Aung, Thiha

[["dc.bibliographiccitation.firstpage","395"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Clinical Cancer Research"],["dc.bibliographiccitation.lastpage","404"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Koch, Raphael"],["dc.contributor.author","Aung, Thiha"],["dc.contributor.author","Vogel, Daniel"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Wenzel, Dirk"],["dc.contributor.author","Becker, Sabrina"],["dc.contributor.author","Sinzig, Ursula"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","von Mach, Tobias"],["dc.contributor.author","Jacob, Ralf"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T10:19:22Z"],["dc.date.available","2018-11-07T10:19:22Z"],["dc.date.issued","2016"],["dc.description.abstract","Purpose: Although R-CHOP-based immunochemotherapy cures significant proportions of patients with aggressive B-cell lymphoma, tumor cell susceptibility to chemotherapy varies, with mostly fatal outcome in cases of resistant disease. We and others have shown before that export of cytostatic drugs contributes to drug resistance. Now we provide a novel approach to overcome exosome-mediated drug resistance in aggressive B-cell lymphomas. Experimental Design: We used well-established centrifugation protocols to purify exosomes from DLBCL cell lines and detected anthracyclines using FACS and HPLC. We used shRNA knockdown of ABCA3 to determine ABCA3 dependence of chemotherapy susceptibility and monitored ABCA3 expression after indomethacin treatment using qPCR. Finally, we established an in vivo assay using a chorioallantoic membrane (CAM) assay to determine the synergy of anthracycline and indomethacin treatment. Results: We show increased efficacy of the anthracycline doxorubicin and the anthracenedione pixantrone by suppression of exosomal drug resistance with indomethacin. B-cell lymphoma cells in vitro efficiently extruded doxorubicin and pixantrone, in part compacted in exosomes. Exosomal biogenesis was critically dependent on the expression of the ATP-transporter A3 (ABCA3). Genetic or chemical depletion of ABCA3 augmented intracellular retention of both drugs and shifted the subcellular drug accumulation to prolonged nuclear retention. Indomethacin increased the cytostatic efficacy of both drugs against DLBCL cell lines in vitro and in vivo in a CAM assay. Conclusions: We propose pretreatment with indomethacin toward enhanced antitumor efficacy of anthracyclines and anthracenediones. (C) 2015 AACR."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft; University Medicine Goettingen"],["dc.identifier.doi","10.1158/1078-0432.CCR-15-0577"],["dc.identifier.isi","000369076500016"],["dc.identifier.pmid","26369630"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41643"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1557-3265"],["dc.relation.issn","1078-0432"],["dc.title","Nuclear Trapping through Inhibition of Exosomal Export by Indomethacin Increases Cytostatic Efficacy of Doxorubicin and Pixantrone"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["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.journal","Onkologie"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Diering, Nina"],["dc.contributor.author","Aung, T."],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Koch, R."],["dc.contributor.author","Becker, S."],["dc.contributor.author","Krause, D."],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T08:38:49Z"],["dc.date.available","2018-11-07T08:38:49Z"],["dc.date.issued","2010"],["dc.format.extent","188"],["dc.identifier.isi","000282988401085"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18846"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","Putative tumor stem cells of SP phenotype in aggressive B-cell lymphoma"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Investigative Dermatology"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Kotzerke, Kristina"],["dc.contributor.author","Aung, T."],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Mempel, Martin"],["dc.contributor.author","Braun, Alexander"],["dc.date.accessioned","2018-11-07T09:06:56Z"],["dc.date.available","2018-11-07T09:06:56Z"],["dc.date.issued","2012"],["dc.format.extent","S1"],["dc.identifier.isi","000307814000007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25670"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","New york"],["dc.relation.conference","42nd Annual Meeting of the European-Society-for-Dermatological-Research (ESDR)"],["dc.relation.eventlocation","Venice, ITALY"],["dc.relation.issn","0022-202X"],["dc.title","Immunostimulatory effects of exosomes from keratinocytes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","650"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Experimental Dermatology"],["dc.bibliographiccitation.lastpage","655"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Kotzerke, Kristina"],["dc.contributor.author","Mempel, Martin"],["dc.contributor.author","Aung, Thiha"],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Wenzel, Dirk"],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Braun, Andrea"],["dc.date.accessioned","2018-11-07T09:19:28Z"],["dc.date.available","2018-11-07T09:19:28Z"],["dc.date.issued","2013"],["dc.description.abstract","It has long been known that keratinocytes influence cutaneous immunity through secretion of soluble factors. Exosomes, small membrane vesicles of endocytotic origin, have been implicated in intercellular communication processes such as the transfer of tumor cell antigens and the activation of recipient dendritic cells (DC). However, little is known about immunomodulatory functions of keratinocyte-derived exosomes. To