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21 results on '"Melcher, Viktoria"'

2. Mitochondrial DNA mutations in Medulloblastoma

Author

Funke, Viktoria L. E., Sandmann, Sarah, Melcher, Viktoria, Seggewiss, Jochen, Horvath, Judit, Jäger, Natalie, Kool, Marcel, Jones, David T. W., Pfister, Stefan M., Milde, Till, Rutkowski, Stefan, Mynarek, Martin, Varghese, Julian, Sträter, Ronald, Rust, Stephan, Seelhöfer, Anja, Reunert, Janine, Fiedler, Barbara, Schüller, Ulrich, Marquardt, Thorsten, and Kerl, Kornelius

Published
2023
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3. Single-cell transcriptomics identifies potential cells of origin of MYC rhabdoid tumors

Author

Graf, Monika, Interlandi, Marta, Moreno, Natalia, Holdhof, Dörthe, Göbel, Carolin, Melcher, Viktoria, Mertins, Julius, Albert, Thomas K., Kastrati, Dennis, Alfert, Amelie, Holsten, Till, de Faria, Flavia, Meisterernst, Michael, Rossig, Claudia, Warmuth-Metz, Monika, Nowak, Johannes, Meyer zu Hörste, Gerd, Mayère, Chloe, Nef, Serge, Johann, Pascal, Frühwald, Michael C., Dugas, Martin, Schüller, Ulrich, and Kerl, Kornelius

Published
2022
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4. Additional file 1 of Group-specific cellular metabolism in Medulloblastoma

Author

Funke, Viktoria L. E., Walter, Carolin, Melcher, Viktoria, Wei, Lanying, Sandmann, Sarah, Hotfilder, Marc, Varghese, Julian, Jäger, Natalie, Kool, Marcel, Jones, David T. W., Pfister, Stefan M., Milde, Till, Mynarek, Martin, Rutkowski, Stefan, Seggewiss, Jochen, Jeising, Daniela, de Faria, Flavia W., Marquardt, Thorsten, Albert, Thomas K., Schüller, Ulrich, and Kerl, Kornelius

Abstract

Additional file 1: Supplementary materials. Supplementary materials include supplementary methods, references and the Supplementary Figures S1–S15.

Published
2023
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5. Group-specific cellular metabolism in Medulloblastoma.

Author

Funke, Viktoria L. E., Walter, Carolin, Melcher, Viktoria, Wei, Lanying, Sandmann, Sarah, Hotfilder, Marc, Varghese, Julian, Jäger, Natalie, Kool, Marcel, Jones, David T. W., Pfister, Stefan M., Milde, Till, Mynarek, Martin, Rutkowski, Stefan, Seggewiss, Jochen, Jeising, Daniela, de Faria, Flavia W., Marquardt, Thorsten, Albert, Thomas K., and Schüller, Ulrich

Subjects
MEDULLOBLASTOMA, GENE expression, INOSITOL phosphates, PHOSPHATE metabolism, REGULATOR genes
Abstract

Background: Cancer metabolism influences multiple aspects of tumorigenesis and causes diversity across malignancies. Although comprehensive research has extended our knowledge of molecular subgroups in medulloblastoma (MB), discrete analysis of metabolic heterogeneity is currently lacking. This study seeks to improve our understanding of metabolic phenotypes in MB and their impact on patients' outcomes. Methods: Data from four independent MB cohorts encompassing 1,288 patients were analysed. We explored metabolic characteristics of 902 patients (ICGC and MAGIC cohorts) on bulk RNA level. Moreover, data from 491 patients (ICGC cohort) were searched for DNA alterations in genes regulating cell metabolism. To determine the role of intratumoral metabolic differences, we examined single-cell RNA-sequencing (scRNA-seq) data from 34 additional patients. Findings on metabolic heterogeneity were correlated to clinical data. Results: Established MB groups exhibit substantial differences in metabolic gene expression. By employing unsupervised analyses, we identified three clusters of group 3 and 4 samples with distinct metabolic features in ICGC and MAGIC cohorts. Analysis of scRNA-seq data confirmed our results of intertumoral heterogeneity underlying the according differences in metabolic gene expression. On DNA level, we discovered clear associations between altered regulatory genes involved in MB development and lipid metabolism. Additionally, we determined the prognostic value of metabolic gene expression in MB and showed that expression of genes involved in metabolism of inositol phosphates and nucleotides correlates with patient survival. Conclusion: Our research underlines the biological and clinical relevance of metabolic alterations in MB. Thus, distinct metabolic signatures presented here might be the first step towards future metabolism-targeted therapeutic options. [ABSTRACT FROM AUTHOR]

