Gallwas, Julia

[["dc.bibliographiccitation.artnumber","7"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Clinical Epigenetics"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Pantelaiou-Prokaki, Garyfallia"],["dc.contributor.author","Mieczkowska, Iga"],["dc.contributor.author","Schmidt, Geske E."],["dc.contributor.author","Fritzsche, Sonja"],["dc.contributor.author","Prokakis, Evangelos"],["dc.contributor.author","Gallwas, Julia"],["dc.contributor.author","Wegwitz, Florian"],["dc.date.accessioned","2022-02-01T10:31:32Z"],["dc.date.accessioned","2022-08-18T12:33:13Z"],["dc.date.available","2022-02-01T10:31:32Z"],["dc.date.available","2022-08-18T12:33:13Z"],["dc.date.issued","2022-01-11"],["dc.date.updated","2022-07-29T12:00:15Z"],["dc.description.abstract","Background Basal-like breast cancer (BLBC) is one of the most aggressive malignant diseases in women with an increased metastatic behavior and poor prognosis compared to other molecular subtypes of breast cancer. Resistance to chemotherapy is the main cause of treatment failure in BLBC. Therefore, novel therapeutic strategies counteracting the gain of aggressiveness underlying therapy resistance are urgently needed. The epithelial-to-mesenchymal transition (EMT) has been established as one central process stimulating cancer cell migratory capacity but also acquisition of chemotherapy-resistant properties. In this study, we aimed to uncover epigenetic factors involved in the EMT-transcriptional program occurring in BLBC cells surviving conventional chemotherapy. Results Using whole transcriptome data from a murine mammary carcinoma cell line (pG-2), we identified upregulation of Hdac4 , 7 and 8 in tumor cells surviving conventional chemotherapy. Subsequent analyses of human BLBC patient datasets and cell lines established HDAC8 as the most promising factor sustaining tumor cell viability. ChIP-sequencing data analysis identified a pronounced loss of H3K27ac at regulatory regions of master transcription factors (TFs) of epithelial phenotype like Gata3 , Elf5 , Rora and Grhl2 upon chemotherapy. Interestingly, impairment of HDAC8 activity reverted epithelial-TFs levels. Furthermore, loss of HDAC8 activity sensitized tumor cells to chemotherapeutic treatments, even at low doses. Conclusion The current study reveals a previously unknown transcriptional repressive function of HDAC8 exerted on a panel of transcription factors involved in the maintenance of epithelial cell phenotype, thereby supporting BLBC cell survival to conventional chemotherapy. Our data establish HDAC8 as an attractive therapeutically targetable epigenetic factor to increase the efficiency of chemotherapeutics. Graphical abstract"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.citation","Clinical Epigenetics. 2022 Jan 11;14(1):7"],["dc.identifier.doi","10.1186/s13148-022-01228-4"],["dc.identifier.pii","1228"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98885"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112916"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-517"],["dc.publisher","BioMed Central"],["dc.relation.eissn","1868-7083"],["dc.relation.issn","1868-7075"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","HDAC8"],["dc.subject","MET"],["dc.subject","EMT"],["dc.subject","BLBC"],["dc.subject","TNBC"],["dc.subject","Chemotherapy"],["dc.subject","Epigenetics"],["dc.subject","H3K27ac"],["dc.subject","Epithelial transcription factors"],["dc.title","HDAC8 suppresses the epithelial phenotype and promotes EMT in chemotherapy-treated basal-like breast cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","479"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal der Deutschen Dermatologischen Gesellschaft"],["dc.bibliographiccitation.lastpage","494"],["dc.bibliographiccitation.volume","19"],["dc.contributor.affiliation","Gross, Gerd E.; 1\r\nDepartment of Dermatology and Venereology\r\nUniversity Hospital Rostock\r\nRostock