Cancer Research and Treatment

Prognostic Significance of KAI-1 and Survivin Expressions in Ovarian Epithelial Carcinomas: Ju Han Lee, Suk Min Lee, Jong Sang Choi; Cancer Res Treat. 2003;35(4):323-329. Published online August 31, 2003; DOI: https://doi.org/10.4143/crt.2003.35.4.323

Abstract PDF: PURPOSE
The purpose of this study was to evaluate the expressions of KAI-1 and survivin, and to investigate their correlation with the clinical stage and survival rate of patients with ovarian carcinomas.
MATERIALS AND METHODS
The expressions of survivin and KAI-1 were immunohistochemically determined in 54 serous and mucinous ovarian adenocarcinomas and borderline malignancy tumors. 10 of the 54 cases were also analyzed for the expressions of survivin and KAI-1 using western blot.
RESULTS
The down-regulation of the expression of KAI-1 was observed by immunohistochemical staining (IHC) in 53.7% of the ovarian cancers, and a negative reaction in 50% by the western blot analysis. From the IHC, the survivin expression was positive and strongly positive in 51.9 and 18% of the ovarian cancers, respectively. From the western blot analysis, 10% of the ovarian cancer showed positive reactions. The down- regulation of the KAI-1 expression was significantly correlated with the clinical stage (p=0.001) and disease free survival rate (p<0.001), but not with the histological type. The expression of survivin was not correlated with the clinical stage or histological type. However, the patients with a negative survivin expression had a significantly longer disease survival rate than those with a strong positive expression.
CONCLUSION
The down- and up-regulation of the KAI-1 and survivin, respectively, might be independent prognostic factors in human ovarian carcinomas.

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Growth Suppression of Ovarian Cancer Cells by Interferon-gama: Jong Sup Park, Eun Joo Kim, Tae Chul Park, Eun Jung Kim, Jin Kim, Joon Mo Lee, Sung Eun Namkoong, Soo Jong Um; Cancer Res Treat. 2001;33(3):236-242. Published online June 30, 2001; DOI: https://doi.org/10.4143/crt.2001.33.3.236

PURPOSE
Growth regulation of cancer cells very frequently involves tumor suppressor gene p53, Rb and cell cycle regulator, however the molecular biologic mechanisms of growth regulation in ovarian carcinoma cells are not fully defined. To assess the mechanism of growth suppression, we treated IFN-gama in ovarian carcinoma cells.
MATERIALS AND METHODS
Growth suppression by treatment of IFN-gama was determined by cell proliferation assay in ovarian carcinoma cell lines. Apoptosis was determined by DNA fragmentation assay and electron microscopy. Molecular mechanism of the apoptosis in ovarian carcinoma cell by IFN-gama was further analyzed by the western blot.
RESULTS
We found that IFN-gama had remarkable growth- suppressive effects in PA-1 and A2774 ovarian carcinoma cells in a time-dependent manner. Apoptosis was observed in PA-1 and A2774 cell following treatment of IFN- gama by DNA fragmentation assay and EM. The expression of IRF-1 protein from A2774 and PA-1 cell extracts was elevated by increasing the concentration of IFN-gama. IFN-gama caused an increased expression of the important apoptosis-related gene, ICE (interleukin-1beta-converting enzyme) protein in A2774 and PA-1.
CONCLUSION
The coordinate induction of IRF-1 and ICE by IFN-gama in ovarian carcinoma cells suggests a functional relationship between these proteins in programmed cell death. The significance of this study is the molecular biologic background of IFN-gama considered as an alternative treatment trial of ovarian cancers.

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Cdk2-dependent phosphorylation of the NF-Y transcription factor is essential for the expression of the cell cycle-regulatory genes and cell cycle G1/S and G2/M transitions
Hee-Don Chae, Jeanho Yun, Yung-Jue Bang, Deug Y Shin
Oncogene.2004; 23(23): 4084. CrossRef
Cdk2-dependent Phosphorylation of the NF-Y Transcription Factor and Its Involvement in the p53-p21 Signaling Pathway
Jeanho Yun, Hee-Don Chae, Tae-Saeng Choi, Eun-Hee Kim, Yung-Jue Bang, Jongkyeong Chung, Kyeong-Sook Choi, Roberto Mantovani, Deug Y. Shin
Journal of Biological Chemistry.2003; 278(38): 36966. CrossRef

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Expression of Cyclin D1 and CDK4 in DMBA-Induced Rat Ovarian Cancer: Ki Kwon Kim; Cancer Res Treat. 2001;33(3):229-235. Published online June 30, 2001; DOI: https://doi.org/10.4143/crt.2001.33.3.229