Published
2023
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7. ETMR-05. Single-cell transcriptomics of ETMR reveals developmental cellular programs and tumor-pericyte communications in the microenvironment

Author

de Faria, Flavia W, primary, Walter, Carolin, additional, Interlandi, Marta, additional, Melcher, Viktoria, additional, Riedel, Nicole, additional, Graf, Monika, additional, Moreno, Natalia, additional, Schoof, Melanie, additional, Holdhof, Dörthe, additional, Thomas, Christian, additional, Frühwald, Michael C, additional, Maerkl, Bruno, additional, Ho, Ben, additional, Sandmann, Sarah, additional, Varghese, Julian, additional, Ebinger, Martin, additional, Schuhmann, Martin, additional, Canak, Aysegül, additional, Huang, Annie, additional, Schüller, Ulrich, additional, Albert, Thomas K, additional, and Kerl, Kornelius, additional

Published
2022
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8. ATRT-16. Mechanisms of myeloid cell-induced resistance in AT/RT

Author

Disch, Alina, primary, Melcher, Viktoria, additional, Walter, Carolin, additional, Interlandi, Marta, additional, Moreno, Natalia, additional, de Faria, Flavia W, additional, Graf, Monika, additional, Hasselblatt, Martin, additional, Albert, Thomas K, additional, and Kerl, Kornelius, additional

Published
2022
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9. OTHR-34. Identifying mechanisms of microglia-tumor cell interactions in retinoblastoma

Author

Pohlmann, Anike, primary, Gerling, Teresa, additional, Walter, Carolin, additional, Melcher, Viktoria, additional, de Faria, Flavia W, additional, Disch, Alina, additional, Kanber, Deniz, additional, Wöstefeld, Julia, additional, Steenpass, Laura, additional, Lohmann, Dietmar, additional, Ryl, Tatsiana, additional, Riedel, Nicole, additional, Ketteler, Petra, additional, Schönberger, Stefan, additional, Ting, Saskia, additional, Bedzhov, Ivan, additional, Kiefer, Tobias, additional, Lever, Mael, additional, Schlüter, Sabrina, additional, Biewald, Eva, additional, Bechrakis, Nikolaos, additional, Albert, Thomas K, additional, and Kerl, Kornelius, additional

Published
2022
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10. ATRT-15. Primordial germ cells identified as one potential cell of origin of MYC rhabdoid tumors

Author

Graf, Monika, primary, Interlandi, Marta, additional, Moreno, Natalia, additional, Roy, Rajanya, additional, Holdhof, Dörthe, additional, Göbel, Carolin, additional, Melcher, Viktoria, additional, Mertins, Julius, additional, Albert, Thomas K, additional, Kastrati, Dennis, additional, Alfert, Amelie, additional, Holsten, Till, additional, de Faria, Flavia, additional, Meisterernst, Michael, additional, Rossig, Claudia, additional, Warmuth-Metz, Monika, additional, Nowak, Johannes, additional, Hörste, Gerd Meyer zu, additional, Mayère, Chloe, additional, Nef, Serge, additional, Johann, Pascal, additional, Frühwald, Michael C, additional, Dugas, Martin, additional, Schüller, Ulrich, additional, and Kerl, Kornelius, additional

Published
2022
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13. Single-cell transcriptomics identifies potential cells of origin of MYC rhabdoid tumors