Germany"],["dc.contributor.affiliation","Avila Valle, Gabriela L.; 3\r\nDepartment of Dermatology\r\nVenereology and Allergology\r\nDivision of Evidence Based Medicine in Dermatology (dEBM)\r\nCharité – University Medical Center Berlin\r\ncorporate member of Free University Berlin\r\nHumboldt University Berlin\r\nand Berlin Institute of Health\r\nBerlin Germany"],["dc.contributor.affiliation","Bickel, Markus; 4\r\nInfektiologikum Frankfurt\r\nFrankfurt am Main\r\nGermany"],["dc.contributor.affiliation","Brockmeyer, Norbert H.; 5\r\nDepartment of Dermatology\r\nVenereology and Allergology\r\nRuhr University Bochum\r\nCenter for Sexual Health – WIR „Walk In Ruhr“\r\nBochum Germany"],["dc.contributor.affiliation","Doubek, Klaus; 6\r\nGynecology Office Dr. Klaus Doubek\r\nWiesbaden Germany"],["dc.contributor.affiliation","Gallwas, Julia; 7\r\nDepartment of Gynecology and Obstetrics\r\nGeorg August University Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Gieseking, Friederike; 8\r\nGynecology Office Heussweg\r\nHamburg Germany"],["dc.contributor.affiliation","Haase, Heidemarie; 9\r\nWomen Support Group Cancer – Federal Association\r\nGermany"],["dc.contributor.affiliation","Hillemanns, Peter; 10\r\nDepartment of Gynecology and Obstetrics\r\nHannover Medical School\r\nHannover Germany"],["dc.contributor.affiliation","Ikenberg, Hans; 11\r\nMVZ for Cytology and Molecular Biology (CytoMol)\r\nFrankfurt am Main\r\nGermany"],["dc.contributor.affiliation","Jongen, Johannes; 12\r\nProctology Office Kiel\r\nKiel Germany"],["dc.contributor.affiliation","Kaufmann, Andreas M.; 13\r\nDepartment of Gynecology\r\nCampus Virchow Hospital\r\nCharité – University Medical Center Berlin, corporate member of Free University Berlin\r\nHumboldt University Berlin and Berlin Institute of Health\r\nBerlin Germany"],["dc.contributor.affiliation","Klußmann, Jens Peter; 14\r\nDepartment of Otorhinolaryngology\r\nHead and Neck Surgery\r\n­University Hospital of Cologne\r\nMedical Faculty\r\nUniversity of Cologne\r\nCologne Germany"],["dc.contributor.affiliation","von Knebel Doeberitz, Magnus; 15\r\nDepartment of Applied Tumor Biology\r\nInstitute of Pathology, University Hospital Heidelberg\r\nClinical Cooperation Unit G105 of the German Cancer Research Center (DKFZ)\r\nHeidelberg Germany"],["dc.contributor.affiliation","Knuf, Markus; 16\r\nHospital for Child and Adolescent Health\r\nHelios Dr. Horst Schmidt Kliniken\r\nWiesbaden Germany"],["dc.contributor.affiliation","Köllges, Ralf; 18\r\nOffice for Child and Adolescent Health\r\nMönchengladbach Germany"],["dc.contributor.affiliation","Laws, Hans‐Jürgen; 19\r\nDepartment of Pediatric Oncology\r\nHematology and Clinical Immunology\r\nUniversity Hospital Düsseldorf\r\nDüsseldorf Germany"],["dc.contributor.affiliation","Mikolajczyk, Rafael; 20\r\nInstitute of Medical Epidemiology\r\nBiometry and Informatics (IMEBI)\r\nMartin Luther University of Halle‐Wittenberg\r\nHalle (Saale) Germany"],["dc.contributor.affiliation","Neis, Klaus J.; 21\r\nGynecology Office am Staden\r\nSaarbrücken Germany"],["dc.contributor.affiliation","Petry, Karl‐Ulrich; 22\r\nGynecology Clinic\r\nHospital Wolfsburg\r\nWolfsburg Germany"],["dc.contributor.affiliation","Pfister, Herbert; 23\r\nInstitute of Virology\r\nUniversity of Cologne\r\nCologne Germany"],["dc.contributor.affiliation","Schlaeger, Martin; 24\r\nOffice Dr. Martin Schlaeger\r\nOldenburg Germany"],["dc.contributor.affiliation","Schneede, Peter; 25\r\nUrology Clinic\r\nHospital Memmingen\r\nMemmingen Germany"],["dc.contributor.affiliation","Schneider, Achim; 26\r\nMVZ in Fürstenberg‐Karree\r\nBerlin Germany"],["dc.contributor.affiliation","Smola, Sigrun; 27\r\nInstitute of Virology, Saarland University Medical Center\r\nMedical Faculty\r\nSaarland University\r\nHomburg/Saar Germany"],["dc.contributor.affiliation","Tiews, Sven; 28\r\nMVZ Laboratory for Cytopathology Dr. Steinberg GmbH\r\nSoest Germany"],["dc.contributor.affiliation","Nast, Alexander; 3\r\nDepartment