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König, Alexander Otto
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König, Alexander Otto
Official Name
König, Alexander Otto
Alternative Name
König, Alexander O.
König, A. O.
König, Alexander
König, A.
Koenig, Alexander Otto
Koenig, Alexander O.
Koenig, A. O.
Koenig, Alexander
Koenig, A.
Main Affiliation
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2022Journal Article [["dc.bibliographiccitation.journal","Langenbeck's Archives of Surgery"],["dc.contributor.author","Azizian, Azadeh"],["dc.contributor.author","König, Alexander"],["dc.contributor.author","Ghadimi, Michael"],["dc.date.accessioned","2022-09-01T09:51:31Z"],["dc.date.available","2022-09-01T09:51:31Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract\n \n Purpose\n VIPoma belongs to the group of neuroendocrine neoplasms. These tumours are located mostly in the pancreas and produce high levels of vasoactive intestinal peptide (VIP). In most cases, a metastatic state has already been reached at the initial diagnosis, with high levels of VIP leading to a wide spectrum of presenting symptoms. These symptoms include intense diarrhoea and subsequent hypopotassaemia but also cardiac complications, with life-threatening consequences. Treatment options include symptomatic therapy, systemic chemotherapy and targeted therapy, as well as radiation and surgery. Due to the low incidence of VIPoma, there are no prospective studies or evidence-based therapeutic standards to date.\n \n \n Methods\n To evaluate the possible impact of different therapy strategies, we performed literature research using PubMed.\n \n \n Results\n All possible treatment modalities for VIPoma have at least one of two therapy goals: antisecretory effects (symptom control) and antitumoural effects (tumour burden reduction). Symptomatic therapy is the most important in the emergency setting to rehydrate, balance electrolytes and stabilise the patient. Symptomatic therapy is also of great importance perioperatively. Somatostatin analogues play a major role in symptom control, although their efficiency is often limited. Chemotherapy may be effective in reaching stable disease for a certain time period, although its impact on symptom control is limited and often delayed. Among targeted therapy options, the usage of sunitinib appears to be the most effective in terms of symptom control and showing antitumoural effects at the same time. Experience with radiation is still limited; however, local ablative procedures seem to be promising options. Peptide receptor radiotherapy (PRRT) with radiolabelled somatostatin analogues (SSAs, 177Lu-DOTATATE) offers a targeted approach, especially in patients with high somatostatin receptor density. Surgery is the first-line therapy for nonmetastatic VIPoma. Additionally, if the resection of all visible tumour lesions is possible, the surgical approach seems preferable to other strategies in highly symptomatic patients. The role of surgery in very advanced stages where only tumour debulking is possible remains debatable. However, a high rate of immediate symptom control can be achieved by tumour debulking followed by somatostatin therapy, although the impact on survival remains unclear.\n \n \n Conclusion\n Surgery is the only curative option for nonmetastatic VIPoma. Additionally, surgery should be a first-line therapy option for highly symptomatic patients, especially if the resection of all tumour lesions (primary tumour and metastasis) is achievable. In frail patients, other modalities can be used."],["dc.identifier.doi","10.1007/s00423-022-02620-7"],["dc.identifier.pii","2620"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113988"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-597"],["dc.relation.eissn","1435-2451"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Treatment options of metastatic and nonmetastatic VIPoma: a review"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2022Journal Article [["dc.bibliographiccitation.journal","Zeitschrift für