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  • American Association for Cancer Research (AACR)  (56)
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  • American Association for Cancer Research (AACR)  (56)
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  • 1
    Online Resource
    Online Resource
    A Functional Variant at 19q13.3, rs967591G〉A, Is Associated with Shorter Survival of Early-Stage Lung Cancer
    American Association for Cancer Research (AACR) ; 2013
    In:  Clinical Cancer Research Vol. 19, No. 15 ( 2013-08-01), p. 4185-4195
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 19, No. 15 ( 2013-08-01), p. 4185-4195
    Abstract: Purpose: This study was conducted to investigate the associations between single-nucleotide polymorphisms (SNP) in 19q13.3 and survival of patients with early-stage non–small cell lung cancer (NSCLC), and to define the causative functional SNP of the association. Experimental Design: A two-stage study design was used to evaluate five SNPs in relation to survival outcomes in 328 patients and then to validate the results in an independent patient population (n = 483). Luciferase assay and real-time PCR were conducted to examine functional relevance of a potentially functional SNP. Results: Of the five SNPs, three SNPs (rs105165C & gt;T, rs967591G & gt;A, and rs735482A & gt;C) were significantly associated with survival outcomes in a stage I study. The rs967591A allele had significantly higher activity of the CD3EAP promoter compared with the rs967591G allele (P = 0.002), but the SNP did not have an effect on the activity of PPP1R13L promoter. The rs967591G & gt;A was associated with the level of CD3EAP mRNA expression in lung tissues (P = 0.01). The rs967591G & gt;A exhibited consistent associations in a stage II study. In combined analysis, the rs967591 AA genotype exhibited a worse overall survival (adjusted HR = 1.69; 95% confidence interval = 1.29–2.20; P = 0.0001). Conclusion: The rs967591G & gt;A affects CD3EAP expression and thus influences survival in early-stage NSCLC. The analysis of the rs967591G & gt;A polymorphism can help identify patients at high risk of a poor disease outcome. Clin Cancer Res; 19(15); 4185–95. ©2013 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-12-2792
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 2
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    Online Resource
    Abstract 3138: Topological analysis of spatial transcriptomics reveals different spatial interaction patterns in tumor microenvironment of lung cancer
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 7_Supplement ( 2023-04-04), p. 3138-3138
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7_Supplement ( 2023-04-04), p. 3138-3138
    Abstract: Background: As the tumor microenvironment (TME) consists of various cell types with complex spatial interaction, its spatial organization patterns affect response to immune-oncology treatment. Therefore, describing the spatial composition and interaction of cells in the tumor microenvironment (TME) is necessary. Here, we developed a tool, STopover, which adopts topological analysis in spatial transcriptomics to reveal cell-cell colocalization patterns in TME and capture the key components and niche of intercellular communication, and applied it to human lung cancer data. Methods: The spatial colocalization pattern of pairs of features was defined using topological data analysis with Morse filtration. The spatial network of spatial gene expression data was generated for each sample and then the patterns were summarized as connected components (CCs) based on the spatial distance between unit tissue regions and the persistence of each CC. The global and local extent of spatial overlap of a feature pair was calculated as Jaccard indices between extracted CC pairs. We applied STopover to 11 barcode-based spatial transcriptomic data of human lung adenocarcinoma with different PD-L1 expressions. Spatial mapping of cell types in TME was performed by CellDART. In addition, image-based spatial transcriptomic data of lung cancer were also used to find key spatial molecular interactions in TME using STopover. Results: First, STopover disclosed the distinct immune and stromal infiltration patterns in lung cancer tissues. Spatial colocalization of cancer cells and T-cells was heterogeneous and correlated with the immune-related markers such as MHC class I signature. The cancer types were clustered according to spatial colocalization patterns of various immune cells with cancer cells, which showed different infiltration patterns of immune cells. Moreover, STopover could estimate the top cell-cell interaction and emphasize the key locations based on the literature-supported ligand-receptor database. Conclusion: STopover is expected to account for significant spatial cell interactions in tumor-immune and tumor-stromal components and could be utilized as a platform to decipher the mechanisms underlying immune-oncology treatment response. Citation Format: Sungwoo Bae, Hyekyoung Lee, Kwon Joong Na, Dong Soo Lee, Hongyoon Choi, Young Tae Kim. Topological analysis of spatial transcriptomics reveals different spatial interaction patterns in tumor microenvironment of lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3138.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2023-3138
