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  1. Book ; Online ; Thesis: Analyse histologischer und transkriptomischer Veränderungen in murinen Schilddrüsengeweben zu verschiedenen Zeitpunkten nach γ-Bestrahlung

    Stauffer, Elena [Verfasser] / Zitzelsberger, Horst [Akademischer Betreuer]

    2023  

    Author's details Elena Stauffer ; Betreuer: Horst Zitzelsberger
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Universitätsbibliothek der Ludwig-Maximilians-Universität
    Publishing place München
    Document type Book ; Online ; Thesis
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  2. Book ; Online ; Thesis: Vergleich von Auswertemethoden einer immunhistochemischen PD-L1-Färbung anhand eines Kopf-Hals-Tumor-Kollektivs

    Rasim, Jan-Niklas [Verfasser] / Zitzelsberger, Horst [Akademischer Betreuer]

    Bedeutung für Therapieresistenz und Rezidiventstehung

    2023  

    Author's details Jan-Niklas Rasim ; Betreuer: Horst Zitzelsberger
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Universitätsbibliothek der Ludwig-Maximilians-Universität
    Publishing place München
    Document type Book ; Online ; Thesis
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  3. Article ; Online: Metabolomic Analysis of Human Cirrhosis and Hepatocellular Carcinoma: A Pilot Study.

    Weber, Sabine / Unger, Kristian / Alunni-Fabbroni, Marianna / Hirner-Eppeneder, Heidrun / Öcal, Elif / Zitzelsberger, Horst / Mayerle, Julia / Malfertheiner, Peter / Ricke, Jens

    Digestive diseases and sciences

    2024  

    Abstract: Background: Molecular changes in HCC development are largely unknown. As the liver plays a fundamental role in the body's metabolism, metabolic changes are to be expected.: Aims: We aimed to identify metabolomic changes in HCC in comparison to liver ... ...

    Abstract Background: Molecular changes in HCC development are largely unknown. As the liver plays a fundamental role in the body's metabolism, metabolic changes are to be expected.
    Aims: We aimed to identify metabolomic changes in HCC in comparison to liver cirrhosis (LC) patients, which could potentially serve as novel biomarkers for HCC diagnosis and prognosis.
    Methods: Metabolite expression from 38 HCC from the SORAMIC trial and 32 LC patients were analyzed by mass spectrometry. Metabolites with significant differences between LC and HCC at baseline were analyzed regarding expression over follow-up. In addition, association with overall survival was tested using univariate Cox proportional-hazard analysis.
    Results: 41 metabolites showed differential expression between LC and HCC patients. 14 metabolites demonstrated significant changes in HCC patients during follow-up. Campesterol, lysophosphatidylcholine, octadecenoic and octadecadienoic acid, and furoylglycine showed a differential expression in the local ablation vs. palliative care group. High expression of eight metabolites (octadecenoic acid, 2-hydroxybutyrate, myo-inositol, isocitrate, erythronic acid, creatinine, pseudouridine, and erythrol) were associated with poor overall survival. The association between poor OS and octadecenoic acid and creatinine remained statistically significant even after adjusting for tumor burden and LC severity.
    Conclusion: Our findings give promising insides into the metabolic changes during HCC carcinogenesis and provide candidate biomarkers for future studies. Campesterol and furoylglycine in particular were identified as possible biomarkers for HCC progression. Moreover, eight metabolites were detected as predictors for poor overall survival.
    Language English
    Publishing date 2024-04-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 304250-9
    ISSN 1573-2568 ; 0163-2116
    ISSN (online) 1573-2568
    ISSN 0163-2116
    DOI 10.1007/s10620-024-08446-1
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  4. Article ; Online: Analysis of clonogenic growth in vitro.

    Brix, Nikko / Samaga, Daniel / Belka, Claus / Zitzelsberger, Horst / Lauber, Kirsten

    Nature protocols

    2021  Volume 16, Issue 11, Page(s) 4963–4991

    Abstract: The clonogenic assay measures the capacity of single cells to form colonies in vitro. It is widely used to identify and quantify self-renewing mammalian cells derived from in vitro cultures as well as from ex vivo tissue preparations of different origins. ...

