Klinik für Gynäkologie und Geburtshilfe

[["dc.bibliographiccitation.firstpage","5050"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Läsche, Matthias"],["dc.contributor.author","Gallwas, Julia"],["dc.contributor.author","Gründker, Carsten"],["dc.date.accessioned","2022-06-01T09:39:57Z"],["dc.date.available","2022-06-01T09:39:57Z"],["dc.date.issued","2022"],["dc.date.updated","2022-09-03T21:08:21Z"],["dc.description.abstract","Despite all precautionary actions and the possibility of using vaccinations to counteract infections caused by human papillomaviruses (HPVs), HPV-related cancers still account for approximately 5% of all carcinomas. Worldwide, many women are still excluded from adequate health care due to their social position and origin. Therefore, immense efforts in research and therapy are still required to counteract the challenges that this disease entails. The special thing about an HPV infection is that it is not only able to trick the immune system in a sophisticated way, but also, through genetic integration into the host genome, to use all the resources available to the host cells to complete the replication cycle of the virus without activating the alarm mechanisms of immune recognition and elimination. The mechanisms utilized by the virus are the metabolic, immune, and hormonal signaling pathways that it manipulates. Since the virus is dependent on replication enzymes of the host cells, it also intervenes in the cell cycle of the differentiating keratinocytes and shifts their terminal differentiation to the uppermost layers of the squamocolumnar transformation zone (TZ) of the cervix. The individual signaling pathways are closely related and equally important not only for the successful replication of the virus but also for the onset of cervical cancer. We will therefore analyze the effects of HPV infection on metabolic signaling, as well as changes in hormonal and immune signaling in the tumor and its microenvironment to understand how each level of signaling interacts to promote tumorigenesis of cervical cancer."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3390/ijms23095050"],["dc.identifier.pii","ijms23095050"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108603"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.title","Like Brothers in Arms: How Hormonal Stimuli and Changes in the Metabolism Signaling Cooperate, Leading HPV Infection to Drive the Onset of Cervical Cancer"],["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","636"],["dc.bibliographiccitation.issue","6898"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","641"],["dc.bibliographiccitation.volume","418"],["dc.contributor.author","Pandur, P."],["dc.contributor.author","Lasche, M."],["dc.contributor.author","Eisenberg, L. M."],["dc.contributor.author","Kuhl, M."],["dc.date.accessioned","2018-11-07T10:10:59Z"],["dc.date.available","2018-11-07T10:10:59Z"],["dc.date.issued","2002"],["dc.description.abstract","Formation of the vertebrate heart requires a complex interplay of several temporally regulated signalling cascades(1). In Xenopus laevis, cardiac specification occurs during gastrulation and requires signals from the dorsal lip and underlying endoderm(2). Among known Xenopus Wnt genes, only Wnt-11 shows a spatiotemporal pattern of expression that correlates with cardiac specification, which indicates that Wnt-11 may be involved in heart development(3,4). Here we show, through loss- and gain-of-function experiments, that XWnt-11 is required for heart formation in Xenopus embryos and is sufficient to induce a contractile phenotype in embryonic explants. Treating the mouse embryonic carcinoma stem cell line P19 with murine Wnt-11 conditioned medium triggers cardiogenesis, which indicates that the function of Wnt-11 in heart development has been conserved in higher vertebrates. XWnt-11 mediates this effect by non-canonical Wnt signalling, which is independent of beta-catenin and involves protein kinase C and Jun amino-terminal kinase. Our results indicate that the cardiac developmental program requires non-canonical Wnt signal transduction."],["dc.identifier.doi","10.1038/nature00921"],["dc.identifier.isi","177305600042"],["dc.identifier.pmid","12167861"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39957"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0028-0836"],["dc.title","Wnt-11 activation of a non-canonical Wnt signalling pathway is required for cardiogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","184"],["dc.bibliographiccitation.issue","02"],["dc.bibliographiccitation.journal","Geburtshilfe und Frauenheilkunde"],["dc.bibliographiccitation.lastpage","188"],["dc.bibliographiccitation.volume","79"],["dc.contributor.author","Gründker, Carsten"],["dc.contributor.author","Läsche, Matthias"],["dc.contributor.author","Hellinger, Johanna"],["dc.contributor.author","Emons, Günter"],["dc.date.accessioned","2020-12-10T18:12:06Z"],["dc.date.available","2020-12-10T18:12:06Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1055/a-0805-9113"],["dc.identifier.eissn","1438-8804"],["dc.identifier.issn","0016-5751"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74247"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Mechanisms of Metastasis and Cell Mobility – The Role of