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  • 1
    Language: English
    In: Metallomics, 2018
    ISSN: 1756-5901
    E-ISSN: 1756-591X
    Source: CrossRef
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  • 2
    Language: English
    In: PLoS ONE, 01 January 2017, Vol.12(7), p.e0181081
    Description: The efficacy of cisplatin-based chemotherapy in cancer is limited by the occurrence of innate and acquired drug resistance. In order to better understand the mechanisms underlying acquired cisplatin resistance, we have compared the adenocarcinoma-derived non-small cell lung cancer (NSCLC) cell line A549 and its cisplatin-resistant sub-line A549rCDDP2000 with regard to cisplatin resistance mechanisms including cellular platinum accumulation, DNA-adduct formation, cell cycle alterations, apoptosis induction and activation of key players of DNA damage response. In A549rCDDP2000 cells, a cisplatin-induced G2/M cell cycle arrest was lacking and apoptosis was reduced compared to A549 cells, although equitoxic cisplatin concentrations resulted in comparable platinum-DNA adduct levels. These differences were accompanied by changes in the expression of proteins involved in DNA damage response. In A549 cells, cisplatin exposure led to a significantly higher expression of genes coding for proteins mediating G2/M arrest and apoptosis (mouse double minute 2 homolog (MDM2), xeroderma pigmentosum complementation group C (XPC), stress inducible protein (SIP) and p21) compared to resistant cells. This was underlined by significantly higher protein levels of phosphorylated Ataxia telangiectasia mutated (pAtm) and p53 in A549 cells compared to their respective untreated control. The results were compiled in a preliminary model of resistance-associated signaling alterations. In conclusion, these findings suggest that acquired resistance of NSCLC cells against cisplatin is the consequence of altered signaling leading to reduced G2/M cell cycle arrest and apoptosis.
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 3
    In: Ahmad, Aamir and Sarin, Navin and Engel, Florian and Kalayda, Ganna V. and Mannewitz, Mareike and Cinatl, Jindrich and Rothweiler, Florian and Michaelis, Martin and Saafan, Hisham and Ritter, Christoph A. and Jaehde, Ulrich and Frötschl, Roland (2017) Cisplatin resistance in non-small cell lung cancer cells is associated with an abrogation of cisplatin-induced G2/M cell cycle arrest. PLOS ONE, 12 (7). e0181081.
    Description: The efficacy of cisplatin-based chemotherapy in cancer is limited by the occurrence of innate and acquired drug resistance. In order to better understand the mechanisms underlying acquired cisplatin resistance, we have compared the adenocarcinoma-derived non-small cell lung cancer (NSCLC) cell line A549 and its cisplatin-resistant sub-line A549rCDDP2000 with regard to cisplatin resistance mechanisms including cellular platinum accumulation, DNA-adduct formation, cell cycle alterations, apoptosis induction and activation of key players of DNA damage response. In A549rCDDP2000 cells, a cisplatin-induced G2/M cell cycle arrest was lacking and apoptosis was reduced compared to A549 cells, although equitoxic cisplatin concentrations resulted in comparable platinum-DNA adduct levels. These differences were accompanied by changes in the expression of proteins involved in DNA damage response. In A549 cells, cisplatin exposure led to a significantly higher expression of genes coding for proteins mediating G2/M arrest and apoptosis (mouse double minute 2 homolog (MDM2), xeroderma pigmentosum complementation group C (XPC), stress inducible protein (SIP) and p21) compared to resistant cells. This was underlined by significantly higher protein levels of phosphorylated Ataxia telangiectasia mutated (pAtm) and p53 in A549 cells compared to their respective untreated control. The results were compiled in a preliminary model of resistance-associated signaling alterations. In conclusion, these findings suggest that acquired resistance of NSCLC cells against cisplatin is the consequence of altered signaling leading to reduced G2/M cell cycle arrest and apoptosis.
    ISSN: 1932-6203
    Source: University of Kent
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  • 4
    Language: English
    In: International journal of clinical pharmacology and therapeutics, August 2017, Vol.55(8), pp.686-689
    Keywords: Antineoplastic Agents -- Therapeutic Use ; Carcinoma, Non-Small-Cell Lung -- Drug Therapy ; Cisplatin -- Therapeutic Use
    ISSN: 0946-1965
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  • 5
    In: Sarin, Navin and Engel, Florian and Kalayda, Ganna V and Frötschl, Roland and Cinatl, Jindrich and Rothweiler, Florian and Michaelis, Martin and Fröhlich, Holger and Jaehde, Ulrich (2016) Knowledge-based approach to identify key determinants of cisplatin sensitivity . International journal of clinical pharmacology and therapeutics, .