    Abstract The clonogenic assay measures the capacity of single cells to form colonies in vitro. It is widely used to identify and quantify self-renewing mammalian cells derived from in vitro cultures as well as from ex vivo tissue preparations of different origins. Varying research questions and the heterogeneous growth requirements of individual cell model systems led to the development of several assay principles and formats that differ with regard to their conceptual setup, 2D or 3D culture conditions, optional cytotoxic treatments and subsequent mathematical analysis. The protocol presented here is based on the initial clonogenic assay protocol as developed by Puck and Marcus more than 60 years ago. It updates and extends the 2006 Nature Protocols article by Franken et al. It discusses different strategies and principles to analyze clonogenic growth in vitro and presents the clonogenic assay in a modular protocol framework enabling a diversity of formats and measures to optimize determination of clonogenic growth parameters. We put particular focus on the phenomenon of cellular cooperation and consideration of how this can affect the mathematical analysis of survival data. This protocol is applicable to any mammalian cell model system from which single-cell suspensions can be prepared and which contains at least a small fraction of cells with self-renewing capacity in vitro. Depending on the cell system used, the entire procedure takes ~2-10 weeks, with a total hands-on time of <20 h per biological replicate.
    MeSH term(s) Models, Biological
    Language English
    Publishing date 2021-10-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2244966-8
    ISSN 1750-2799 ; 1754-2189
    ISSN (online) 1750-2799
    ISSN 1754-2189
    DOI 10.1038/s41596-021-00615-0
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  5. Book ; Online ; Thesis: Validation and functional characterization of a prognostic 4-miRNA signature in Glioblastoma

    Piehlmaier, Daniel [Verfasser] / Zitzelsberger, Horst [Akademischer Betreuer]

    2020  

    Author's details Daniel Piehlmaier ; Betreuer: Horst Zitzelsberger
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language English
    Publisher Universitätsbibliothek der Ludwig-Maximilians-Universität
    Publishing place München
    Document type Book ; Online ; Thesis
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  6. Article ; Online: The clonogenic assay: robustness of plating efficiency-based analysis is strongly compromised by cellular cooperation.

    Brix, Nikko / Samaga, Daniel / Hennel, Roman / Gehr, Katharina / Zitzelsberger, Horst / Lauber, Kirsten

    Radiation oncology (London, England)

    2020  Volume 15, Issue 1, Page(s) 248

    Abstract: Background: The clonogenic assay is a versatile and frequently used tool to quantify reproductive cell survival in vitro. Current state-of-the-art analysis relies on plating efficiency-based calculations which assume a linear correlation between the ... ...

    Abstract Background: The clonogenic assay is a versatile and frequently used tool to quantify reproductive cell survival in vitro. Current state-of-the-art analysis relies on plating efficiency-based calculations which assume a linear correlation between the number of cells seeded and the number of colonies counted. The present study was designed to test the validity of this assumption and to evaluate the robustness of clonogenic survival results obtained.
    Methods: A panel of 50 established cancer cell lines was used for comprehensive evaluation of the clonogenic assay procedure and data analysis. We assessed the performance of plating efficiency-based calculations and examined the influence of critical experimental parameters, such as cell density seeded, assay volume, incubation time, as well as the cell line-intrinsic factor of cellular cooperation by auto-/paracrine stimulation. Our findings were integrated into a novel mathematical approach for the analysis of clonogenic survival data.
    Results: For various cell lines, clonogenic growth behavior failed to be adequately described by a constant plating efficiency, since the density of cells seeded severely influenced the extent and the dynamics of clonogenic growth. This strongly impaired the robustness of survival calculations obtained by the current state-of-the-art method using plating efficiency-based normalization. A novel mathematical approach utilizing power regression and interpolation of matched colony numbers at different irradiation doses applied to the same dataset substantially reduced the impact of cell density on survival results. Cellular cooperation was observed to be responsible for the non-linear clonogenic growth behavior of a relevant number of cell lines and the impairment of survival calculations. With 28/50 cell lines of different tumor entities showing moderate to high degrees of cellular cooperation, this phenomenon was found to be unexpectedly common.
    Conclusions: Our study reveals that plating efficiency-based analysis of clonogenic survival data is profoundly compromised by cellular cooperation resulting in strongly underestimated assay-intrinsic errors in a relevant proportion of established cancer cell lines. This severely questions the use of plating efficiency-based calculations in studies aiming to achieve more than semiquantitative results. The novel approach presented here accounts for the phenomenon of cellular cooperation and allows the extraction of clonogenic survival results with clearly improved robustness.
    MeSH term(s) Cell Communication ; Cell Survival ; Humans ; Tumor Cells, Cultured ; Tumor Stem Cell Assay/methods
    Language English
    Publishing date 2020-10-29
    Publishing country England
    Document type Journal Article
    ISSN 1748-717X
    ISSN (online) 1748-717X
    DOI 10.1186/s13014-020-01697-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: A Novel Subgroup of UCHL1-Related Cancers Is Associated with Genomic Instability and Sensitivity to DNA-Damaging Treatment.