address this question, we analysed exosome secretion of the murine keratinocyte cell line MPEK under steady state as well as inflammatory conditions (+/- IFN). These exosomes were readily taken up by bone marrow-derived DC (BMDC) in vitro resulting in a matured phenotype, as evidenced by increased CD40 expression as well as by the production of large amounts of IL-6, IL-10 and IL-12. When the transfer of antigen-specific information through exosomes was investigated, it was found that keratinocytes took up antigen (ovalbumin) and transferred it to their exosomes. However, these antigen-harbouring exosomes failed to induce antigen-specific T cell responses via BMDC. Together, this novel biological function suggests that keratinocytes are able to direct unspecific immune processes but do not elicit specific immune responses."],["dc.identifier.doi","10.1111/exd.12230"],["dc.identifier.isi","000325008600005"],["dc.identifier.pmid","24079734"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28641"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0906-6705"],["dc.title","Immunostimulatory activity of murine keratinocyte-derived exosomes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0200343"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Blesinger, Hannah"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Aung, Thiha"],["dc.contributor.author","Schwoch, Sonja"],["dc.contributor.author","Prantl, Lukas"],["dc.contributor.author","Rößler, Jochen"],["dc.contributor.author","Wilting, Jörg"],["dc.contributor.author","Becker, Jürgen"],["dc.date.accessioned","2019-07-09T11:45:49Z"],["dc.date.available","2019-07-09T11:45:49Z"],["dc.date.issued","2018"],["dc.description.abstract","Lymphatic malformations (LM) are characterized by the overgrowth of lymphatic vessels during pre- and postnatal development. Macrocystic, microcystic and combined forms of LM are known. The cysts are lined by lymphatic endothelial cells (LECs). Resection and sclerotherapy are the most common treatment methods. Recent studies performed on LM specimens in the United States of America have identified activating mutations in the phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) gene in LM. However, whole tissue but not isolated cell types were studied. Here, we studied LM tissues resected at the University Hospitals Freiburg and Regensburg, Germany. We isolated LECs and fibroblasts separately, and sequenced the commonly affected exons 8, 10, and 21 of the PIK3CA gene. We confirm typical monoallelic mutations in 4 out of 6 LM-derived LEC lines, and describe two new mutations i.) in exon 10 (c.1636C>A; p.Gln546Lys), and ii.) a 3bp in-frame deletion of GAA (Glu109del). LM-derived fibroblasts did not possess such mutations, showing cell-type specificity of the gene defect. High activity of the PIK3CA-AKT- mTOR pathway was demonstrated by hyperphosphorylation of AKT-Ser473 in all LM-derived LECs (including the ones with newly identified mutations), as compared to normal LECs. Additionally, hyperphosphorylation of ERK was seen in all LM-derived LECs, except for the one with Glu109del. In vitro, the small molecule kinase inhibitors Buparlisib/BKM-120, Wortmannin, and Ly294002, (all inhibitors of PIK3CA), CAL-101 (inhibitor of PIK3CD), MK-2206 (AKT inhibitor), Sorafenib (multiple kinases inhibitor), and rapamycin (mTOR inhibitor) significantly blocked proliferation of LM-derived LECs in a concentration-dependent manner, but also blocked proliferation of normal LECs. However, MK-2206 appeared to be more specific for mutated LECs, except in case of Glu109 deletion. In sum, children that are, or will be, treated with kinase inhibitors must be monitored closely."],["dc.identifier.doi","10.1371/journal.pone.0200343"],["dc.identifier.pmid","29985963"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15320"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59313"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","PIK3CA mutations are specifically localized to lymphatic endothelial cells of lymphatic malformations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","35"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Lymphatic Research and Biology"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Felmerer, Gunther"],["dc.contributor.author","Dowlatshahi, A. S."],["dc.contributor.author","Stark, G. Bjoern"],["dc.contributor.author","Foeldi, Ethelka"],["dc.contributor.author","Foeldi, Martha"],["dc.contributor.author","Ahls, Maria G."],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Aung, Thiha"],["dc.date.accessioned","2018-11-07T10:17:37Z"],["dc.date.available","2018-11-07T10:17:37Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Stewart-Treves syndrome is a rare complication of breast cancer treatment, representing a lymphangiosarcoma commonly associated with lymphedema and severely impacting patient's outcome. The tumor typically develops in the atrophic, pachydermatous, hyperkeratotic skin of limbs affected by long-standing lymphedema. Clinical data associated with Stewart-Treves syndrome and lymphedema management have rarely been published. Methods and Results: In the period between 1980 and 2009, ten patients with Stewart-Treves syndrome were diagnosed and treated at the Foeldiklinik, Hinterzarten, Germany. Nine of the ten patients were female. Five patients had previously suffered from breast cancer (and were treated with mastectomy); two from other malignancies; two patients had primary lymphedema, and one had undergone lower extremity lymphadenectomy. All cancer patients had undergone radiation treatment. In all cases, the sarcoma developed in non-irradiated areas 6-48 