Author

Graf, Monika, Interlandi, Marta, Moreno, Natalia, Holdhof, Dörthe, Göbel, Carolin, Melcher, Viktoria, Mertins, Julius, Albert, Thomas K., Kastrati, Dennis, Alfert, Amelie, Holsten, Till, de Faria, Flavia, Meisterernst, Michael, Rossig, Claudia, Warmuth-Metz, Monika, Nowak, Johannes, Meyer zu Hörste, Gerd, Mayère, Chloe, Nef, Serge, Johann, Pascal, Frühwald, Michael C., Dugas, Martin, Schüller, Ulrich, and Kerl, Kornelius

Subjects
Mice, Germ Cells, Animals, Humans, ddc:610, SMARCB1 Protein, Single-Cell Analysis, Transcriptome, Rhabdoid Tumor
Abstract

Rhabdoid tumors (RT) are rare and highly aggressive pediatric neoplasms. Their epigenetically-driven intertumoral heterogeneity is well described; however, the cellular origin of RT remains an enigma. Here, we establish and characterize different genetically engineered mouse models driven under the control of distinct promoters and being active in early progenitor cell types with diverse embryonic onsets. From all models only Sox2-positive progenitor cells give rise to murine RT. Using single-cell analyses, we identify distinct cells of origin for the SHH and MYC subgroups of RT, rooting in early stages of embryogenesis. Intra- and extracranial MYC tumors harbor common genetic programs and potentially originate from fetal primordial germ cells (PGCs). Using PGC specific Smarcb1 knockout mouse models we validate that MYC RT originate from these progenitor cells. We uncover an epigenetic imbalance in MYC tumors compared to PGCs being sustained by epigenetically-driven subpopulations. Importantly, treatments with the DNA demethylating agent decitabine successfully impair tumor growth in vitro and in vivo. In summary, our work sheds light on the origin of RT and supports the clinical relevance of DNA methyltransferase inhibitors against this disease.

Published
2020

15. ATRT-13. DIFFERENT CELLS OF ORIGIN PAVE THE WAY FOR MOLECULAR HETEROGENEITY IN RHABDOID TUMORS

Author

Graf, Monika, primary, Interlandi, Marta, additional, Moreno, Natalia, additional, Holdhof, Dörthe, additional, Melcher, Viktoria, additional, Kastrati, Dennis, additional, zu Hörste, Gerd Meyer, additional, Dugas, Martin, additional, Frühwald, Michael C, additional, Albert, Thomas K, additional, Schüller, Ulrich, additional, and Kerl, Kornelius, additional

Published
2020
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16. ATRT-14. MACROPHAGE-TUMOR CELL INTERACTION PROMOTES ATRT PROGRESSION AND CHEMORESISTANCE

Author

Melcher, Viktoria, primary, Graf, Monika, additional, Interlandi, Marta, additional, Moreno, Natalia, additional, de Faria, Flavia W, additional, Kim, Su Na, additional, Kastrati, Dennis, additional, Korbanka, Sonja, additional, Alfert, Amelie, additional, Gerß, Joachim, additional, zu Hörste, Gerd Meyer, additional, Hartmann, Wolfgang, additional, Frühwald, Michael C, additional, Dugas, Martin, additional, Schüller, Ulrich, additional, Hasselblatt, Martin, additional, Albert, Thomas K, additional, and Kerl, Kornelius, additional

Published
2020
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17. An extracellular vesicle-related gene expression signature identifies high-risk patients in medulloblastoma

Author

Albert, Thomas K, primary, Interlandi, Marta, additional, Sill, Martin, additional, Graf, Monika, additional, Moreno, Natalia, additional, Menck, Kerstin, additional, Rohlmann, Astrid, additional, Melcher, Viktoria, additional, Korbanka, Sonja, additional, Meyer zu Hörste, Gerd, additional, Lautwein, Tobias, additional, Frühwald, Michael C, additional, Krebs, Christian F, additional, Holdhof, Dörthe, additional, Schoof, Melanie, additional, Bleckmann, Annalen, additional, Missler, Markus, additional, Dugas, Martin, additional, Schüller, Ulrich, additional, Jäger, Natalie, additional, Pfister, Stefan M, additional, and Kerl, Kornelius, additional

