001     154244
005     20240229120023.0
024 7 _ |a 10.1155/2019/2902985
|2 doi
024 7 _ |a pmid:31929796
|2 pmid
024 7 _ |a pmc:PMC6942867
|2 pmc
024 7 _ |a 1687-8450
|2 ISSN
024 7 _ |a 1687-8469
|2 ISSN
024 7 _ |a altmetric:74047354
|2 altmetric
037 _ _ |a DKFZ-2020-00680
041 _ _ |a eng
082 _ _ |a 610
100 1 _ |a Borchert, Sabrina
|0 0000-0002-0447-3206
|b 0
245 _ _ |a Screening of Pleural Mesothelioma Cell Lines for Kinase Activity May Identify New Mechanisms of Therapy Resistance in Patients Receiving Platin-Based Chemotherapy.
260 _ _ |a New York, NY
|c 2019
|b Hindawi Publ. Corp.
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1585306247_8314
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Malignant pleural mesothelioma (MPM) is a rare, predominantly asbestos-related and biologically highly aggressive tumor associated with a dismal prognosis. Multimodal therapy consisting of platinum-based chemotherapy is the treatment of choice. The reasons underlying the rather poor efficacy of platinum compounds remain largely unknown. Kinase activity might influence cellular response to these regimens.For this exploratory study, we screened MPM cell lines (NCI-H2452, NCI-H2052, and MSTO-211H) differing in response to cisplatin and benign control fibroblasts (MRC-5) for overall phosphorylation patterns as well as kinase activity with respect to cellular response to cisplatin-based therapeutics. We analysed the cell lines for cellular kinases in a high-throughput manner using the highly innovative technique PamGene. Cell state analysis including apoptosis, necrosis, and cell viability was performed by using enzyme activity and fluorescent-based assays.Cisplatin alters cellular phosphorylation patterns affecting cell cycle, migration, adhesion, signal transduction, immune modulation, and apoptosis. In cisplatin-responsive cell lines, phosphorylation of AKT1 and GSK3B was decreased but could not be influenced in cisplatin-resistant NCI-H2452 cells. Cisplatin-responsive cell lines showed increased phosphorylation levels of JNK1/2/3 but decreased phosphorylation in cisplatin-resistant NCI-H2452 cells.Kinase phosphorylation and activity might play a crucial role in cellular response to cytostatic agents. Cisplatin influences phosphorylation patterns with distinct features in cisplatin-resistant cells. These alterations exert a significant impact on cell cycle, migration, adhesion, signal transduction, immune modulation, and apoptosis of the respective tumor cells. Based on our results, the induction of p38 or JNK1/3, or inhibition of AKT1 by, for example, BIA-6, might offer a positive synergistic effect by induction of an apoptotic response to cisplatin-based treatment, thus potentially enhancing the clinical outcome of MPM patients.
536 _ _ |a 899 - ohne Topic (POF3-899)
|0 G:(DE-HGF)POF3-899
|c POF3-899
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
700 1 _ |a Suckrau, Pia-Maria
|b 1
700 1 _ |a Wessolly, Michael
|0 0000-0002-4399-8646
|b 2
700 1 _ |a Mairinger, Elena
|0 P:(DE-HGF)0
|b 3
700 1 _ |a Hegedus, Balazs
|b 4
700 1 _ |a Hager, Thomas
|0 P:(DE-HGF)0
|b 5
700 1 _ |a Herold, Thomas
|0 P:(DE-He78)0ecb73a869d20caca507c5781ffc8b11
|b 6
700 1 _ |a Eberhardt, Wildfried E E
|b 7
700 1 _ |a Wohlschlaeger, Jeremias
|b 8
700 1 _ |a Aigner, Clemens
|b 9
700 1 _ |a Bankfalvi, Agnes
|0 P:(DE-HGF)0
|b 10
700 1 _ |a Schmid, Kurt Werner
|0 P:(DE-HGF)0
|b 11
700 1 _ |a Walter, Robert F H
|b 12
700 1 _ |a Mairinger, Fabian D
|0 0000-0003-1067-0051
|b 13
773 _ _ |a 10.1155/2019/2902985
|g Vol. 2019, p. 1 - 11
|0 PERI:(DE-600)2461349-6
|p 2902985
|t Journal of oncology
|v 2019
|y 2019
|x 1687-8469
909 C O |o oai:inrepo02.dkfz.de:154244
|p VDB
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 0
|6 0000-0002-0447-3206
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 2
|6 0000-0002-4399-8646
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 3
|6 P:(DE-HGF)0
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 5
|6 P:(DE-HGF)0
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 6
|6 P:(DE-He78)0ecb73a869d20caca507c5781ffc8b11
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 10
|6 P:(DE-HGF)0
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 11
|6 P:(DE-HGF)0
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 13
|6 0000-0003-1067-0051
913 1 _ |a DE-HGF
|b Programmungebundene Forschung
|l ohne Programm
|1 G:(DE-HGF)POF3-890
|0 G:(DE-HGF)POF3-899
|2 G:(DE-HGF)POF3-800
|v ohne Topic
|x 0
|4 G:(DE-HGF)POF
|3 G:(DE-HGF)POF3
914 1 _ |y 2019
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b J ONCOL : 2017
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0310
|2 StatID
|b NCBI Molecular Biology Database
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0320
|2 StatID
|b PubMed Central
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0501
|2 StatID
|b DOAJ Seal
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0500
|2 StatID
|b DOAJ
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b DOAJ : Blind peer review
915 _ _ |a Creative Commons Attribution CC BY (No Version)
|0 LIC:(DE-HGF)CCBYNV
|2 V:(DE-HGF)
|b DOAJ
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
915 _ _ |a WoS
|0 StatID:(DE-HGF)0111
|2 StatID
|b Science Citation Index Expanded
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1110
|2 StatID
|b Current Contents - Clinical Medicine
915 _ _ |a IF < 5
|0 StatID:(DE-HGF)9900
|2 StatID
920 1 _ |0 I:(DE-He78)L401-20160331
|k L401
|l DKTK Essen
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a I:(DE-He78)L401-20160331
980 _ _ |a UNRESTRICTED


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21