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
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    Online Resource
    Tumor Genomic Profiling Guides Patients with Metastatic Gastric Cancer to Targeted Treatment: The VIKTORY Umbrella Trial
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Discovery Vol. 9, No. 10 ( 2019-10-01), p. 1388-1405
    Details
    In: Cancer Discovery, American Association for Cancer Research (AACR), Vol. 9, No. 10 ( 2019-10-01), p. 1388-1405
    Abstract: The VIKTORY (targeted agent eValuation In gastric cancer basket KORea) trial was designed to classify patients with metastatic gastric cancer based on clinical sequencing and focused on eight different biomarker groups (RAS aberration, TP53 mutation, PIK3CA mutation/amplification, MET amplification, MET overexpression, all negative, TSC2 deficient, or RICTOR amplification) to assign patients to one of the 10 associated clinical trials in second-line (2L) treatment. Capivasertib (AKT inhibitor), savolitinib (MET inhibitor), selumetinib (MEK inhibitor), adavosertib (WEE1 inhibitor), and vistusertib (TORC inhibitor) were tested with or without chemotherapy. Seven hundred seventy-two patients with gastric cancer were enrolled, and sequencing was successfully achieved in 715 patients (92.6%). When molecular screening was linked to seamless immediate access to parallel matched trials, 14.7% of patients received biomarker-assigned drug treatment. The biomarker-assigned treatment cohort had encouraging response rates and survival when compared with conventional 2L chemotherapy. Circulating tumor (ctDNA) analysis demonstrated good correlation between high MET copy number by ctDNA and response to savolitinib. Significance: Prospective clinical sequencing revealed that baseline heterogeneity between tumor samples from different patients affected response to biomarker-selected therapies. VIKTORY is the first and largest platform study in gastric cancer and supports both the feasibility of tumor profiling and its clinical utility. This article is highlighted in the In This Issue feature, p. 1325
    Type of Medium: Online Resource
    ISSN: 2159-8274 , 2159-8290
    URL: Article
    DOI: 10.1158/2159-8290.CD-19-0442
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 2607892-2
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  • 4
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    Online Resource
    Methyl-CpG Binding Domain 1 Gene Polymorphisms and Risk of Primary Lung Cancer
    American Association for Cancer Research (AACR) ; 2005
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 14, No. 11 ( 2005-11-01), p. 2474-2480
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 14, No. 11 ( 2005-11-01), p. 2474-2480
    Abstract: The methyl-CpG binding domain 1 (MBD1) protein plays an important role for transcriptional regulation of gene expression. Polymorphisms and haplotypes of the MBD1 gene may have an influence on MBD1 activity on gene expression profiles, thereby modulating an individual's susceptibility to lung cancer. To test this hypothesis, we investigated the association of MBD1 −634G & gt;A, −501delT (−501 T/T, T/−, −/−), and Pro401Ala genotypes and their haplotypes with the risk of lung cancer in a Korean population. The MBD1 genotype was determined in 432 lung cancer patients and in 432 healthy control subjects who were frequency matched for age and gender. The −634GG genotype was associated with a significantly increased risk of overall lung cancer compared with the −634AA genotype [adjusted odds ratio (OR), 3.10; 95% confidence interval (95% CI), 1.24-7.75; P = 0.016]. When analyses were stratified according to the tumor histology, the −634GG genotype was associated with a significantly increased risk of adenocarcinoma compared with the −634AA genotype (adjusted OR, 4.72; 95% CI, 1.61-13.82; P = 0.005). For the MBD1 −501delT and Pro401Ala polymorphisms, the −501 T/T genotype was associated with a marginal significantly increased risk of adenocarcinoma compared with the −501−/− genotype (adjusted OR, 2.07; 95% CI, 1.02-4.20; P = 0.045), and the Pro/Pro genotype was associated with a significantly increased risk of adenocarcinoma compared with the Ala/Ala genotype (adjusted OR, 3.41; 95% CI, 1.21-9.60; P = 0.02). Consistent with the genotyping analyses, the −634G/−501T/401Pro haplotype was associated with a significantly increased risk of overall lung cancer and adenocarcinoma compared with the −634A/−501−/401Ala haplotype (adjusted OR, 1.44; 95% CI, 1.08-1.91; P = 0.012 and Pc = 0.048; adjusted OR, 1.75; 95% CI, 1.20-2.56; P = 0.004 and Pc = 0.016, respectively). On a promoter assay, the −634A allele had significantly higher promoter activity compared with the −634G allele in the Chinese hamster ovary cells and A549 cells (P & lt; 0.05 and P & lt; 0.001, respectively), but the −501delT polymorphism did not have an effect on the promoter activity. When comparing the promoter activity of the MBD1 haplotypes, the −634A/−501− haplotype had a significantly higher promoter activity than the −634G/−501T haplotype (P & lt; 0.001). These results suggest that the MBD1 −634G & gt;A, −501delT, and Pro401Ala polymorphisms and their haplotypes contribute to the genetic susceptibility for lung cancer and particularly for adenocarcinoma.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-05-0423