    Keywords: RM Therapeutics. Pharmacology
    ISSN: 0946-1965
    Source: University of Kent
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  • 6
    Language: English
    In: International Journal of Molecular Sciences, 01 March 2018, Vol.19(3), p.767
    Description: The major obstacle in the clinical use of the antitumor drug cisplatin is inherent and acquired resistance. Typically, cisplatin resistance is not restricted to a single mechanism demanding for a systems pharmacology approach to understand a whole cell’s reaction to the drug. In this study, the cellular transcriptome of untreated and cisplatin-treated A549 non-small cell lung cancer cells and their cisplatin-resistant sub-line A549rCDDP2000 was screened with a whole genome array for relevant gene candidates. By combining statistical methods with available gene annotations and without a previously defined hypothesis HRas, MAPK14 (p38), CCL2, DOK1 and PTK2B were identified as genes possibly relevant for cisplatin resistance. These and related genes were further validated on transcriptome (qRT-PCR) and proteome (Western blot) level to select candidates contributing to resistance. HRas, p38, CCL2, DOK1, PTK2B and JNK3 were integrated into a model of resistance-associated signalling alterations describing differential gene and protein expression between cisplatin-sensitive and -resistant cells in reaction to cisplatin exposure.
    Keywords: Cisplatin Resistance ; Cellular Signalling ; Hras ; P38 ; Ccl2 ; Dok1 ; Ptk2b ; Jnk3 ; Biology
    E-ISSN: 1422-0067
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  • 7
    In: Sarin, Navin and Engel, Florian and Rothweiler, Florian and Cinatl, Jindrich and Michaelis, Martin and Frötschl, Roland and Fröhlich, Holger and Kalayda, Ganna V (2018) Key Players of Cisplatin Resistance: Towards a Systems Pharmacology Approach. International Journal of Molecular Sciences, 19 (3). pp. 767-785.
    Description: The major obstacle in the clinical use of the antitumor drug cisplatin is inherent and acquired resistance. Typically, cisplatin resistance is not restricted to a single mechanism demanding for a systems pharmacology approach to understand a whole cell’s reaction to the drug. In this study, the cellular transcriptome of untreated and cisplatin-treated A549 non-small cell lung cancer cells and their cisplatin-resistant sub-line A549rCDDP2000 was screened with a whole genome array for relevant gene candidates. By combining statistical methods with available gene annotations and without a previously defined hypothesis HRas, MAPK14 (p38), CCL2, DOK1 and PTK2B were identified as genes possibly relevant for cisplatin resistance. These and related genes were further validated on transcriptome (qRT-PCR) and proteome (Western blot) level to select candidates contributing to resistance. HRas, p38, CCL2, DOK1, PTK2B and JNK3 were integrated into a model of resistance-associated signalling alterations describing differential gene and protein expression between cisplatin-sensitive and -resistant cells in reaction to cisplatin exposure.
    ISSN: 1422-0067
    Source: University of Kent
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  • 8
    Language: English
    In: International journal of clinical pharmacology and therapeutics, January 2014, Vol.52(1), pp.92-4
    Keywords: Epithelial-Mesenchymal Transition ; Carcinoma, Non-Small-Cell Lung -- Drug Therapy ; Erbb Receptors -- Antagonists & Inhibitors ; Lung Neoplasms -- Drug Therapy ; Micrornas -- Physiology
    ISSN: 0946-1965
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  • 9
    Language: English
    In: International journal of clinical pharmacology and therapeutics, January 2014, Vol.52(1), pp.89-91
    Keywords: Carcinoma, Non-Small-Cell Lung -- Drug Therapy ; Erbb Receptors -- Physiology ; Lung Neoplasms -- Drug Therapy
    ISSN: 0946-1965
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  • 10
    Language: English
    In: Diagnostic Cytopathology, July 2013, Vol.41(7), pp.640-643
    Description: Hepatocellular carcinoma (HCC) with atypical cytomorphological features and presenting with bone and soft tissue metastasis is very rare. We report a 65‐year‐old male patient of HCC who presented with bone and soft tissue metastases and was clinically and radiologically suspected to have a soft tissue sarcoma. The patient presented with severe cervical pain with palpable masses in right scapular, nape of neck, and occiput area of scalp. Radiologically, these were large, bulky soft tissue masses expansile, destructive, and lytic in nature. Cytomorphologic studies revealed HCC with uncommon features of multinucleated osteoclast‐like giant cell and very prominent intracytoplasmic hyaline bodies (IHBs). Cytology, immunohistochemistry on cell block preparation, rising serum α‐fetoprotein (AFP) levels (1121.93–5000 ng/ml), and PIVKA II levels confirmed the diagnosis. The patient has been on follow‐up on sorafinib for 2 months and is doing well. This case emphasizes the need for systematic approach in cases of HCC with atypical clinical presentation and unusual cytomorphology. Diagn. Cytopathol. 2013. © 2011 Wiley Periodicals, Inc.
    Keywords: Hepatocellular Carcinoma ; Intracytoplasmic Hyline Bodies ; Osteoclastic Giant Cells ; Bone And Soft Tissue Metastases
    ISSN: 8755-1039
    E-ISSN: 1097-0339
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