo Ho Potamitis Press 2012 Anticancer research Vol.32 No.8
<P>This study aimed at examining the association of gene silencing and promoter methylation of glutathione peroxidase 1 (GPX1) and glutathione peroxidase 3 (GPX3) in gastric cancer cells and determined the clinical significance of GPX1 and GPX3 expression loss in gastric cancer tissue.</P>
Myricetin induces cell death of human colon cancer cells via BAX/BCL2-dependent pathway.
Kim, Mi Eun,Ha, Tae Kwun,Yoon, Ju Hwa,Lee, Jun Sik Potamitis Press 2014 Anticancer research Vol.34 No.2
<P>Myricetin is a flavonol found in various berries, herbs, and walnuts. Previous studies have demonstrated that myricetin has anticancer effects against several types of cancer, including hepatocarcinoma, skin carcinoma, and pancreatic cancer. However, the anticancer activity of myricetin on human colon cancer has not been yet established. In the present study, we investigated the anticancer effects of myricetin on HCT-15 human colon cancer cells. We found that myricetin induces cytotoxicity and DNA condensation in human colon cancer cells in a dose-dependent manner. We also determined that myricetin increases the BCL2-associated X protein/B-cell lymphoma 2 ratio, but not cleavage of caspase-3 and -9. In addition, myricetin induced the release of apoptosis-inducing factor from mitochondria. These results suggest that myricetin induces apoptosis of HCT-15 human colon cancer cells and may prove useful in the development of therapeutic agents for human colon cancer.</P>
Hong, Il Ki,Kim, Seog Young,Chung, Jin Hwa,Lee, Seung Jin,Oh, Seung Jun,Lee, Sang Ju,Oh, Jungsu,Ryu, Jin-Sook,Kim, Tae Won,Kim, Deog Yoon,Moon, Dae Hyuk Potamitis Press 2014 Anticancer research Vol.34 No.2
<P>We aimed to investigate whether 3'-deoxy-3'-[(18)F]fluorothymidine ([(18)F]FLT) positron emission tomography (PET) can estimate thymidine kinase 1 (TK1) activity after thymidylate synthase (TS) inhibition by 5-fluorouracil (5-FU) in a mouse tumor model.</P>
Kim, Si Hyoung,Kang, Jun Goo,Kim, Chul Sik,Ihm, Sung-Hee,Choi, Moon Gi,Yoo, Hyung Joon,Lee, Seong Jin Potamitis Press 2015 Anticancer research Vol.35 No.10
<P>The aim of the present study was to evaluate the effect of heat-shock protein 90 (HSP90) inhibitors, 17-allylamino-17-demethoxygeldanamycin (17-AAG) and herbimycin A (HMA) on survival of anaplastic thyroid carcinoma (ATC) cells.</P>
Kim, Young Wan,Jan, Khalilullah Mia,Jung, Duck Hyun,Cho, Mee Yon,Kim, Nam Kyu Potamitis Press 2013 Anticancer research Vol.33 No.11
<P>Antitumor immune response is suggested to be a factor affecting the number of nodes retrieved after colorectal cancer surgery. The purpose of this study was to evaluate the correlation of antitumor immune response with the number of retrieved nodes.</P>
Yang, Si Hyung,Suh, Jung Hwa,Lee, Myung Gull,Kim, So Hee Potamitis Press 2013 Anticancer research Vol.33 No.2
<P>Tamoxifen, which is used to treat breast cancer, and ondansetron, used for the treatment of chemotherapy-induced nausea, are commonly metabolized via cytochrome P450 (CYP) 2D subfamily and 3A1/2 in rats, as in humans. This study was conducted to investigate the pharmacokinetic interactions between ondansetron and tamoxifen after intravenous and oral administration of ondansetron (both 8 mg/kg) and/or tamoxifen (2 and 10 mg/kg for intravenous and oral administration, respectively), in rats bearing 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammarian tumors (DMBA rats), used as an animal model of human breast cancer. The total area under the plasma concentration-time curve, from time zero to infinity (AUC) of tamoxifen was significantly greater after both intravenous and oral administration with ondansetron, compared to that after administration of tamoxifen-alone. The hepatic and intestinal metabolism of tamoxifen in DMBA rats was inhibited by ondansetron. Taken together, the significant increase in tamoxifen AUC in DMBA rats after intravenous or oral administration with ondansetron may be attributed to non-competitive hepatic (intravenous) and competitive intestinal (oral) inhibition of CYP2D subfamily- and 3A1/2-mediated tamoxifen metabolism by ondansetron.</P>