Gastroenterologie"],["dc.contributor.author","Brunner, Marius"],["dc.contributor.author","Ammer-Herrmenau, Christoph"],["dc.contributor.author","Biggemann, Lorenz"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","König, Alexander"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Petzold, Golo"],["dc.date.accessioned","2022-10-04T10:22:18Z"],["dc.date.available","2022-10-04T10:22:18Z"],["dc.date.issued","2022"],["dc.description.abstract","Zusammenfassung\n Hintergrund Granulomatöse Erkrankungen wie Sarkoidose können die Diagnostik bei onkologischen Erkrankungen erschweren, da Metastasen bildmorphologisch häufig nicht von Granulomen zu unterscheiden sind. Die vorliegende Kasuistik beschreibt Diagnostik und Therapie eines Patienten mit fortgeschrittener Sarkoidose und einem hepatisch metastasierten Rektumkarzinom mit schlussendlichem Erreichen eines kurativen Stadiums.\n Fallbeschreibung Bei einem 71-jährigen Patienten wurde im Rahmen der Abklärung ungewollten Gewichtsverlustes sowie einer Anämie ein Adenokarzinom des Rektums diagnostiziert. Die weitere Umfelddiagnostik ergab bildmorphologisch den hochgradigen Verdacht auf multiple rechtshepatische, pulmonale und splenische Metastasen. Histologisch zeigten sich nach bronchoskopischer Biopsie der mediastinalen Lymphknoten jedoch nichtverkäsende Epitheloidzellgranulome als Manifestation einer bis dato nicht bekannten Sarkoidose. Aufgrund des stenosierenden Tumors erfolgte eine Rektumresektion mit Milzextirpation bei intraoperativ hochgradigem Verdacht auf Milzmetastasen. Histologisch zeigten sich in der Milz eine Beteiligung im Rahmen der Sarkoidose. Bei bildmorphologisch weiterhin suspekten rechtshepatischen Leberläsionen erfolgte postoperativ eine Stanzbiopsie einer Läsion, die histologisch sowohl eine Metastase des bekannten Rektumkarzinoms als auch eine Sarkoidose ergab. Es erfolgte eine pseudo(neo)adjuvante Therapie mit 5-Fluorouracil, Leukovorin und Oxaliplatin (FOLFOX) und Panitumumab (Anti-EGF-Antikörper). Bildmorphologisch zeigten sich posttherapeutisch 2 Leberläsionen regredient, mehrere weitere größenstabil. Es erfolgte eine erweiterte Hemihepatektomie rechts mit histologischem Nachweis von sowohl Metastasen als auch Sarkoidose-Herden. Der zu diesem Zeitpunkt tumorfreie Patient wurde in die engmaschige Nachsorge entlassen, die sich im weiteren Verlauf (13 Monate) bildmorphologisch ohne Rezidivhinweis zeigte.\n Diskussion Das gleichzeitige Auftreten von metastasierten Tumorerkrankungen und Sarkoidoseherden führt zu einem diagnostischen Dilemma, da die Manifestationen bildmorphologisch kaum unterschieden werden können. Dieser Fallbereich zeigt, dass eine umfassende histologische Aufarbeitung der unterschiedlichen betroffenen Organe mit konsekutiven Resektionen schlussendlich zu einer Tumorfreiheit des Patienten führen kann."],["dc.identifier.doi","10.1055/a-1880-1639"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114638"],["dc.language.iso","de"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","1439-7803"],["dc.relation.issn","0044-2771"],["dc.title","Metastase oder Sarkoidose – eine diagnostische Herausforderung beim metastasierten Rektumkarzinom"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2017Journal Article [["dc.bibliographiccitation.firstpage","S1448"],["dc.bibliographiccitation.issue","S15"],["dc.bibliographiccitation.journal","Journal of Thoracic Disease"],["dc.bibliographiccitation.lastpage","S1457"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Dinter, Helen"],["dc.contributor.author","König, Alexander"],["dc.contributor.author","Ströbel, Philipp"],["dc.date.accessioned","2020-12-10T18:42:54Z"],["dc.date.available","2020-12-10T18:42:54Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.21037/jtd.2017.02.02"],["dc.identifier.eissn","2077-6624"],["dc.identifier.issn","2072-1439"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78124"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Neuroendocrine tumors of the thymus and mediastinum"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2017Journal Article Discussion [["dc.bibliographiccitation.firstpage","S29"],["dc.bibliographiccitation.journal","Translational Cancer Research"],["dc.bibliographiccitation.lastpage","S30"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Koenig, Alexander