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  • 1
    Online Resource
    Online Resource
    BCAR1/p130Cas expression in untreated and acquired tamoxifen-resistant human breast carcinomas
    Wiley ; 2000
    In:  International Journal of Cancer Vol. 89, No. 5 ( 2000-09-20), p. 465-468
    Details
    In: International Journal of Cancer, Wiley, Vol. 89, No. 5 ( 2000-09-20), p. 465-468
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Journal
    URL: Article
    DOI: 10.1002/1097-0215(20000920)89:5〈〉1.0.CO;2-U
    DOI: 10.1002/(ISSN)1097-0215
    DOI: 10.1002/1097-0215(20000920)89:5〈465::AID-IJC11〉3.0.CO;2-O
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2000
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  • 2
    Online Resource
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    Protein pathway activation mapping reveals molecular networks associated with antiestrogen resistance in breast cancer cell lines
    Wiley ; 2012
    In:  International Journal of Cancer Vol. 131, No. 9 ( 2012-11-01), p. 1998-2007
    Details
    In: International Journal of Cancer, Wiley, Vol. 131, No. 9 ( 2012-11-01), p. 1998-2007
    Type of Medium: Online Resource
    ISSN: 0020-7136
    URL: Article
    DOI: 10.1002/ijc.27489
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2012
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  • 3
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    Cell-free MicroRNA miR-505-3p in Graft Preservation Fluid Is an Independent Predictor of Delayed Graft Function After Kidney Transplantation
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Transplantation Vol. 103, No. 2 ( 2019-2), p. 329-335
    Details
    In: Transplantation, Ovid Technologies (Wolters Kluwer Health), Vol. 103, No. 2 ( 2019-2), p. 329-335
    Abstract: Delayed graft function (DGF), a common complication after transplantation of deceased donor kidneys, affects both short- and long-term outcomes. Currently available biomarkers during graft preservation lack sensitivity in predicting risk for DGF. The aim of this study is to identify cell-free micro ribonucleic acid (miRNA) biomarkers in graft preservation fluid predictive of DGF after kidney transplantation. Methods Vascular bed preservation fluid was collected from 48 kidney grafts from donation after circulatory death (DCD) or donation after brain death (DBD) donors. miRNA profiles were determined by polymerase chain reaction (PCR) array (n = 8) and validated by reverse transcription and quantitative PCR (n = 40). Graft function posttransplantation was defined as immediate good function (IF) or DGF. Results A total of 223 miRNAs fulfilled the preset parameters (Ct 〈 40 in 3 or more samples) and were included in the analysis. Thirty-two miRNAs were significantly different between DGF and IF kidney grafts ( P 〈 0.05) but, after correction for multiple testing, only miR-505-3p remained significant. The significant association of high miR-505-3p levels with DGF was confirmed in an independent validation cohort using conventional reverse transcription and quantitative PCR detection. Multivariate analyses showed miR-505-3p as an independent predictor for DGF (odds ratio, 1.12; P = 0.028). If stratified for donor type, miR-505-3p levels remained significantly different between IF and DGF in DCD grafts ( P 〈 0.01), but not in DBD grafts. Receiver operating characteristic curve analysis showed a high sensitivity and specificity (area under the curve, 0.833). Conclusions In DCD grafts, high levels of miR-505-3p in preservation fluid are associated with increased risk of DGF after kidney transplantation. Further study is required to confirm the utility of cell-free miR-505-3p as prognostic biomarker for DGF.
