Chapuy, Björn

[["dc.bibliographiccitation.firstpage","362"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Oncology"],["dc.bibliographiccitation.lastpage","370"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Overbeck, Tobias R."],["dc.contributor.author","Hupfeld, Timo"],["dc.contributor.author","Krause, Doris"],["dc.contributor.author","Waldmann-Beushausen, Regina"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Guedenzoph, Bjoern"],["dc.contributor.author","Aung, Thiha"],["dc.contributor.author","Inagaki, Nobuya"],["dc.contributor.author","Schoendube, Friedrich Albert"],["dc.contributor.author","Danner, Bernhard Christoph"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T09:29:56Z"],["dc.date.available","2018-11-07T09:29:56Z"],["dc.date.issued","2013"],["dc.description.abstract","Patients with advanced-stage bronchial cancer benefit from systemic cytostatic therapy, in particular from regimens integrating cisplatin and taxanes. However, eventual disease progression leads to a fatal outcome in most cases, originating from tumor cells resisting chemotherapy. We here show that the intracellular ATP-binding cassette transporter A3 (ABCA3), previously recognized as critical for the secretion of surfactant components from type 2 pneumocytes, is expressed in non-small-cell lung cancer (NSCLC) cells. With some heterogeneity in a given specimen, expression levels detected immunohistochemically in primary cancer tissue were highest in adenocarcinomas and lowest in small cell lung cancers. Genetic silencing of ABCA3 in the NSCLC cell line models A549, NCI-H1650 and NCI-H1975 significantly increased tumor cell susceptibility to the cytostatic effects of both cisplatin (in all cell lines) and paclitaxel (in two of three cell lines). Taken together, ABCA3 emerges as a modulator of NSCLC cell susceptibility to cytostatic therapy. Copyright (c) 2013 S. Karger AG, Basel"],["dc.description.sponsorship","Faculty of Medicine, Georg August University Gottingen, Germany"],["dc.identifier.doi","10.1159/000348884"],["dc.identifier.isi","000320219100007"],["dc.identifier.pmid","23689165"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10826"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31175"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0030-2414"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Intracellular ATP-Binding Cassette Transporter A3 is Expressed in Lung Cancer Cells and Modulates Susceptibility to Cisplatin and Paclitaxel"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1576"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Leukemia"],["dc.bibliographiccitation.lastpage","1586"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Koch, R."],["dc.contributor.author","Radunski, Ulf"],["dc.contributor.author","Corsham, Sabrina"],["dc.contributor.author","Cheong, Naeun"],["dc.contributor.author","Inagaki, Nobuya"],["dc.contributor.author","Ban, N."],["dc.contributor.author","Wenzel, D."],["dc.contributor.author","Reinhardt, D."],["dc.contributor.author","Zapf, Antonia"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Kosari, F."],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T11:12:37Z"],["dc.date.available","2018-11-07T11:12:37Z"],["dc.date.issued","2008"],["dc.description.abstract","Multidrug resistance (MDR) seriously limits the efficacy of chemotherapy in patients with cancer and leukemia. Active transport across membranes is essential for such cellular drug resistance, largely provided by ATP-binding cassette (ABC) transport proteins. Intracellular drug sequestration contributes to MDR; however, a genuine intracellular ABC transport protein with MDR function has not yet been identified. Analyzing the intrinsic drug efflux capacity of leukemic stem cells, we found the ABC transporter A3 (ABCA3) to be expressed consistently in acute myeloid leukemia (AML) samples. Greater expression of ABCA3 is associated with unfavorable treatment outcome, and in vitro, elevated expression induces resistance toward a broad spectrum of cytostatic agents. ABCA3 remains localized within the limiting membranes of lysosomes and multivesicular bodies, in which cytostatics are efficiently sequestered. In addition to AML, we also detected ABCA3 in a panel of lymphohematopoietic tissues and transformed cell lines. In conclusion, we identified subcellular drug sequestration mediated by the genuinely intracellular ABCA3 as being a clinically relevant mechanism of intrinsic MDR."],["dc.identifier.doi","10.1038/leu.2008.103"],["dc.identifier.isi","000258413400013"],["dc.identifier.pmid","18463677"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6063"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53706"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0887-6924"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Intracellular ABC transporter A3 confers multidrug resistance in leukemia cells by lysosomal drug sequestration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","181"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","eJHaem"],["dc.bibliographiccitation.lastpage","187"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Høhloch, Karin"],["dc.contributor.author","Ziepert, Marita"],["dc.contributor.author","Trümper, Lorenz"],["dc.contributor.author","Buske, Christian"],["dc.contributor.author","Held, Gerhard"],["dc.contributor.author","Poeschel, Viola"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Altmann, Bettina"],["dc.date.accessioned","2020-12-11T11:48:55Z"],["dc.date.accessioned","2021-10-27T13:22:25Z"],["dc.date.available","2020-12-11T11:48:55Z"],["dc.date.available","2021-10-27T13:22:25Z"],["dc.date.issued","2020"],["dc.description.abstract","Serum albumin a well‐known risk factor predicting outcome in many solid tumors. We explore the role of low serum albumin (≤3.5 g/dL) as an independent risk factor in elderly patients with aggressive B‐cell lymphoma. Outcome