O."],["dc.date.accessioned","2018-11-07T10:27:48Z"],["dc.date.available","2018-11-07T10:27:48Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.21037/tcr.2017.02.32"],["dc.identifier.isi","000397306100010"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43301"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Ame Publ Co"],["dc.relation.issn","2219-6803"],["dc.relation.issn","2218-676X"],["dc.title","Interaction of tumor and stromal cells in pancreatic cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]Details DOI WOS2014Journal Article [["dc.bibliographiccitation.firstpage","688"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Cancer Discovery"],["dc.bibliographiccitation.lastpage","701"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Baumgart, Sandra"],["dc.contributor.author","Chen, Nai-Ming"],["dc.contributor.author","Siveke, Jens T."],["dc.contributor.author","Koenig, Alexander O."],["dc.contributor.author","Zhang, J."],["dc.contributor.author","Singh, Shiv K."],["dc.contributor.author","Wolf, Elmar"],["dc.contributor.author","Bartkuhn, Marek"],["dc.contributor.author","Esposito, Irene"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Reinecke, Johanna"],["dc.contributor.author","Nikorowitsch, Julius"],["dc.contributor.author","Brunner, Marius"],["dc.contributor.author","Singh, Garima"],["dc.contributor.author","Fernandez-Zapico, Martin E."],["dc.contributor.author","Smyrk, Thomas C."],["dc.contributor.author","Bamlet, William R."],["dc.contributor.author","Eilers, Martin"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.author","Gress, Thomas M."],["dc.contributor.author","Billadeau, Daniel D."],["dc.contributor.author","Tuveson, David A."],["dc.contributor.author","Urrutia, Raul"],["dc.contributor.author","Ellenrieder, Volker"],["dc.date.accessioned","2018-11-07T09:39:31Z"],["dc.date.available","2018-11-07T09:39:31Z"],["dc.date.issued","2014"],["dc.description.abstract","Cancer-associated inflammation is a molecular key feature in pancreatic ductal adenocarcinoma. Oncogenic KRAS in conjunction with persistent inflammation is known to accelerate carcinogenesis, although the underlying mechanisms remain poorly understood. Here, we outline a novel pathway whereby the transcription factors NFATc1 and STAT3 cooperate in pancreatic epithelial cells to promote Kras(G12D) -driven carcinogenesis. NFATc1 activation is induced by inflammation and itself accelerates inflammation-induced carcinogenesis in Kras(G12D) mice, whereas genetic or pharmacologic ablation of NFATc1 attenuates this effect. Mechanistically, NFATc1 complexes with STAT3 for enhancer-promoter communications at jointly regulated genes involved in oncogenesis, for example, Cyclin, EGFR and WNT family members. The NFATc1-STAT3 cooperativity is operative in pancreatitis-mediated carcinogenesis as well as in established human pancreatic cancer. Together, these studies unravel new mechanisms of inflammatory-driven pancreatic carcinogenesis and suggest beneficial effects of chemopreventive strategies using drugs that are currently available for targeting these factors in clinical trials. SIGNIFICANCE: Our study points to the existence of an oncogenic NFATc1-STAT3 cooperativity that mechanistically links inflammation with pancreatic cancer initiation and progression. Because NFATc1STAT3 nucleoprotein complexes control the expression of gene networks at the intersection of inflammation and cancer, our study has significant relevance for potentially managing pancreatic cancer and other inflammatory-driven malignancies. (C) 2014 AACR."],["dc.identifier.doi","10.1158/2159-8290.CD-13-0593"],["dc.identifier.isi","000337185500025"],["dc.identifier.pmid","24694735"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33304"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","2159-8290"],["dc.relation.issn","2159-8274"],["dc.title","Inflammation-Induced NFATc1-STAT3 Transcription Complex Promotes Pancreatic Cancer Initiation by Kras(G12D)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2019Journal Article [["dc.bibliographiccitation.firstpage","234"],["dc.bibliographiccitation.issue","4_suppl"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.lastpage","234"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Ettrich, Thomas