    Type of Medium: Online Resource
    ISSN: 1534-6080 , 0041-1337
    URL: Article
    DOI: 10.1097/TP.0000000000002527
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2035395-9
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  • 4
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    Identification of genes involved in development of hormone independence in human breast cancer
    Elsevier BV ; 1990
    In:  European Journal of Cancer and Clinical Oncology Vol. 26, No. 2 ( 1990-2), p. 182-
    Details
    In: European Journal of Cancer and Clinical Oncology, Elsevier BV, Vol. 26, No. 2 ( 1990-2), p. 182-
    Type of Medium: Online Resource
    ISSN: 0277-5379
    URL: Article
    DOI: 10.1016/0277-5379(90)90433-T
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1990
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    detail.hit.zdb_id: 283367-0
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  • 5
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    Cloning and expression of interleukin-3 genes of chimpanzee and New World monkeys
    Elsevier BV ; 1994
    In:  Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression Vol. 1217, No. 2 ( 1994-3), p. 195-198
    Details
    In: Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression, Elsevier BV, Vol. 1217, No. 2 ( 1994-3), p. 195-198
    Type of Medium: Online Resource
    ISSN: 0167-4781
    URL: Article
    DOI: 10.1016/0167-4781(94)90034-5
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1994
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    SSG: 12
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  • 6
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    ERRATUM : Structural homology between the human fur gene product and the subtilisin-like protease encoded by yeast KEX2
    Oxford University Press (OUP) ; 1990
    In:  Nucleic Acids Research Vol. 18, No. 5 ( 1990), p. 1332-1332
    Details
    In: Nucleic Acids Research, Oxford University Press (OUP), Vol. 18, No. 5 ( 1990), p. 1332-1332
    Type of Medium: Online Resource
    ISSN: 0305-1048 , 1362-4962
    URL: Article
    DOI: 10.1093/nar/18.5.1332-a
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 1990
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    SSG: 12
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  • 7
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    Chromosome 3p25.3 Gain Is Associated With Cisplatin Resistance and Is an Independent Predictor of Poor Outcome in Male Malignant Germ Cell Tumors
    American Society of Clinical Oncology (ASCO) ; 2022
    In:  Journal of Clinical Oncology Vol. 40, No. 26 ( 2022-09-10), p. 3077-3087
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 40, No. 26 ( 2022-09-10), p. 3077-3087
    Abstract: Cisplatin is the main systemic treatment modality for male type II germ cell tumors (GCTs). Although generally very effective, 5%-10% of patients suffer from cisplatin-resistant disease. Identification of the driving mechanisms of resistance will enable improved risk stratification and development of alternative treatments. METHODS We developed and characterized cisplatin-resistant GCT cell line models and compared their molecular characteristics with patient samples with cisplatin resistance and/or a poor clinical outcome. Subsequently, the association between the overlapping genetic features and clinical data was assessed. Finally, we used Cox regression to determine the prognostic relevance of these features within the currently used risk classification. RESULTS Gain of chromosome 3p25.3 was detected in all cisplatin-resistant cell lines, and copy number of this region correlated with the level of resistance (R = 0.96, P = 1.5e-04). Gain of this region was detected at low frequencies in primary tumors and at higher frequencies in relapsed and/or cisplatin-resistant tumors. Chromosome 3p25.3 gain was associated with shorter progression-free survival and overall survival, with the strongest association observed in nonseminomas excluding pure teratomas. 3p25.3 gain was more frequently observed in tumors with yolk sac tumor histology and predicted adverse outcome independent of the International Germ Cell Cancer Collaborative Group risk classification and the presence of TP53/ MDM2 alterations. CONCLUSION On the basis of both in vitro analyses and clinical data, we found 3p25.3 to be strongly associated with cisplatin resistance and poor clinical outcome in male type II GCTs. Using genomic profiling, 3p25.3 status could help to improve risk stratification in male patients with type II GCT. Further characterization of this locus and underlying mechanisms of resistance is warranted to guide development of novel treatment approaches for cisplatin-resistant disease.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.21.02809
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2022
    detail.hit.zdb_id: 2005181-5
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  • 8
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    Functional Screen for Genes Responsible for Tamoxifen Resistance in Human Breast Cancer Cells
    American Association for Cancer Research (AACR) ; 2006
    In:  Molecular Cancer Research Vol. 4, No. 6 ( 2006-06-01), p. 379-386
    Details
    In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 4, No. 6 ( 2006-06-01), p. 379-386
    Abstract: Antiestrogens, such as tamoxifen, are widely used for endocrine treatment of estrogen receptor–positive breast cancer. However, as breast cancer progresses, development of tamoxifen resistance is inevitable. The mechanisms underlying this resistance are not well understood. To identify genes involved in tamoxifen resistance, we have developed a rapid screening method. To alter the tamoxifen-sensitive phenotype of human ZR-75-1 breast cancer cells into a tamoxifen-resistant phenotype, the cells were infected with retroviral cDNA libraries derived from human placenta, human brain, and mouse embryo. Subsequently, the cells were selected for proliferation in the presence of 4-hydroxy-tamoxifen (OH-TAM) and integrated cDNAs were identified by sequence similarity searches. From 155 OH-TAM-resistant cell colonies, a total of 25 candidate genes were isolated. Seven of these genes were identified in multiple cell colonies and thus cause antiestrogen resistance. The epidermal growth factor receptor, platelet-derived growth factor receptor-α, platelet-derived growth factor receptor-β, colony-stimulating factor 1 receptor, neuregulin1, and fibroblast growth factor 17 that we have identified have been described as key regulators in the mitogen-activated protein kinase pathway. Therefore, this pathway could be a valuable target in the treatment of patients with breast cancer resistant to endocrine treatment. In addition, the putative gene LOC400500, predicted by in silico analysis, was identified. We showed that ectopic expression of this gene, designated as breast cancer antiestrogen resistance 4 (BCAR4), caused OH-TAM resistance and anchorage-independent cell growth in ZR-75-1 cells and that the intact open reading frame was required for its function. We conclude that retroviral transfer of cDNA libraries into human breast cancer cells is an efficient method for identifying genes involved in tamoxifen resistance. (Mol Cancer Res 2006;4(6):379–86)
