Rieken, Stefan

[["dc.bibliographiccitation.firstpage","6563"],["dc.bibliographiccitation.journal","Cancer Management and Research"],["dc.bibliographiccitation.lastpage","6569"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Bernhardt, Denise"],["dc.contributor.author","Aufderstrasse, Sophie"],["dc.contributor.author","König, Laila"],["dc.contributor.author","Adeberg, Sebastian"],["dc.contributor.author","Bozorgmehr, Farastuk"],["dc.contributor.author","Christopoulos, Petros"],["dc.contributor.author","Shafie, Rami A El"],["dc.contributor.author","Hörner-Rieber, Juliane"],["dc.contributor.author","Kappes, Jutta"],["dc.contributor.author","Thomas, Michael"],["dc.contributor.author","Herth, Felix"],["dc.contributor.author","Steins, Martin"],["dc.contributor.author","Debus, Jürgen"],["dc.contributor.author","Rieken, Stefan"],["dc.date.accessioned","2020-07-16T10:32:15Z"],["dc.date.available","2020-07-16T10:32:15Z"],["dc.date.issued","2018"],["dc.description.abstract","Systemic inflammation appears to play a role in the progression of numerous solid tumors by promoting tumor proliferation. Our current study aimed to evaluate the role of inflammatory markers in limited disease (LD) small-cell lung cancer (SCLC) patients undergoing thoracic chemoradiotherapy (TCR)."],["dc.identifier.doi","10.2147/CMAR.S180990"],["dc.identifier.pmid","30555261"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/67162"],["dc.language.iso","en"],["dc.relation.issn","1179-1322"],["dc.title","Impact of inflammatory markers on survival in patients with limited disease small-cell lung cancer undergoing chemoradiotherapy"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","782"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Thoracic Disease"],["dc.bibliographiccitation.lastpage","793"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","von Eiff, Damian"],["dc.contributor.author","Bozorgmehr, Farastuk"],["dc.contributor.author","Chung, Inn"],["dc.contributor.author","Bernhardt, Denise"],["dc.contributor.author","Rieken, Stefan"],["dc.contributor.author","Liersch, Stephan"],["dc.contributor.author","Muley, Thomas"],["dc.contributor.author","Kobinger, Sonja"],["dc.contributor.author","Thomas, Michael"],["dc.contributor.author","Christopoulos, Petros"],["dc.contributor.author","Steins, Martin"],["dc.date.accessioned","2020-07-16T10:32:04Z"],["dc.date.available","2020-07-16T10:32:04Z"],["dc.date.issued","2020-03"],["dc.description.abstract","Etoposide-/platinum-based chemotherapy is the standard first-line treatment for extensive-disease small cell lung cancer (SCLC), but responses are short-lived and subsequent options limited. Here, we present our experience with paclitaxel in advanced treatment lines."],["dc.identifier.doi","10.21037/jtd.2019.12.74"],["dc.identifier.pmid","32274145"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/67159"],["dc.language.iso","en"],["dc.relation.issn","2072-1439"],["dc.title","Paclitaxel for treatment of advanced small cell lung cancer (SCLC): a retrospective study of 185 patients"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2589"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","2598"],["dc.bibliographiccitation.volume","142"],["dc.contributor.author","Christopoulos, Petros"],["dc.contributor.author","Endris, Volker"],["dc.contributor.author","Bozorgmehr, Farastuk"],["dc.contributor.author","Elsayed, Mei"],["dc.contributor.author","Kirchner, Martina"],["dc.contributor.author","Ristau, Jonas"],["dc.contributor.author","Buchhalter, Ivo"],["dc.contributor.author","Penzel, Roland"],["dc.contributor.author","Herth, Felix J"],["dc.contributor.author","Heussel, Claus P"],["dc.contributor.author","Eichhorn, Martin"],["dc.contributor.author","Muley, Thomas"],["dc.contributor.author","Meister, Michael"],["dc.contributor.author","Fischer, Jürgen R"],["dc.contributor.author","Rieken, Stefan"],["dc.contributor.author","Warth, Arne"],["dc.contributor.author","Bischoff, Helge"],["dc.contributor.author","Schirmacher, Peter"],["dc.contributor.author","Stenzinger, Albrecht"],["dc.contributor.author","Thomas, Michael"],["dc.date.accessioned","2020-07-10T08:19:50Z"],["dc.date.available","2020-07-10T08:19:50Z"],["dc.date.issued","2018"],["dc.description.abstract","In order to identify anaplastic lymphoma kinase-driven non-small cell lung cancer (ALK+ NSCLC) patients with a worse outcome, who might require alternative therapeutic approaches, we retrospectively analyzed all stage IV cases treated at our institutions with one of the main echinoderm microtubule-associated protein-like 4 (EML4)-ALK fusion variants V1, V2 and V3 as detected by next-generation sequencing or reverse transcription-polymerase chain reaction (n = 67). Progression under tyrosine kinase inhibitor (TKI) treatment was evaluated both according to Response Evaluation Criteria in Solid Tumors (RECIST) and by the need to change systemic therapy. EML4-ALK fusion variants V1, V2 and V3 were found in 39%, 10% and 51% of cases, respectively. Patients with V3-driven tumors had more metastatic sites at diagnosis than cases with the V1 and V2 variants (mean 3.3 vs. 1.9 and 1.6, p = 0.005), which suggests increased disease aggressiveness. Furthermore, V3-positive status was associated with earlier failure after treatment with first and second-generation ALK TKI (median progression-free survival [PFS] by RECIST in the first line 7.3 vs. 39.3 months, p = 0.01), platinum-based combination chemotherapy (median PFS 5.4 vs. 15.2 months for the first line, p = 0.008) and cerebral radiotherapy (median brain PFS 6.1 months vs. not reached for cerebral radiotherapy during first-line treatment, p = 0.028), and with inferior overall survival (39.8 vs. 59.6 months in median, p = 0.017). Thus, EML4-ALK fusion variant V3 is a high-risk feature for ALK+ NSCLC. Determination of V3 status should be considered as part of the initial workup for this entity in order to select patients for more aggressive surveillance and treatment strategies."],["dc.identifier.doi","10.1002/ijc.31275"],["dc.identifier.pmid","29363116"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66979"],["dc.language.iso","en"],["dc.relation.eissn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.title","EML4-ALK fusion variant V3 is a high-risk feature conferring accelerated metastatic spread, early treatment failure and worse overall survival in ALK+ non-small cell lung cancer"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]