of 429 patients treated with R‐CHOP‐14 in the RICOVER‐60 trial and available serum albumin were analyzed in this retrospective study. Of the 429 patients in the RICOVER‐60 trial, 137 (32%) had low and 292 (68%) had normal serum albumin levels (>3.5 g/dL). In the low albumin group, patients had significantly higher International Prognostic Index (IPI), bulky disease, extralymphatic involvement, and B‐symptoms. Event‐free survival (EFS) (P < .001), progression‐free survival (PFS) (P < .001), and overall survival (OS) (P < .001) were significantly inferior for patients with low compared to those with normal serum albumin. Multivariate analysis adjusted for IPI shows following Hazard ratios (HR) for low serum albumin: EFS (HR = 1.5; 95% confidance interval [CI] [1.1; 2.1], P = .009), PFS (HR = 1.7; 95% CI [1.2; 2.4], P = .001) and OS (HR = 1.6; 95% CI [1.1; 2.3], P = .006). Results were confirmed in 185 patients from the DENSE‐R‐CHOP‐14 and SMARTE‐R‐CHOP‐14 trials. In conclusion, low serum albumin is an independent risk factor in elderly patients with aggressive B‐cell lymphoma treated with R‐CHOP."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2020"],["dc.identifier.doi","10.1002/jha2.61"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17695"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92093"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","2688-6146"],["dc.relation.issn","2688-6146"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Low serum albumin is an independent risk factor in elderly patients with aggressive B‐cell lymphoma: Results from prospective trials of the German High‐Grade Non‐Hodgkin's Lymphoma Study Group"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","580"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Białopiotrowicz, Emilia"],["dc.contributor.author","Noyszewska-Kania, Monika"],["dc.contributor.author","Kachamakova-Trojanowska, Neli"],["dc.contributor.author","Łoboda, Agnieszka"],["dc.contributor.author","Cybulska, Magdalena"],["dc.contributor.author","Grochowska, Aleksandra"],["dc.contributor.author","Kopczyński, Michał"],["dc.contributor.author","Mikula, Michał"],["dc.contributor.author","Prochorec-Sobieszek, Monika"],["dc.contributor.author","Firczuk, Małgorzata"],["dc.contributor.author","Graczyk-Jarzynka, Agnieszka"],["dc.contributor.author","Zagożdżon, Radosław"],["dc.contributor.author","Ząbek, Adam"],["dc.contributor.author","Młynarz, Piotr"],["dc.contributor.author","Dulak, Józef"],["dc.contributor.author","Górniak, Patryk"],["dc.contributor.author","Szydłowski, Maciej"],["dc.contributor.author","Pyziak, Karolina"],["dc.contributor.author","Martyka, Justyna"],["dc.contributor.author","Sroka-Porada, Agnieszka"],["dc.contributor.author","Jabłońska, Ewa"],["dc.contributor.author","Polak, Anna"],["dc.contributor.author","Kowalczyk, Piotr"],["dc.contributor.author","Szumera-Ciećkiewicz, Anna"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Rzymski, Tomasz"],["dc.contributor.author","Brzózka, Krzysztof"],["dc.contributor.author","Juszczyński, Przemysław"],["dc.date.accessioned","2021-04-14T08:26:59Z"],["dc.date.available","2021-04-14T08:26:59Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3390/cancers12030580"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82131"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","MDPI"],["dc.relation.eissn","2072-6694"],["dc.relation.orgunit","Klinik für Hämatologie und Medizinische Onkologie"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Serine Biosynthesis Pathway Supports MYC–miR-494–EZH2 Feed-Forward Circuit Necessary to Maintain Metabolic and Epigenetic Reprogramming of Burkitt Lymphoma Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1528"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","HAEMATOLOGICA-THE HEMATOLOGY JOURNAL"],["dc.bibliographiccitation.lastpage","1536"],["dc.bibliographiccitation.volume","94"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Panse, Melanie"],["dc.contributor.author","Radunski, Ulf"],["dc.contributor.author","Koch, Raphael"],["dc.contributor.author","Wenzel, Dirk"],["dc.contributor.author","lnagaki, Nobuya"],["dc.contributor.author","Haase, Detlef"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T11:22:41Z"],["dc.date.available","2018-11-07T11:22:41Z"],["dc.date.issued","2009"],["dc.description.abstract","Background Inhibition of BCR-ABL tyrosine kinase activity has evolved as a mainstay of therapy for patients with chronic myeloid leukemia. However, a fraction of leukemic cells persists under targeted therapy and can lead to disease progression on cessation of treatment. Design and Methods We analyzed bone marrow progenitor cells with the side population phenotype, and characterized the role of the intracellular ABC transporter A3 in imatinib detoxification. Results BCR-ABL-positive leukemic cells contribute to the side population cell compartment in untreated patients. Such leukemic side population cells, as well as CD34-positive progenitors from chronic myeloid leukemia samples, strongly express the intracellular ABCA3. Functionally, ABCA3 levels are critical for the susceptibility of chronic myeloid leukemia blast cell lines to specific BCR-A-BL inhibition by imatinib. The transporter is localized in the limiting membrane of lysosomes and multivesicular bodies, and intracellular [(14)C]-labeled imatinib accumulates in such organelles. The lysosomal storage capacity increases with ABCA3 expression, thus regulating imatinib sequestration. Conclusions The intracellular ABC transporter A3 is expressed in chronic myeloid leukemia progenitor cells and may contribute to intrinsic imatinib resistance by facilitating lysosomal sequestration in chronic myeloid leukemia cells."],["dc.identifier.doi","10.3324/haematol.2009.008631"],["dc.identifier.isi","000272165800009"],["dc.identifier.pmid","19880777"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5958"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56030"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0390-6078"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","ABC