of Dermatology\r\nVenereology and Allergology\r\nDivision of Evidence Based Medicine in Dermatology (dEBM)\r\nCharité – University Medical Center Berlin\r\ncorporate member of Free University Berlin\r\nHumboldt University Berlin\r\nand Berlin Institute of Health\r\nBerlin Germany"],["dc.contributor.affiliation","Gaskins, Matthew; 3\r\nDepartment of Dermatology\r\nVenereology and Allergology\r\nDivision of Evidence Based Medicine in Dermatology (dEBM)\r\nCharité – University Medical Center Berlin\r\ncorporate member of Free University Berlin\r\nHumboldt University Berlin\r\nand Berlin Institute of Health\r\nBerlin Germany"],["dc.contributor.affiliation","Wieland, Ulrike; 29\r\nNational Reference Center for Papilloma and Polyoma Viruses\r\nInstitute of Virology\r\nUniversity Hospital of Cologne\r\nUniversity of Cologne\r\nCologne Germany"],["dc.contributor.author","Gross, Gerd E."],["dc.contributor.author","Werner, Ricardo N."],["dc.contributor.author","Avila Valle, Gabriela L."],["dc.contributor.author","Bickel, Markus"],["dc.contributor.author","Brockmeyer, Norbert H."],["dc.contributor.author","Doubek, Klaus"],["dc.contributor.author","Gallwas, Julia"],["dc.contributor.author","Gieseking, Friederike"],["dc.contributor.author","Haase, Heidemarie"],["dc.contributor.author","Hillemanns, Peter"],["dc.contributor.author","Ikenberg, Hans"],["dc.contributor.author","Jongen, Johannes"],["dc.contributor.author","Kaufmann, Andreas M."],["dc.contributor.author","Klußmann, Jens Peter"],["dc.contributor.author","von Knebel Doeberitz, Magnus"],["dc.contributor.author","Knuf, Markus"],["dc.contributor.author","Köllges, Ralf"],["dc.contributor.author","Laws, Hans‐Jürgen"],["dc.contributor.author","Mikolajczyk, Rafael"],["dc.contributor.author","Neis, Klaus J."],["dc.contributor.author","Petry, Karl‐Ulrich"],["dc.contributor.author","Pfister, Herbert"],["dc.contributor.author","Schlaeger, Martin"],["dc.contributor.author","Schneede, Peter"],["dc.contributor.author","Schneider, Achim"],["dc.contributor.author","Smola, Sigrun"],["dc.contributor.author","Tiews, Sven"],["dc.contributor.author","Nast, Alexander"],["dc.contributor.author","Gaskins, Matthew"],["dc.contributor.author","Wieland, Ulrike"],["dc.date.accessioned","2021-04-14T08:28:20Z"],["dc.date.available","2021-04-14T08:28:20Z"],["dc.date.issued","2021"],["dc.date.updated","2022-02-09T13:21:00Z"],["dc.description.abstract","Summary Anogenital and oropharyngeal infections with human papilloma viruses (HPV) are common. Clinically manifest disease may significantly impact quality of life; the treatment of HPV‐associated lesions is associated with a high rate of recurrence and invasive neoplasms, such as cervical, anal, vulvar, penile, and oropharyngeal cancers, which are characterized by significant morbidity and mortality. Vaccination against HPV is an effective and safe measure for the primary prevention of HPV‐associated lesions, but immunization rates are still low in Germany. The present publication is an abridged version of the German evidence and consensus‐based guideline “Vaccination recommendations for the prevention of HPV‐associated lesions”, which is available on the website of the German Association of the Scientific Medical Societies (AWMF). On the basis of a systematic review with meta‐analyses, a representative panel developed and agreed upon recommendations for the vaccination of different populations against HPV. In addition, consensus‐based recommendations were developed for specific issues relevant to everyday practice. Based on current evidence and a representative expert consensus, these recommendations are intended to provide guidance in a field in which there is often uncertainty and in which both patients and health care providers are sometimes confronted with controversial and emotionally charged points of