    Type of Medium: Online Resource
    ISSN: 1541-7786 , 1557-3125
    URL: Article
    DOI: 10.1158/1541-7786.MCR-05-0156
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2006
    detail.hit.zdb_id: 2097884-4
    SSG: 12
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  • 9
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    Abstract 358: Identification of signaling pathways activated by BCAR4 expression in human breast cancer
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 358-358
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 358-358
    Abstract: Background: The development of resistance to the antiestrogen tamoxifen remains a major challenge in the management of estrogen receptor alpha (ER)-positive breast cancer. Understanding the mechanisms leading to resistance is essential to develop more efficient therapies. In a functional screening for genes causing tamoxifen resistance, we have identified the breast cancer antiestrogen resistance 4 (BCAR4) gene. BCAR4 mRNA is expressed in 27% of primary breast tumors. High BCAR4 mRNA levels predict resistance to tamoxifen treatment and poor outcome, and are associated with a shorter metastasis-free survival and overall survival. Forced expression of BCAR4 in the estrogen-dependent breast cancer cell line ZR-75-1 induced antiestrogen resistance and phosphorylation of ERBB2, ERBB3, and their down-stream mediators ERK1/2 and AKT. The knockdown of ERBB2 or ERBB3 with specific siRNA inhibited cell proliferation, confirming the role of these receptors in BCAR4-induced tamoxifen resistance in vitro. These findings suggest that tumors expressing BCAR4 may rely on ERBB2/ERBB3 signaling and patients with such tumors may be eligible to receive ERBB-targeted therapy. Although ER is functional in ZR/BCAR4 cells, the knockdown of the receptor had no effect on the proliferation rate of BCAR4-expressing cells, showing that this mechanism of resistance is independent of ER signaling. Objective: To identify signaling pathways activated by BCAR4 expression and investigate the consequences of perturbations of the pathways. Experimental design: Reverse-phase protein microarray (RPPA) using phospho-specific antibodies was done to examine the activation status of several key signaling molecules in a cellular model for endocrine resistance of breast cancer. A panel of ZR-75-1-derived cell lines, each containing a different transgene conferring anti-estrogen resistance, was analyzed by RPPA. Results: By measuring the activity of a large number of phospho-protein isoforms in cell lysates from vector-containing control and BCAR4-expressing cells (ZR/BCAR4), it was confirmed that ERBB2 and ERBB3 were strongly phosphorylated in ZR/BCAR4 cells. This was observed in estradiol-containing medium and in medium supplemented with tamoxifen. Furthermore, many established down-stream signaling molecules of ERBB2/3 were found to be activated. Conclusions: ERBB2/ERBB3signaling is strongly activated in cells with forced expression of BCAR4 and completely independent of estrogen signaling. Both ERBB2 and ERBB3 are required for BCAR4-mediated tamoxifen resistance. Our results suggest that patients with ER-positive breast tumors expressing BCAR4 may benefit from ERBB-targeted therapies combined with tamoxifen treatment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 358. doi:10.1158/1538-7445.AM2011-358
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-358
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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    detail.hit.zdb_id: 410466-3
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  • 10
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    Abstract 5225: MicroRNA profiling in serum samples from donors with germ cell cancer
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 5225-5225
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 5225-5225
    Abstract: MicroRNAs are short non-coding RNA molecules (∼21 bases) that have been identified as important regulators of gene expression at the translational and transcriptional level. They are known to play a crucial role in cell development, differentiation, and disease. Dysregulation of miRNAs has been linked to cancer development and tumor progression. In addition, miRNAs have been identified as tumor classifiers and disease biomarkers. Recent studies have shown that miRNAs are present in body fluids (serum, saliva, semen, urine) thus providing a non-invasive tool to study and monitor disease states. Earlier research studies identified specific miRNAs as characteristic for germ cell tumors, such as testicular cancer (miR-372, miR-373). miRNA Profiling (∼760 miRNAs) was performed to identify additional miRNAs as candidate biomarkers in serum samples for testicular cancer (seminoma and non-seminoma types), from normal and cancer tissue in parallel with their matched serum samples collected from patients with testicular cancer. For this research study we used a miRNA specific bead capture system to isolate miRNAs from serum and TaqMan® Array Card platform for profiling. We will present results from this research study comparing the miRNA expression patterns in matched normal, cancer tissue, and serum. For Research Use Only. Not for use in diagnostic procedures. Citation Format: Kathy Y. Lee, Sunali Patel, Kathleen Hayashibara, Shirley Chu, Ad J. M Gillis, Martin Rijlaarsdam, Lambert C.J Dorssers, Leendert H. J Looijenga. MicroRNA profiling in serum samples from donors with germ cell 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 5225. doi:10.1158/1538-7445.AM2014-5225
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-5225
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
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