Abstract PDF

PURPOSE
Ovarian cancer is a common gynecologic malignancy and the leading cause of death in women. It is typically not diagnosed until it has reached the advanced stages. We performed this study to investigate the roles of the proteins related to the G1 cell cycle in ovarian carcinogenesis.
MATERIALS AND METHODS
Immunohistochemistry and Western blot were used to analyse the expression of cyclin Dl and CDK4 in 7, 12-dimethylbenzanthracene- induced ovarian cancer in rats.
RESULTS
The Cyclin D1 and CDK4 labelling index was significantly higher in the ovarian cancers than in the normal ovarian surface epithelium of rats. There was no difference among the cancer types. In Western blot analyses, the expression of cyclin Dl and CDK4 in the ovarian cancers was higher than that in the normal ovarian surface epithelium. A positive correlation was observed between the expressions of the CDK4 and Cyclin D1.
CONCLUSION
The upregulation of cyclin Dl and CDK4 that occurs in DMBA-induced rat ovarian carcinogenesis is likely to be associated with tumor progression. Further studies are needed to investigate the role and function of cyclin Dl and CDK4 in human ovarian cancer.

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CDK4/6i enhances the antitumor effect of PD1 antibody by promoting TLS formation in ovarian cancer
Wangyou Feng, Dongbo Jiang, Ying Xu, Yuanfeng Li, Lin Chen, Minye Zhao, Yujie Shen, Wenjing Liao, Hong Yang, Jia Li
Heliyon.2023; 9(9): e19760. CrossRef

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Alterations of HLA Class I and II Antigen Expressions in Borderline, Invasive and Metastatic Ovarian Cancers: Yun Kyong Kim, Young Oak Lew, Sung Bae Jee, Gyu Moon Kim, Mi Young Choi, Mi Ji Kang, Yong Seok Lee, Jin Woo Kim; J Korean Cancer Assoc. 2000;32(6):1031-1042.

Abstract PDF: PURPOSE
The relationship between altered HLA expressions and ovarian carcinogenesis is not fully elucidated.
MATERIALS AND METHODS
Histological evaluation comprised 20 serous adenocarcinoma, 5 borderline serous malignancy, 10 mucinous adenocarcinoma, 15 borderline mucinous malignancy. We used monoclonal antibodys to HLA class I beta2-microglobulin, class I B/C and class II heavy chain.
RESULTS
There was no statistical difference in HLA expressions between borderline serous malignancy and normal ovarian tissue. In serous adenocarcinoma, beta2-microglobulin, B/C and class II heavy chain expressions were down-regulated. In metastatic cancer, B/C and class II ex pressions were also down-regulated. But the HLA expression of tumor or normal stromal tissue in primary tumor, were not down-regulated compared with the tissues in metastasis. In borderline mucinous malignancy, class II expressions were down-regulated. In mucinous adenocarcinoma, beta2-microglobulin, B/C and class II expressions were down-regulated. In metastatic ovarian cancer, B/C and class II expressions were down-regulated. But, in borderline malignancy, the result failed to reach statistical significance except class II of borderline mucinous malignancy.
CONCLUSION
Loss of HLA class I and II molecules in invasive ovarian cancers raises the possibility that this could be a mechanism for tumor cells to have invasiveness.

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Phase I Clinical Trial of Paclitaxel Plus Ifosfamide for the Patients with Refractory Ovarian Cancer: Ho Sawk Saw, Jae Kwan Lee; J Korean Cancer Assoc. 2000;32(5):895-903.

Abstract PDF: PURPOSE
Patients with advanced ovarian carcinoma and refractory to platinum based chemotherapy have a very poor prognosis and effective salvage regimens are needed. This study was conducted in order to determine the maximum tolerated dose (MTD) and dose limiting toxicity of combination with paclitaxel and ifosfamide.
MATERIALS AND METHODS
After premedication, patients received paclitaxel (110~225 mg/m2) as a 24 hour IV infusion on day 1. Ifosfamide (1,000~1,500 mg/m2) was given as a 12 hour IV infusion with standard dose of mesna on day 2~6. All patients received G-CSF (granulocyte colony stimulating factor) on day 6~15.
RESULTS
12 patients with advanced ovarian cancer entered this trial. Toxicity included bone marrow suppression, neuromuscular toxicity, urothelial toxicity, gastrointestinal toxicity, which occurred in 84.6%, 65.3%, 30.7%, 88.4% of cycles.
CONCLUSION
Neuromuscular toxicity was dose limiting toxicity. Maximum tolerated dose in com bination with paclitaxel and ifosfamide was 175 mg/m2 of paclitaxel and 1,500 mg/m2 of ifosfamide.

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A Case of Triple-Alkylating Regimen and Peripheral Blood Stem Cell Transplantation for a Patient with Relapsed Ovarian Carcinoma: Jun Mo Lee, Seok Goo Cho, Jin No Park, Young Sun Hong, Hoon Kyo Kim, Sung Eun Namkoong, Kyung Shick Lee, Chun Choo Kim; J Korean Cancer Assoc. 2000;32(4):817-821.