Published
2020
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18. Macrophage-tumor cell interaction promotes ATRT progression and chemoresistance

Author

Melcher, Viktoria, primary, Graf, Monika, additional, Interlandi, Marta, additional, Moreno, Natalia, additional, de Faria, Flavia W., additional, Kim, Su Na, additional, Kastrati, Dennis, additional, Korbanka, Sonja, additional, Alfert, Amelie, additional, Gerß, Joachim, additional, Meyer zu Hörste, Gerd, additional, Hartmann, Wolfgang, additional, Frühwald, Michael C., additional, Dugas, Martin, additional, Schüller, Ulrich, additional, Hasselblatt, Martin, additional, Albert, Thomas K., additional, and Kerl, Kornelius, additional

Published
2019
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19. An extracellular vesicle-related gene expression signature identifies high-risk patients in medulloblastoma.

Author

Albert, Thomas K, Interlandi, Marta, Sill, Martin, Graf, Monika, Moreno, Natalia, Menck, Kerstin, Rohlmann, Astrid, Melcher, Viktoria, Korbanka, Sonja, Hörste, Gerd Meyer zu, Lautwein, Tobias, Frühwald, Michael C, Krebs, Christian F, Holdhof, Dörthe, Schoof, Melanie, Bleckmann, Annalen, Missler, Markus, Dugas, Martin, Schüller, Ulrich, and Jäger, Natalie

Published
2021
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20. Macrophage-tumor cell interaction promotes ATRT progression and chemoresistance.

Author

Melcher, Viktoria, Graf, Monika, Interlandi, Marta, Moreno, Natalia, de Faria, Flavia W., Kim, Su Na, Kastrati, Dennis, Korbanka, Sonja, Alfert, Amelie, Gerß, Joachim, Meyer zu Hörste, Gerd, Hartmann, Wolfgang, Frühwald, Michael C., Dugas, Martin, Schüller, Ulrich, Hasselblatt, Martin, Albert, Thomas K., and Kerl, Kornelius

Subjects
*DRUG resistance in cancer cells, *RNA sequencing, *CELL communication, *TUMOR microenvironment, *CELLS, *MACROPHAGES
Abstract

Atypical teratoid/rhabdoid tumors (ATRT) are known for their heterogeneity concerning pathophysiology and outcome. However, predictive factors within distinct subgroups still need to be uncovered. Using multiplex immunofluorescent staining and single-cell RNA sequencing we unraveled distinct compositions of the immunological tumor microenvironment (TME) across ATRT subgroups. CD68+ cells predominantly infiltrate ATRT-SHH and ATRT-MYC and are a negative prognostic factor for patients' survival. Within the murine ATRT-MYC and ATRT-SHH TME, Cd68+ macrophages are core to intercellular communication with tumor cells. In ATRT-MYC distinct tumor cell phenotypes express macrophage marker genes. These cells are involved in the acquisition of chemotherapy resistance in our relapse xenograft mouse model. In conclusion, the tumor cell-macrophage interaction contributes to ATRT-MYC heterogeneity and potentially to tumor recurrence. [ABSTRACT FROM AUTHOR]

Published
2020
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21. ATRT-07. MURINE SOX2-POSITIVE EARLY PRECURSOR CELLS GIVE RISE TO RHABDOID TUMORS WITH FEATURES OF THE HUMAN ATRT-MYC GROUP

Author

Galarza, Natalia Moreno, primary, Holdhof, Dörthe, additional, Interlandi, Marta, additional, Melcher, Viktoria, additional, Graf, Monika, additional, Kastrati, Dennis, additional, Meisterernst, Michael, additional, Johann, Pascal, additional, Kool, Marcel, additional, Frühwald, Michael, additional, Schüller, Ulrich, additional, and Kerl, Kornelius, additional

Published
2018
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