Metabolism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Oncology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Läsche, Matthias"],["dc.contributor.author","Emons, Günter"],["dc.contributor.author","Gründker, Carsten"],["dc.date.accessioned","2021-04-14T08:26:59Z"],["dc.date.available","2021-04-14T08:26:59Z"],["dc.date.issued","2020"],["dc.description.abstract","Since the earliest findings of Otto Warburg, who discovered the first metabolic differences between lactate production of cancer cells and non-malignant tissues in the 1920s, much time has passed. He explained the increased lactate levels with dysfunctional mitochondria and aerobic glycolysis despite adequate oxygenation. Meanwhile, we came to know that mitochondria remain instead functional in cancer cells; hence, metabolic drift, rather than being linked to dysfunctional mitochondria, was found to be an active act of direct response of cancer cells to cell proliferation and survival signals. This metabolic drift begins with the use of sugars and the full oxidative phosphorylation via the mitochondrial respiratory chain to form CO2, and it then leads to the formation of lactic acid via partial oxidation. In addition to oncogene-driven metabolic reprogramming, the oncometabolites themselves alter cell signaling and are responsible for differentiation and metastasis of cancer cells. The aberrant metabolism is now considered a major characteristic of cancer within the past 15 years. However, the proliferating anabolic growth of a tumor and its spread to distal sites of the body is not explainable by altered glucose metabolism alone. Since a tumor consists of malignant cells and its tumor microenvironment, it was important for us to understand the bilateral interactions between the primary tumor and its microenvironment and the processes underlying its successful metastasis. We here describe the main metabolic pathways and their implications in tumor progression and metastasis. We also portray that metabolic flexibility determines the fate of the cancer cell and ultimately the patient. This flexibility must be taken into account when deciding on a therapy, since singular cancer therapies only shift the metabolism to a different alternative path and create resistance to the medication used. As with Otto Warburg in his days, we primarily focused on the metabolism of mitochondria when dealing with this scientific question."],["dc.identifier.doi","10.3389/fonc.2020.00409"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17392"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82134"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","2234-943X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Shedding New Light on Cancer Metabolism: A Metabolic Tightrope Between Life and Death"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","714"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Läsche, Matthias"],["dc.contributor.author","Urban, Horst"],["dc.contributor.author","Gallwas, Julia"],["dc.contributor.author","Gründker, Carsten"],["dc.date.accessioned","2021-06-01T09:42:32Z"],["dc.date.available","2021-06-01T09:42:32Z"],["dc.date.issued","2021"],["dc.description.abstract","Cervical cancer is responsible for around 5% of all human cancers worldwide. It develops almost exclusively from an unsolved, persistent infection of the squamocolumnar transformation zone between the endo- and ecto-cervix with various high-risk (HR) human papillomaviruses (HPVs). The decisive turning point on the way to persistent HPV infection and malignant transformation is an immune system weakened by pathobionts and oxidative stress and an injury to the cervical mucosa, often caused by sexual activities. Through these injury and healing processes, HPV viruses, hijacking activated keratinocytes, move into the basal layers of the cervical epithelium and then continue their development towards the distal prickle cell layer (Stratum spinosum). The microbial microenvironment of the cervical tissue determines the tissue homeostasis and the integrity of the protective mucous layer through the maintenance of a healthy immune and metabolic signalling. Pathological microorganisms and the resulting dysbiosis disturb this signalling. Thus, pathological inflammatory reactions occur, which manifest the HPV infection. About 90% of all women contract an HPV infection in the course of their lives. In about 10% of cases, the virus persists and cervical intra-epithelial neoplasia (CIN) develops. Approximately 1% of women with a high-risk HPV infection incur a cervical carcinoma after 10 to 20 years. In this non-systematic review article, we summarise how the sexually and microbial mediated pathogenesis of the cervix proceeds through aberrant immune and metabolism signalling via CIN to cervical carcinoma. We show how both the virus and the cancer benefit from the same changes in the immune and metabolic environment."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/cells10030714"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85278"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","2073-4409"],["dc.relation.orgunit","Klinik für Gynäkologie und Geburtshilfe"],["dc.rights","CC BY 4.0"],["dc.title","HPV and Other Microbiota; Who’s Good and Who’s Bad: Effects of the Microbial Environment on the Development of Cervical Cancer—A Non-Systematic Review"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]