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2005
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 5
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    Online Resource
    Tumor Suppressive Effects of Bromodomain-Containing Protein 7 (BRD7) in Epithelial Ovarian Carcinoma
    American Association for Cancer Research (AACR) ; 2014
    In:  Clinical Cancer Research Vol. 20, No. 3 ( 2014-02-01), p. 565-575
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 20, No. 3 ( 2014-02-01), p. 565-575
    Abstract: Purpose: Bromodomain-containing protein 7 (BRD7), which is a subunit of SWI/SNF complex, has been recently suggested as a novel tumor suppressor in several cancers. In this study, we investigated the tumor suppressive effect of BRD7 in epithelial ovarian cancer. Experimental Design: We analyzed the expression of BRD7 in human ovarian tissues with real-time PCR. To investigate the functional role of BRD7, we transfected ovarian cancer cells (A2780 and SKOV3) with BRD7 plasmid and checked the cell viability, apoptosis, and invasion. The activities of BRD7 in the signaling pathways associated with carcinogenesis were also tested. In addition, we used the orthotopic mouse model for ovarian cancer to evaluate tumor growth-inhibiting effect by administration of BRD7 plasmid. Results: The BRD7 expression was downregulated in the ovarian cancer tissues compared with normal (P & lt; 0.05), high-grade serous cancer exhibited significantly decreased expression of BRD7 compared with low-grade (P & lt; 0.01) serous cancer. Transfection of BRD7 plasmid to A2780 (p53-wild) or SKOV3 (p53-null) ovarian cancer cells showed the tumor suppressive effects assessed by cell viability, apoptosis, and invasion assay and especially significantly decreased tumor weight in orthotopic mouse model (A2780). Moreover, we found that tumor suppressive effects of BRD7 are independent to the presence of p53 activity in ovarian cancer cells. BRD7 negatively regulated β-catenin pathway, resulting in decreased its accumulation in the nucleus. Conclusions: These results suggested that BRD7 acts as a tumor suppressor in epithelial ovarian cancers independently of p53 activity, via negative regulation of β-catenin pathway. Clin Cancer Res; 20(3); 565–75. ©2013 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-13-1271
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 6
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    Online Resource
    Abstract 2607: Antitumor activity of the selective RAF inhibitor HM95573 in solid tumors and hematologic malignancies
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 2607-2607
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 2607-2607
    Abstract: The mitogen-activated protein kinase (MAPK) pathway is particularly important for the survival and proliferation of tumor cells. Activation of the MAPK pathway due to mutations in BRAF, NRAS and KRAS is considered one of the causes of solid tumors (NSCLC, CRC,HCC, andthyroid cancers) and hematologic malignancies. HM95573 is a novel, highly potent RAF kinase inhibitor. Biochemically assayed for over 120 kinases, HM95573 showed the high selectivity toward BRAF mutant and CRAF kinases. The half maximal inhibition concentrations (IC50) of HM95573 against BRAFWT, BRAFV600E and CRAF kinases were 41nM, 7nM and 2nM, respectively. The strongly inhibited kinases subsequent to RAF kinases appeared to be CSF1R (44nM), DDR1 (77nM) and DDR2 (182 nM). HM95573 potently inhibited the growth of BRAFmutation CRC cell lines (e.g. IC50: 118nM for Colo-205) and thyroid cancer cell lines (43nM for B-CPAP); KRAS mutation NSCLC cell lines(297nM for Calu-6),CRC cell lines(65nM for HCT-116) and thyroid cancer cell lines(479nM for CAL-62); and NRAS mutation HCC cell lines(28nM for HepG2) andleukemia cell lines (39nM for HL-60). HM95573 effectively inhibited the phosphorylations of MEK and ERK, downstream kinases associated with cell proliferation in tumor cell lines mutated in BRAF, KRAS and NRAS. In addition, the phosphorylation of downstream kinases of RAF such as MEK and ERK was effectively inhibited with treatment of HM95573 in mutant KRAS NSCLC and CRC cells. HM95573 showed the excellent antitumor activity in mouse models xenografted with BRAF mutation cell line (Colo-205), KRAS mutation cell lines (Calu-6 and HCT-116)and NRAS mutation cell line (HepG2)two RAF inhibitors approved in melanoma which were effective to only BRAF mutation cell lines under conditions tested. The in vivo antitumor activity of HM95573 was potentiated with MEK inhibitors. Now, HM95573 is currently in phase I development in patients with advanced solid tumors including KRAS mutation NSCLC in Korea. Citation Format: Young-Mi Lee, InHwan Bae, Namgoong Gwang Mo, Jae Ho Lee, Suhyeon Kim, Ji Yeon Song, Kyu Hang Lee, Tae Hun Song, Young Gil Ahn, Young Hoon Kim, Kwee Hyun Suh. Antitumor activity of the selective RAF inhibitor HM95573 in solid tumors and hematologic malignancies. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2607. doi:10.1158/1538-7445.AM2015-2607
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-2607
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 7
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    Online Resource
    Abstract 4009: N-ras codon 61 mutation is associated with distant metastasis in patients with follicular thyroid carcinoma
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 4009-4009
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 4009-4009
    Abstract: Distant metastasis is a main cause of death in follicular thyroid carcinoma (FTC) patients. Factors related to distant metastasis in FTC had been known as age, primary tumor size, and invasiveness. Ras mutations were also supposed to be associated with poor clinical outcomes. We analyzed Ras mutations in FTC with a distant metastasis (FTC M1, n=28), size matched-FTC without a distant metastasis (FTC M0, n=28), follicular adenoma (FA, n=17), and nodular hyperplasia (NH, n=12) to figure out the roles of Ras mutations in follicular thyroid carcinogenesis and metastasis. In addition, we assess the relationship between Ras mutations and clinical outcomes in FTC patients. NRAS, HRAS, and KRAS mutations were assessed using direct sequencing method. Among 85 patients, 39 patients (46%) had Ras mutations. NRAS codon 61 mutation (n=21; 25%) was the most common point mutation. HRAS codon 61, KRAS codon 12/13, and KRAS codon 61 mutations were found in 7, 6, and 4 patients, respectively. NRAS codon 12/13 mutation was found in only 1 patient, and HRAS codon 12/13 mutation was not found. Ras mutations were significantly more common in the FTC than FA or NH groups. Especially, NRAS codon 61 mutation was associated with distant metastasis in patients with FTC. However, there was no significant difference in survival between the Ras mutation positive-FTC and Ras mutation negative-FTC patients. Ras mutation, especially NRAS codon 61 mutation, was significantly associated with the presence of distant metastases. NRAS codon 61 mutation status might be a potential prognostic factor in FTC patients. Citation Format: MinJi Jeon, Eun Kyung Jang, Dong Eun Song, So Young Sim, Eui Young Kim, Yun Mi Choi, Ji Min Han, Won Gu Kim, Tae Yong Kim, Young Kee Shong, Won Bae Kim. N-ras codon 61 mutation is associated with distant metastasis in patients with follicular thyroid carcinoma. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4009. doi:10.1158/1538-7445.AM2014-4009
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-4009
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
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    Online Resource
    Abstract 1709: The effect of a XIAP inhibitor, embelin, on apoptosis of thyroid cancer cell lines
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1709-1709
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1709-1709
    Abstract: X-linked inhibitor of apoptosis protein (XIAP) is a member of the inhibitor of apoptosis (IAP) protein family that selectively blocks caspases-3, -7, -9 and inhibits cell death. Embelin, a XIAP inhibitor, is known to exhibit anti-inflammatory and apoptotic activities. Recent reports suggest that embelin interferes the signal transducer and activator of transcription 3 (STAT3) pathway and nuclear factor-kB (NF-kB) signal pathway. In this study, we investigated the anti-cancer efficacy of embelin by measuring its effects on apoptosis of thyroid cancer cell lines. We also explored the mechanism underlying these effects. We found that embelin induced the apoptosis of human thyroid cancer cell lines, such as FTC-133, CAL-62, KTC-1, and 8505C. The effect was stronger in BRAF V600E-mutant thyroid cancer cell lines (KTC-1 and 8505C) than wild-type cell lines (FTC-133 and CAL-62). The effect of embelin on cell apoptosis was associated with increased phosphorylation of p38. SB203580 inhibited the embelin mediated induction of cleaved caspase-3 activity in V600E mutant thyroid cancer cell lines. Interestingly, embelin induced apoptosis in BRAF wild type cancer cell lines, even after treatment of SB203580. These results indicated that another signaling pathway, not a p38 pathway, might be existed for embelin induced apoptosis in BRAF wild type thyroid cancer cell. In conclusion, embelin-induced XIAP suppression resulted in an increase of apoptosis via phosphorylation of p38 in BRAF V600E-mutant thyroid cancer cell lines. Regulation of XIAP activity may be potentially useful as a treatment of thyroid cancer, especially in BRAF V600E-mutant thyroid cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1709. doi:1538-7445.AM2012-1709