Abstract PDF: Despite an aggressive surgical debulking followed by front-line chemotherapy, most patients with advanced ovarian carcinoma die of drug-resistant disease. Drug resistance can be overcome in a subset of patients with hematologic malignancies and lymphoma with high-dose therapy (HDT) and hematopoietic stem cell transplantation, suggesting that this therapy may also be value in ovarian carcinoma. We report the successful outcome of HDT and peripheral blood stem cell transplantation (PBSCT) in a 41-year-old nulliparous woman who initially was diagnosed with advanced ovarian carcicnoma with FIGO stage IIIc. Her disease relapsed after 19 months from initial therapy of definitive surgery and intra- and post-operative chemotherapy. Subsequently, she received optimal debulking surgery and salvage chemotherapy followed by HDT with triple- alkylating regimen, composed of cyclophosphamide (100 mg/kg), thiotepa (500 mg/m2), and melphalan (100 mg/m2). Her pretranplant characteristics were platinum-sensitive and complete response state. She showed rapid hematologic recovery and mild regimen-related toxicity (Bear man's toxicity criteria), stomatitis (grade I), cardiac toxicitiy (grade II). She has been followed up for 36 months after the inital therapy and is doing well without relapse.

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Changes of Telomerase Activity by Protein Kinase C Modulators in Human Ovarian Cancer Cell Lines: Soo Young Hur, Joon Mo Lee, Sung Eun Namkoong, Jin Woo Kim; J Korean Cancer Assoc. 2000;32(4):724-733.

Abstract PDF: PURPOSE
This study was designed to find out whether protein kinase C (PKC) may affect telomerase activity in human ovarian cancers.
MATERIALS AND METHODS
To determine whether PKC modulators influence PKC activities, NIH: OVCAR-3 and CUMO-2, cells were treated with PKC inhibitors, G 6976 and bisindolyl maleimide I, and PKC activator, 12-O-tetradecanoyl phorbol 13-acetate (TPA). Telomerase acti vity was determined by telomeric repeat amplification protocol (TRAP). Analysis of the expres sion of each telomerase subunits, human telomerase RNA (hTR) and human telomerase reverse transcriptase (hTERT), was performed by RT-PCR. We also examined the alternative splicing of hTERT.
RESULTS
G 6976 and bisindolylmaleimide I inhibited PKC activity. Telomerase activities appeared to be affected in a time-dependent manner by these two PKC inhibitors. PKC activities were increased in parallel with telomerase activity by TPA at the low dose (10 nM), but their activities were down-regulated at the high dose (1 micrometer). RT-PCR demonstrated the presence of hTR and hTERT mRNA before and after the treatment of PKC modulators, respectively, and showed the presence of one alternatively spliced transcript and full-length hTERT transcripts.
CONCLUSION
These results showed that telomerase activity was affected by PKC and suggested PKC modulation may serve as an useful tool in the regulation of telomerase activity.

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Chromosomal Aberrations in Ovarian Carcinoma Cell Line, SNU - S , Using Chromosome Painting: Jae Seong Kang, Dae Woon Kim, Yong Hyuck Chun, Sun Hwa Park; J Korean Cancer Assoc. 2000;32(1):120-128.

Abstract PDF: PURPOSE
The characterization of all recognizable chromosomal rearrangements was dis- turbed by technical limitation of conventional cytogenetic methods. Recently, the strong usefullness of generation of chromosome specific painting probes in identification of marker chromosomes has proven. This study was intended to analyze the chromosomal aberrations in human ovarian cancer cell line, SNU-8, by G-banding and multiple paintings.
MATERIALS AND METHODS
Human ovarian cancer cell line, SNU-8 was cultured and harvested for cytogenetic analysis. Routine karyotyping was performed. For complete analysis of chromosomal aberrations, human chromosome-specific painting probes were constructed from somatic hybrid cells. The origins of the unidentified marker chromosomes were analyzed by fluorescent in situ hybridization (FISH) with these painting probes.
RESULTS
All chromosome alterations were confirmed by the use of multiple chromosome paintings, which also demonstrated a number of additional alterations. SNU-8 had the karyotype 62-69,XXX, + der(1;10)(q10;p10),der(3;18) (q10;p10)X2,-4,+ 5,+ 7,del(9)(q21)X2,-11,-13,-15,-16,der(17;19)(q10;q10) X2, + 20,-22[cp51].
CONCLUSION
The chromosomal aberrations of SNU-8 cell line was effectively analyzed by FISH with these painting probes, and the approach methods of this study can be applied to cytogenetic analysis of chromosomal aberrations in the other cancers.

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