view."],["dc.identifier.doi","10.1111/ddg.14438"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82572"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1610-0387"],["dc.relation.issn","1610-0379"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes."],["dc.title","German evidence and consensus‐based (S3) guideline: Vaccination recommendations for the prevention of HPV‐associated lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Oncology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Wulf, Svenja"],["dc.contributor.author","Gallwas, Julia"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-01-11T14:06:15Z"],["dc.date.available","2022-01-11T14:06:15Z"],["dc.date.issued","2021"],["dc.description.abstract","Ado-trastuzumab emtansine (T-DM1) is an antibody–drug conjugate consisting of the monoclonal antibody trastuzumab linked to the maytansinoid DM1 with potential antineoplastic activity and is approved for human epidermal growth factor receptor 2 (HER2)-positive breast cancer. An analysis of the US Food and Drug Administration (FDA) Adverse Event Reporting System identified 124/1,243 (10%) renal adverse events for trastuzumab. However, there are no published case reports describing kidney biopsy findings related to nephrotoxicity of either trastuzumab or T-DM1. We report kidney biopsy findings in a case of nephrotic range proteinuria due to collapsing focal segmental glomerulosclerosis (FSGS) and tubular injury after initiation of T-DM1 therapy. After systematic exclusion of other causes, it is likely that the observed collapsing FSGS was associated with the prior initiation of T-DM1 therapy. This is further supported by the clinical course with improvement of proteinuria and kidney function 3 weeks after discontinuation of T-DM1 therapy without further specific treatment. In summary, we provide the first report of kidney biopsy findings in a case of nephrotic range proteinuria after initiation of T-DM1 therapy due to collapsing FSGS. This issue is especially relevant since T-DM1 is widely used, and nephrologists have to be aware of this potentially rare but severe complication."],["dc.description.abstract","Ado-trastuzumab emtansine (T-DM1) is an antibody–drug conjugate consisting of the monoclonal antibody trastuzumab linked to the maytansinoid DM1 with potential antineoplastic activity and is approved for human epidermal growth factor receptor 2 (HER2)-positive breast cancer. An analysis of the US Food and Drug Administration (FDA) Adverse Event Reporting System identified 124/1,243 (10%) renal adverse events for trastuzumab. However, there are no published case reports describing kidney biopsy findings related to nephrotoxicity of either trastuzumab or T-DM1. We report kidney biopsy findings in a case of nephrotic range proteinuria due to collapsing focal segmental glomerulosclerosis (FSGS) and tubular injury after initiation of T-DM1 therapy. After systematic exclusion of other causes, it is likely that the observed collapsing FSGS was associated with the prior initiation of T-DM1 therapy. This is further supported by the clinical course with improvement of proteinuria and kidney function 3 weeks after discontinuation of T-DM1 therapy without further specific treatment. In summary, we provide the first report of kidney biopsy findings in a case of nephrotic range proteinuria after initiation of T-DM1 therapy due to collapsing FSGS. This issue is especially relevant since T-DM1 is widely used, and nephrologists have to be aware of this potentially rare but severe complication."