Jens"],["dc.contributor.author","Berger, Andreas Wolfgang"],["dc.contributor.author","Schwerdel, Daniel"],["dc.contributor.author","Reinacher-Schick, Anke C."],["dc.contributor.author","Uhl, Waldemar"],["dc.contributor.author","Alguel, Hana"],["dc.contributor.author","Friess, Helmut"],["dc.contributor.author","Koenig, Alexander"],["dc.contributor.author","Ghadimi, Michael"],["dc.contributor.author","Gallmeier, Eike"],["dc.contributor.author","Bartsch, Detlef K."],["dc.contributor.author","Geissler, Michael"],["dc.contributor.author","Staib, Ludger"],["dc.contributor.author","Tannapfel, Andrea"],["dc.contributor.author","Kleger, Alexander"],["dc.contributor.author","Seufferlein, Thomas"],["dc.date.accessioned","2020-12-10T18:41:37Z"],["dc.date.available","2020-12-10T18:41:37Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1200/JCO.2019.37.4_suppl.234"],["dc.identifier.eissn","1527-7755"],["dc.identifier.issn","0732-183X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77632"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","A blood-based assay for diagnosis of early-stage pancreatic cancer."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2015Journal Article [["dc.bibliographiccitation.firstpage","1024"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Gastroenterology"],["dc.bibliographiccitation.lastpage","U502"],["dc.bibliographiccitation.volume","148"],["dc.contributor.author","Chen, Nai-Ming"],["dc.contributor.author","Singh, Garima"],["dc.contributor.author","Koenig, Alexander O."],["dc.contributor.author","Liou, Geou-Yarh"],["dc.contributor.author","Storz, Peter"],["dc.contributor.author","Zhang, J."],["dc.contributor.author","Regul, Lisanne"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Kuehnemuth, Benjamin"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Hebrok, Matthias"],["dc.contributor.author","Siveke, Jens T."],["dc.contributor.author","Billadeau, Daniel D."],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Heßmann, Elisabeth"],["dc.date.accessioned","2018-11-07T09:57:58Z"],["dc.date.available","2018-11-07T09:57:58Z"],["dc.date.issued","2015"],["dc.description.abstract","BACKGROUND & AIMS: Oncogenic mutations in KRAS contribute to the development of pancreatic ductal adenocarcinoma, but are not sufficient to initiate carcinogenesis. Secondary events, such as inflammation-induced signaling via the epidermal growth factor receptor (EGFR) and expression of the SOX9 gene, are required for tumor formation. Herein we sought to identify the mechanisms that link EGFR signaling with activation of SOX9 during acinar-ductal metaplasia, a transdifferentiation process that precedes pancreatic carcinogenesis. METHODS: We analyzed pancreatic tissues from KrasG12D; pdx1-Cre and KrasG12D; NFATc1D/D; pdx1-Cre mice after intraperitoneal administration of caerulein, vs cyclosporin A or dimethyl sulfoxide (controls). Induction of EGFR signaling and its effects on the expression of Nuclear factor of activated T cells c1 (NFATc1) or SOX9 were investigated by quantitative reverse-transcription polymerase chain reaction, immunoblot, and immunohistochemical analyses of mouse and human tissues and acinar cell explants. Interactions between NFATc1 and partner proteins and effects on DNA binding or chromatin modifications were studied using co-immunoprecipitation and chromatin immunoprecipitation assays in acinar cell explants and mouse tissue. RESULTS: EGFR activation induced expression of NFATc1 in metaplastic areas from patients with chronic pancreatitis and in pancreatic tissue from KrasG12D mice. EGFR signaling also promoted formation of a complex between NFATc1 and C-JUN in dedifferentiating mouse acinar cells, leading to activation of Sox9 transcription and induction of acinar-ductal metaplasia. Pharmacologic inhibition of NFATc1 or disruption of the Nfatc1 gene inhibited EGFR-mediated induction of Sox9 transcription and blocked acinar-ductal transdifferentiation and pancreatic cancer initiation in mice. CONCLUSIONS: EGFR signaling induces expression of NFATc1 and Sox9, leading to acinar cell