    Burkart, Sebastian / Weusthof, Christopher / Khorani, Karam / Steen, Sonja / Stögbauer, Fabian / Unger, Kristian / Hess, Julia / Zitzelsberger, Horst / Belka, Claus / Kurth, Ina / Hess, Jochen

    Cancers

    2023  Volume 15, Issue 6

    Abstract: Purpose: Identification of molecularly-defined cancer subgroups and targeting tumor-specific vulnerabilities have a strong potential to improve treatment response and patient outcomes but remain an unmet challenge of high clinical relevance, especially ... ...

    Abstract Purpose: Identification of molecularly-defined cancer subgroups and targeting tumor-specific vulnerabilities have a strong potential to improve treatment response and patient outcomes but remain an unmet challenge of high clinical relevance, especially in head and neck squamous cell carcinoma (HNSC).
    Experimental design: We established a UCHL1-related gene set to identify and molecularly characterize a UCHL1-related subgroup within TCGA-HNSC by integrative analysis of multi-omics data. An extreme gradient boosting model was trained on TCGA-HNSC based on GSVA scores for gene sets of the MSigDB to robustly predict UCHL1-related cancers in other solid tumors and cancer cell lines derived thereof. Potential vulnerabilities of UCHL1-related cancer cells were elucidated by an in-silico drug screening approach.
    Results: We established a 497-gene set, which stratified the TCGA-HNSC cohort into distinct subgroups with a UCHL1-related or other phenotype. UCHL1-related HNSC were characterized by higher frequencies of genomic alterations, which was also evident for UCHL1-related cancers of other solid tumors predicted by the classification model. These data indicated an impaired maintenance of genomic integrity and vulnerability for DNA-damaging treatment, which was supported by a favorable prognosis of UCHL1-related tumors after radiotherapy, and a higher sensitivity of UCHL1-related cancer cells to irradiation or DNA-damaging compounds (e.g., Oxaliplatin).
    Conclusion: Our study established UCHL1-related cancers as a novel subgroup across most solid tumor entities with a unique molecular phenotype and DNA-damaging treatment as a specific vulnerability, which requires further proof-of-concept in pre-clinical models and future clinical trials.
    Language English
    Publishing date 2023-03-08
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers15061655
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  8. Article ; Online: DNA-methylation and genomic copy number in primary tumors and corresponding lymph node metastases in prostate cancer from patients with low and high Gleason score.

    Unger, Kristian / Hess, Julia / Link, Vera / Buchner, Alexander / Eze, Chukwuka / Li, Minglun / Stief, Christian / Kirchner, Thomas / Klauschen, Frederick / Zitzelsberger, Horst / Niyazi, Maximilian / Ganswindt, Ute / Schmidt-Hegemann, Nina-Sophie / Belka, Claus

    Clinical and translational radiation oncology

    2023  Volume 39, Page(s) 100586

    Abstract: Purpose: In prostate cancer, the indication to irradiate the pelvic lymphatic pathways in clinical node-negative patients is solely based on clinical nomograms. To define biological risk patterns of lymphatic spread, we studied DNA-methylation and ... ...