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3389/fonc.2021.796223"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97865"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","2234-943X"],["dc.relation.orgunit","Klinik für Nephrologie und Rheumatologie"],["dc.rights","CC BY 4.0"],["dc.title","Case Report: Collapsing Focal Segmental Glomerulosclerosis After Initiation of Ado-Trastuzumab Emtansine Therapy"],["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","4529"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","21"],["dc.contributor.affiliation","Eppich, Simon; \t\t \r\n\t\t Department of Obstetrics and Gynecology, University Hospital, Ludwig Maximilians University (LMU), Marchioninistraße 15, 81377 Munich, Germany, simon.eppich@gmx.de"],["dc.contributor.affiliation","Kuhn, Christina; \t\t \r\n\t\t Department of Obstetrics and Gynecology, University Hospital, Ludwig Maximilians University (LMU), Marchioninistraße 15, 81377 Munich, Germany, christina.kuhn@med.uni-muenchen.de"],["dc.contributor.affiliation","Schmoeckel, Elisa; \t\t \r\n\t\t Department of Pathology, LMU Munich, Thalkirchner Str. 56, 80337 Munich, Germany, elisa.schmoeckel@med.uni-muenchen.de"],["dc.contributor.affiliation","Mayr, Doris; \t\t \r\n\t\t Department of Pathology, LMU Munich, Thalkirchner Str. 56, 80337 Munich, Germany, doris.mayr@med.uni-muenchen.de"],["dc.contributor.affiliation","Mahner, Sven; \t\t \r\n\t\t Department of Obstetrics and Gynecology, University Hospital, Ludwig Maximilians University (LMU), Marchioninistraße 15, 81377 Munich, Germany, sven.mahner@med.uni-muenchen.de"],["dc.contributor.affiliation","Jeschke, Udo; \t\t \r\n\t\t Department of Obstetrics and Gynecology, University Hospital, Ludwig Maximilians University (LMU), Marchioninistraße 15, 81377 Munich, Germany, udo.jeschke@med.uni-muenchen.de\t\t \r\n\t\t Department of Obstetrics and Gynecology, University Hospital Augsburg, Stenglinstr. 2, 86156 Augsburg, Germany, udo.jeschke@med.uni-muenchen.de"],["dc.contributor.affiliation","Gallwas, Julia; \t\t \r\n\t\t Department of Obstetrics and Gynecology, University Hospital, Ludwig Maximilians University (LMU), Marchioninistraße 15, 81377 Munich, Germany, julia.gallwas@med.uni-muenchen.de\t\t \r\n\t\t Department of Gynecology and Obstetrics, Georg August University Goettingen, University Medicine, 37075 Goettingen, Germany, julia.gallwas@med.uni-muenchen.de"],["dc.contributor.affiliation","Heidegger, Helene Hildegard; \t\t \r\n\t\t Department of Obstetrics and Gynecology, University Hospital, Ludwig Maximilians University (LMU), Marchioninistraße 15, 81377 Munich, Germany, Helene.heidegger@med.uni-muenchen.de"],["dc.contributor.author","Eppich, Simon"],["dc.contributor.author","Kuhn, Christina"],["dc.contributor.author","Schmoeckel, Elisa"],["dc.contributor.author","Mayr, Doris"],["dc.contributor.author","Mahner, Sven"],["dc.contributor.author","Jeschke, Udo"],["dc.contributor.author","Gallwas, Julia"],["dc.contributor.author","Heidegger, Helene Hildegard"],["dc.date.accessioned","2021-04-14T08:25:04Z"],["dc.date.available","2021-04-14T08:25:04Z"],["dc.date.issued","2020"],["dc.date.updated","2022-09-06T10:50:59Z"],["dc.identifier.doi","10.3390/ijms21124529"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81515"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","MSX1—A Potential Marker for Uterus-Preserving Therapy of Endometrial Carcinomas"],["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","2398"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Steifensand, Friederike"],["dc.contributor.author","Gallwas, Julia"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Gründker, Carsten"],["dc.date.accessioned","2021-10-01T09:58:24Z"],["dc.date.available","2021-10-01T09:58:24Z"],["dc.date.issued","2021"],["dc.description.abstract","Cancer cells have an increased need for glucose and, despite aerobic conditions, obtain their energy through aerobic oxidation and lactate fermentation, instead of aerobic oxidation alone. Glutamine is an essential amino acid in the human body. Glutaminolysis and glycolysis are crucial for cancer cell survival. In the therapy of estrogen receptor α (ERα)-positive breast cancer (BC), the focus lies on hormone sensitivity targeting therapy with selective estrogen receptor modulators (SERMs) such as 4-hydroxytamoxifen (4-OHT), although this therapy is partially limited by the development of resistance. Therefore, further targets for therapy improvement of ERα-positive