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-1709
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
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    Abstract 4618: Therapeutic targeting for sphingosine kinase 1 in epithelial ovarian cancer
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 4618-4618
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 4618-4618
    Abstract: Purpose: Sphingosine kinase 1 (SK1) is over-expressed in various human cancers with pro-growth effects and its inhibitors has been suggested potential anti-cancer agents. This study was designed to investigate the therapeutic potential of SK1 inhibitor in epithelial ovarian carcinoma (EOC). Experimental design: The expression of SK1 protein was evaluated using immunohistochemistry in patients with EOC. EOC cell lines (A2780, SKOV3ip1, A2780-CP20, SKOV3-TR, ES2 and RMG2) were used in this study to test SK1 siRNA or inhibitors. We used two kinds of SK inhibitor including SK inhibitor (for both SK1 and 2) and FTY720 (specifically inhibiting SK1) to check cell proliferation, apoptosis, angiogenesis and invasion using MTT, FACS, ELISA and wound-healing assay, respectively. Furthermore, in vivo experiments were performed to test the FTY720 on tumor growth in orthotopic EOC mouse model. Results: The expression of SK1 protein in primary EOC tissues was strongly observed in all of patients; however, there was no expression of SK1 protein in the normal ovarian epithelium (n=5). Blocking SK1 by its siRNA or inhibitors significantly affected cell proliferation, apoptosis, angiogenesis and invasion in A2780-PAR and SKOV3ip1 cells. SK1 inhibitors led to decrease of SK enzymatic activity in cells. Furthermore, utilizing the in vivo animal model (A2780-PAR), FTY720 treatment significantly decreased the total tumor weight compared with control (P & lt; 0.05). Conclusions: These results show that therapeutic targeting of SK1 with its inhibitor could have potentials of novel therapeutics for EOC. Citation Format: Jeong-Won Lee, Ji Yoon Ryu, Hye-Kyung Jeon, Young-Ae Park, Young-Jae Cho, Jung-Joo Choi, Yoo-Young Lee, Tae-Joong Kim, Chel Hun Choi, Byoung-Gie Kim, Duk-Soo Bae. Therapeutic targeting for sphingosine kinase 1 in epithelial ovarian cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4618. doi:10.1158/1538-7445.AM2014-4618
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-4618
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
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    Abstract 2105: High Galectin-1 expression correlates with poor prognosis and is involved in epithelial ovarian cancer proliferation and invasion
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 2105-2105
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 2105-2105
    Abstract: Purpose: Galectin-1 (Gal-1) is a 14-kDa laminin-binding galectin involved in several biologic events including regulation of tumor proliferation and metastasis. In this study, we investigated the clinical significance of Gal-1 expression and its functional role in cell proliferation and invasion in epithelial ovarian cancer (EOC). Experimental Design: We evaluated the expression of Gal-1 in 52 serous, 11 endometrioid, and 3 mucinous type EOC tumor samples from 66 patients by immunohistochemistry. In vitro experiments were performed to determine the function of Gal-1 in cell survival, proliferation, and invasion in EOC cells using siRNA and anginex, a Gal-1 inhibitor, as well as recombinant Gal-1 protein. Results: Patients with strong Gal-1 peritumoral staining had poorer progression-free survival (PFS) than patients with weak peritumoral staining (P = 0.03). Inhibition of Gal-1 by siRNA or anginex resulted in the inhibition of cell growth and proliferation of HeyA8 and SKOV3ip1 cells. Moreover, the ability of cells to migrate was significantly reduced by treatment of cells with Gal-1 siRNA but was increased by treatment of cells with recombinant Gal-1. When we evaluated the interaction between fibroblasts (H HESC) and cancer cells (A2780-CP20), we found that MMP-2 expression in cancer cells was affected by Gal-1 secreted by fibroblast cells, which suggests that Gal-1 in human fibroblasts might affect the invasive abilities of tumor cells. Conclusion: Our results suggest that Gal-1 expression is a potential prognostic factor for PFS and that Gal-1 could be a novel treatment target in EOC patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2105. doi:1538-7445.AM2012-2105
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-2105
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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