years (average 16.3 years) after the onset of lymphedema. None of the patients had received complex decongestive physical therapy (CDT). Two patients had above-elbow amputation, one had shoulder exarticulation, two patients had wide excision and skin grafting, two patients had above-knee amputation procedure, two patients had a below-knee amputation procedure, and one patient had no surgical treatment at all. The time to recurrence after surgery, time to metastasis, patient survival and CDT were recorded. Conclusions: Patients with lymphedema should be closely examined starting 5 years from the time of lymphedema onset, paying special attention to those with associated malignancies. Only early diagnosis and treatment by radical ablative surgery confers a reasonable prognosis with this rare but aggressive disease. A potential effect of CDT on lymphangiosarcoma has to be studied in a greater patient cohort."],["dc.identifier.doi","10.1089/lrb.2015.0006"],["dc.identifier.isi","000372184300007"],["dc.identifier.pmid","26584023"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41264"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mary Ann Liebert, Inc"],["dc.relation.issn","1557-8585"],["dc.relation.issn","1539-6851"],["dc.title","Lymphangiosarcoma: Is Stewart-Treves Syndrome a Preventable Condition?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Aung, T."],["dc.contributor.author","Kiecke, Christina"],["dc.contributor.author","Kueffer, Stefan"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T09:19:02Z"],["dc.date.available","2018-11-07T09:19:02Z"],["dc.date.issued","2013"],["dc.format.extent","20"],["dc.identifier.isi","000326360900043"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28544"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","1423-0240"],["dc.relation.issn","0378-584X"],["dc.title","The biological relevance of the Amyloid Precursor Protein (APP) in prostate cancer"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","204"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","British Journal of Haematology"],["dc.bibliographiccitation.lastpage","213"],["dc.bibliographiccitation.volume","161"],["dc.contributor.author","Hupfeld, Timo"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Schrader, Verena"],["dc.contributor.author","Beutler, Markus"],["dc.contributor.author","Veltkamp, Christian"],["dc.contributor.author","Koch, Raphael"],["dc.contributor.author","Cameron, Silke"],["dc.contributor.author","Aung, Thiha"],["dc.contributor.author","Haase, Detlef"],["dc.contributor.author","LaRosee, Paul"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T09:26:30Z"],["dc.date.available","2018-11-07T09:26:30Z"],["dc.date.issued","2013"],["dc.description.abstract","Although BCR-ABL1 tyrosine kinase inhibitors reliably induce disease remission for patients with chronic myeloid leukaemia (CML), unlimited extension of therapy is necessary to prevent relapse from persistent leukaemic cells. Here, we analysed model cell lines and primary CML cells for the expression and functions of the ABC transporter A3 (ABCA3) as well as the embryonic stem cell-associated transcription factor SALL4. ABCA3 protected leukaemic cells from the cytotoxic effects of the tyrosine kinase inhibitors imatinib, dasatinib, and nilotinib. In the surviving cells, exposure to tyrosine kinase inhibitors significantly enhanced ABCA3 expression in vivo and in vitro, and was associated with increased expression of SALL4, which binds the ABCA3 promoter. Inhibition of ABCA3 or SALL4 by genetic silencing or indomethacin, but not interferon gamma, interrupted SALL4-dependent regulation of ABCA3 and restored susceptibility of leukaemic cells to tyrosine kinase inhibition. Tyrosine kinase inhibitor exposure facilitates a protective loop of SALL4 and ABCA3 cooperation in persistent leukaemic cells."],["dc.identifier.doi","10.1111/bjh.12246"],["dc.identifier.isi","000317124200008"],["dc.identifier.pmid","23432194"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30318"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0007-1048"],["dc.title","Tyrosinekinase inhibition facilitates cooperation of transcription factor SALL4 and ABC transporter A3 towards intrinsic CML cell drug resistance"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","453"],["dc.bibliographiccitation.issue","3-4"],["dc.bibliographiccitation.journal","Clinical Hemorheology and Microcirculation"],["dc.bibliographiccitation.lastpage","457"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Kauffmann, P."],["dc.contributor.author","Troeltzsch, M."],["dc.contributor.author","Cordesmeyer, R."],["dc.contributor.author","Heidekrueger, P.I."],["dc.contributor.author","Schliephake, H."],["dc.contributor.author","Canis, M."],["dc.contributor.author","Wolff, H.A."],["dc.contributor.author","Rave-Fraenk, M."],["dc.contributor.author","Stroebel, P."],["dc.contributor.author","Kehrer, A."],["dc.contributor.author","Prantl, L."],["dc.contributor.author","Aung, T."],["dc.contributor.editor","Jünger, M."],["dc.contributor.editor","Krüger-Genge, A."],["dc.contributor.editor","Jung, F."],["dc.date.accessioned","2020-12-10T18:44:09Z"],["dc.date.available","2020-12-10T18:44:09Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.3233/CH-179226"],["dc.identifier.eissn","1875-8622"],["dc.identifier.issn","1386-0291"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78345"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Presentation of a variation of the chorioallantoic membrane set up as a potential model for individual therapy for squamous cell carcinoma of the oropharynx"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]