BC with secondary 4-OHT resistance are needed. Hence, increased glucose requirement and upregulated glutaminolysis in BC cells could be used. We have established sublines of ERα-positive MCF7 and T47D BC cells, which were developed to be resistant to 4-OHT. Further, glycolysis inhibitor 2-Deoxy-D-Glucose (2-DG) and glutaminase inhibitor CB-839 were analyzed. Co-treatments using 4-OHT and CB-839, 2-DG and CB-839, or 4-OHT, 2-DG and CB-839, respectively, showed significantly stronger inhibitory effects on viability compared to single treatments. It could be shown that tamoxifen-resistant BC cell lines, compared to the non-resistant cell lines, exhibited a stronger reducing effect on cell viability under co-treatments. In addition, the tamoxifen-resistant BC cell lines showed increased expression of proto-oncogene c-Myc compared to the parental cell lines. This could be reduced depending on the treatment. Suppression of c-Myc expression using specific siRNA completely abolished resistance to 4OH-tamoxifen. In summary, our data suggest that combined treatments affecting the metabolism of BC are suitable depending on the cellularity and resistance status. In addition, the anti-metabolic treatments affected the expression of the proto-oncogene c-Myc, a key player in the regulation of cancer cell metabolism."],["dc.description.abstract","Cancer cells have an increased need for glucose and, despite aerobic conditions, obtain their energy through aerobic oxidation and lactate fermentation, instead of aerobic oxidation alone. Glutamine is an essential amino acid in the human body. Glutaminolysis and glycolysis are crucial for cancer cell survival. In the therapy of estrogen receptor α (ERα)-positive breast cancer (BC), the focus lies on hormone sensitivity targeting therapy with selective estrogen receptor modulators (SERMs) such as 4-hydroxytamoxifen (4-OHT), although this therapy is partially limited by the development of resistance. Therefore, further targets for therapy improvement of ERα-positive BC with secondary 4-OHT resistance are needed. Hence, increased glucose requirement and upregulated glutaminolysis in BC cells could be used. We have established sublines of ERα-positive MCF7 and T47D BC cells, which were developed to be resistant to 4-OHT. Further, glycolysis inhibitor 2-Deoxy-D-Glucose (2-DG) and glutaminase inhibitor CB-839 were analyzed. Co-treatments using 4-OHT and CB-839, 2-DG and CB-839, or 4-OHT, 2-DG and CB-839, respectively, showed significantly stronger inhibitory effects on viability compared to single treatments. It could be shown that tamoxifen-resistant BC cell lines, compared to the non-resistant cell lines, exhibited a stronger reducing effect on cell viability under co-treatments. In addition, the tamoxifen-resistant BC cell lines showed increased expression of proto-oncogene c-Myc compared to the parental cell lines. This could be reduced depending on the treatment. Suppression of c-Myc expression using specific siRNA completely abolished resistance to 4OH-tamoxifen. In summary, our data suggest that combined treatments affecting the metabolism of BC are suitable depending on the cellularity and resistance status. In addition, the anti-metabolic treatments affected the expression of the proto-oncogene c-Myc, a key player in the regulation of cancer cell metabolism."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/cells10092398"],["dc.identifier.pii","cells10092398"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90055"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.relation.eissn","2073-4409"],["dc.relation.orgunit","Klinik für Gynäkologie und Geburtshilfe"],["dc.rights","CC BY 4.0"],["dc.title","Inhibition of Metabolism as a Therapeutic Option for Tamoxifen-Resistant Breast Cancer Cells"],["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","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","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"]]