transporter A3 facilitates lysosomal sequestration of imatinib and modulates susceptibility of chronic myeloid leukemia cell lines to this drug"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Li, Amy"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Varelas, Xaralabos"],["dc.contributor.author","Sebastiani, Paola"],["dc.contributor.author","Monti, Stefano"],["dc.date.accessioned","2020-12-10T18:11:08Z"],["dc.date.available","2020-12-10T18:11:08Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1038/s41598-019-52886-z"],["dc.identifier.eissn","2045-2322"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16923"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73905"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.relation.orgunit","Klinik für Hämatologie und Medizinische Onkologie"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Identification of candidate cancer drivers by integrative Epi-DNA and Gene Expression (iEDGE) data analysis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","509"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","511"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Chapuy, Bjoern"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Huenlich, Mark"],["dc.date.accessioned","2017-09-07T11:46:53Z"],["dc.date.available","2017-09-07T11:46:53Z"],["dc.date.issued","2009"],["dc.identifier.doi","10.1007/s00392-009-0034-0"],["dc.identifier.gro","3143081"],["dc.identifier.isi","000268511200006"],["dc.identifier.pmid","19499163"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5027"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/555"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","1861-0684"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A rare cause of sudden cardiac arrest: primary cardiac lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1655"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Biomedicines"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Thobe, Kirsten"],["dc.contributor.author","Konrath, Fabian"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Wolf, Jana"],["dc.contributor.editor","Baud, Veronique"],["dc.date.accessioned","2022-01-11T14:07:50Z"],["dc.date.available","2022-01-11T14:07:50Z"],["dc.date.issued","2021"],["dc.description.abstract","Personalized medicine aims to tailor treatment to patients based on their individual genetic or molecular background. Especially in diseases with a large molecular heterogeneity, such as diffuse large B-cell lymphoma (DLBCL), personalized medicine has the potential to improve outcome and/or to reduce resistance towards treatment. However, integration of patient-specific information into a computational model is challenging and has not been achieved for DLBCL. Here, we developed a computational model describing signaling pathways and expression of critical germinal center markers. The model integrates the regulatory mechanism of the signaling and gene expression network and covers more than 50 components, many carrying genetic lesions common in DLBCL. Using clinical and genomic data of 164 primary DLBCL patients, we implemented mutations, structural variants and copy number alterations as perturbations in the model using the CoLoMoTo notebook. Leveraging patient-specific genotypes and simulation of the expression of marker genes in specific germinal center conditions allows us to predict the consequence of the modeled pathways for each patient. Finally, besides modeling how genetic perturbations alter physiological signaling, we also predicted for each patient model the effect of rational inhibitors, such as Ibrutinib, that are currently discussed as possible DLBCL treatments, showing patient-dependent variations in effectiveness and synergies."],["dc.description.abstract","Personalized medicine aims to tailor treatment to patients based on their individual genetic or molecular background. Especially in diseases with a large molecular heterogeneity, such as diffuse large B-cell lymphoma (DLBCL), personalized medicine has the potential to improve outcome and/or to reduce resistance towards treatment. However, integration of patient-specific information into a computational model is challenging and has not been achieved for DLBCL. Here, we developed a computational model describing signaling pathways and expression of critical germinal center markers. The model integrates the regulatory mechanism of the signaling and gene expression network and covers more than 50 components, many carrying genetic lesions common in DLBCL. Using clinical and genomic data of 164 primary DLBCL patients, we implemented mutations, structural variants and copy number alterations as perturbations in the model using the CoLoMoTo notebook. Leveraging patient-specific genotypes and simulation of the expression of marker genes in specific germinal center conditions allows us to predict the consequence of the modeled pathways for each patient. Finally, besides modeling how genetic perturbations alter physiological signaling, we also predicted for each patient model the effect of rational inhibitors, such as Ibrutinib, that are currently discussed as possible DLBCL treatments, showing patient-dependent variations in effectiveness and synergies."],["dc.identifier.doi","10.3390/biomedicines9111655"],["dc.identifier.pii","biomedicines9111655"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97875"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.publisher","MDPI"],["dc.relation.eissn","2227-9059"],["dc.rights","Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)."],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Patient-Specific Modeling of Diffuse Large B-Cell Lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]