transdifferentiation and initiation of pancreatic cancer. Strategies designed to disrupt this pathway might be developed to prevent pancreatic cancer initiation in high-risk patients with chronic pancreatitis."],["dc.identifier.doi","10.1053/j.gastro.2015.01.033"],["dc.identifier.isi","000353335700033"],["dc.identifier.pmid","25623042"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37276"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co-elsevier Inc"],["dc.relation.issn","1528-0012"],["dc.relation.issn","0016-5085"],["dc.title","NFATc1 Links EGFR Signaling to Induction of Sox9 Transcription and Acinar-Ductal Transdifferentiation in the Pancreas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2019Journal Article [["dc.bibliographiccitation.firstpage","4128"],["dc.bibliographiccitation.issue","15_suppl"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.lastpage","4128"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Uhl, Waldemar"],["dc.contributor.author","Ettrich, Thomas Jens"],["dc.contributor.author","Reinacher-Schick, Anke C."],["dc.contributor.author","Algül, Hana"],["dc.contributor.author","Friess, Helmut"],["dc.contributor.author","Kornmann, Marko"],["dc.contributor.author","Koenig, Alexander"],["dc.contributor.author","Ghadimi, Michael"],["dc.contributor.author","Wittel, Uwe A"],["dc.contributor.author","Gallmeier, Eike"],["dc.contributor.author","Wille, Kai"],["dc.contributor.author","Geissler, Michael"],["dc.contributor.author","Schimanski, Carl Christoph"],["dc.contributor.author","Prasnikar, Nicole"],["dc.contributor.author","Tannapfel, Andrea"],["dc.contributor.author","Perkhofer, Lukas"],["dc.contributor.author","Berger, Andreas W."],["dc.contributor.author","Seufferlein, Thomas"],["dc.date.accessioned","2020-12-10T18:41:36Z"],["dc.date.available","2020-12-10T18:41:36Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1200/JCO.2019.37.15_suppl.4128"],["dc.identifier.eissn","1527-7755"],["dc.identifier.issn","0732-183X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77625"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","NEONAX trial: Neoadjuvant plus adjuvant or only adjuvant nab-paclitaxel plus gemcitabine for resectable pancreatic cancer, a phase II study of the AIO pancreatic cancer group (AIO-PAK-0313)—Safety interim analysis."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2021Journal Article [["dc.bibliographiccitation.firstpage","jnumed.120.258533"],["dc.bibliographiccitation.journal","Journal of Nuclear Medicine"],["dc.contributor.author","Treiber, Hannes"],["dc.contributor.author","Koenig, Alexander"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.author","Richter, Annika"],["dc.contributor.author","Sahlmann, Carsten Oliver"],["dc.contributor.author","Strauss, Arne"],["dc.date.accessioned","2021-06-01T10:48:40Z"],["dc.date.available","2021-06-01T10:48:40Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.2967/jnumed.120.258533"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86016"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","2159-662X"],["dc.relation.issn","0161-5505"],["dc.title","Liver enzyme elevation after 177 Lu-PSMA radioligand therapy for metastasized castration-resistant prostate cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2020Journal Article [["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Azizian, Azadeh"],["dc.contributor.author","Rühlmann, Felix"],["dc.contributor.author","Krause, Tanja"],["dc.contributor.author","Bernhardt, Markus"],["dc.contributor.author","Jo, Peter"],["dc.contributor.author","König, Alexander"],["dc.contributor.author","Kleiß, Mathias"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Ghadimi, Michael"],["dc.contributor.author","Gaedcke, Jochen"],["dc.date.accessioned","2021-04-14T08:27:35Z"],["dc.date.available","2021-04-14T08:27:35Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41598-020-57930-x"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82341"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2045-2322"],["dc.title","CA19-9 for detecting recurrence of pancreatic cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI
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