    Abstract Purpose: In prostate cancer, the indication to irradiate the pelvic lymphatic pathways in clinical node-negative patients is solely based on clinical nomograms. To define biological risk patterns of lymphatic spread, we studied DNA-methylation and genomic copy number in primary tumors and corresponding lymph nodes metastases.
    Methods/patients: DNA-methylation and genomic copy number profiles of primary tumors (PT) and paired synchronous lymph node metastases (LN) from Gleason Score (GS)-6/7a (n = 20 LN-positive, n = 20 LN-negative) and GS-9/10 patients (LN-positive n = 20) after prostatectomy and lymphonodectomy were analyzed.
    Results: GS-6/7a pN0 PTs and GS-6/7a pN1 PTs differed in histone H3K27me3/H3K9me3 mediated methylation. PTs compared to LNs, in both, GS-6/7a pN1 and GS-9/10 pN1 patients showed large differences in DNA-methylation mediated by histones H3K4me1/2, in addition to copy number changes of chromosomal regions 11q13.1, 14q11.2 and 15q26.1. Between GS-6/7a pN1 and GS-9/10 pN1 patients, methylation levels differed more when comparing LNs than PTs. 16q21-22.1 was specifically lost in GS-9/10 pN0 PTs. Immune system-related pathways characterized the differences between PTs and LNs in both GS-6/7a pN1 and GS-9/10 pN1 patients. Comparing PTs and LKs between GS-6/7a pN1 and GS-9/10 pN1 patients revealed altered transmembrane and G-protein-coupled receptor signaling.
    Conclusions: Our data suggest that progression of prostate cancer, including lymphatic spread, is associated with histone-mediated DNA-methylation and we hypothesize a methylation signature predicting lymphatic spread in GS-6/7a patients from primary tumors. Lymphatic spread in GS-6/7a patients, flanked by DNA-methylation and CNA alterations, appears to be more complex than in GS-9/10 patients, in whom the primary tumors already appear to bear lymph node metastasis-enabling alterations.
    Language English
    Publishing date 2023-01-21
    Publishing country Ireland
    Document type Journal Article
    ISSN 2405-6308
    ISSN (online) 2405-6308
    DOI 10.1016/j.ctro.2023.100586
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  9. Book ; Online ; Thesis: Aufklärung von Markern und deregulierten Netzwerken der strahleninduzierten Mammakarzinogenese durch integrative Analyse von genomischer Kopienzahl, microRNA-, mRNA- und Protein-Expression

    Wilke, Christina Maria [Verfasser] / Zitzelsberger, Horst [Akademischer Betreuer]

    2019  

    Author's details Christina Maria Wilke ; Betreuer: Horst Zitzelsberger
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Universitätsbibliothek der Ludwig-Maximilians-Universität
    Publishing place München
    Document type Book ; Online ; Thesis
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  10. Article ; Online: Metformin Protects against Radiation-Induced Acute Effects by Limiting Senescence of Bronchial-Epithelial Cells.

    Hansel, Christine / Barr, Samantha / Schemann, Alina V / Lauber, Kirsten / Hess, Julia / Unger, Kristian / Zitzelsberger, Horst / Jendrossek, Verena / Klein, Diana

    International journal of molecular sciences

    2021  Volume 22, Issue 13

    Abstract: Radiation-induced damage to normal lung parenchyma remains a dose-limiting factor in thorax-associated radiotherapy (RT). Severe early and late complications with lungs can increase the risk of morbidity in cancer patients after RT. Herein, senescence of ...

    Abstract Radiation-induced damage to normal lung parenchyma remains a dose-limiting factor in thorax-associated radiotherapy (RT). Severe early and late complications with lungs can increase the risk of morbidity in cancer patients after RT. Herein, senescence of lung epithelial cells following RT-induced cellular stress, or more precisely the respective altered secretory profile, the senescence-associated secretory phenotype (SASP), was suggested as a central process for the initiation and progression of pneumonitis and pulmonary fibrosis. We previously reported that abrogation of certain aspects of the secretome of senescent lung cells, in particular, signaling inhibition of the SASP-factor Ccl2/Mcp1 mediated radioprotection especially by limiting endothelial dysfunction. Here, we investigated the therapeutic potential of a combined metformin treatment to protect normal lung tissue from RT-induced senescence and associated lung injury using a preclinical mouse model of radiation-induced pneumopathy. Metformin treatment efficiently limited RT-induced senescence and SASP expression levels, thereby limiting vascular dysfunctions, namely increased vascular permeability associated with increased extravasation of circulating immune and tumor cells early after irradiation (acute effects). Complementary in vitro studies using normal lung epithelial cell lines confirmed the senescence-limiting effect of metformin following RT finally resulting in radioprotection, while fostering RT-induced cellular stress of cultured malignant epithelial cells accounting for radiosensitization. The radioprotective action of metformin for normal lung tissue without simultaneous protection or preferable radiosensitization of tumor tissue might increase tumor control probabilities and survival because higher radiation doses could be used.
    MeSH term(s) Animals ; Bronchi/metabolism ; Bronchi/pathology ; Cellular Senescence/drug effects ; Cellular Senescence/radiation effects ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Metformin/pharmacology ; Mice ; Radiation Injuries, Experimental/metabolism ; Radiation Injuries, Experimental/pathology ; Radiation Injuries, Experimental/prevention & control ; Radiation-Protective Agents/pharmacology
    Chemical Substances Radiation-Protective Agents ; Metformin (9100L32L2N)
    Language English
    Publishing date 2021-06-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22137064
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