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151. Additional file 8: of Integrative analysis of the microRNA-mRNA response to radiochemotherapy in primary head and neck squamous cell carcinoma cells

Author

Summerer, Isolde, Hess, Julia, Pitea, Adriana, Unger, Kristian, Hieber, Ludwig, Selmansberger, Martin, Lauber, Kirsten, and Zitzelsberger, Horst

Subjects
body regions, nervous system, fungi
Abstract

Pathway enrichment analysis of differentially expressed genes in HN1957 after radiochemotherapy treatment. (PDF 66Â kb)

Published
2015
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154. Additional file 6: of Integrative analysis of the microRNA-mRNA response to radiochemotherapy in primary head and neck squamous cell carcinoma cells

Author

Summerer, Isolde, Hess, Julia, Pitea, Adriana, Unger, Kristian, Hieber, Ludwig, Selmansberger, Martin, Lauber, Kirsten, and Zitzelsberger, Horst

Subjects
body regions, nervous system, fungi
Abstract

Significantly deregulated mRNAs in primary HN1957 after in vitro radiochemotherapy treatment. (PDF 146Â kb)

Published
2015
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155. Additional file 7: of Integrative analysis of the microRNA-mRNA response to radiochemotherapy in primary head and neck squamous cell carcinoma cells

Author

Summerer, Isolde, Hess, Julia, Pitea, Adriana, Unger, Kristian, Hieber, Ludwig, Selmansberger, Martin, Lauber, Kirsten, and Zitzelsberger, Horst

Subjects
body regions, nervous system, fungi
Abstract

Significantly deregulated mRNAs in primary HN2092 after in vitro radiochemotherapy treatment. (PDF 143Â kb)

Published
2015
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156. Murine Liver Organoids as a Genetically Flexible System to Study Liver Cancer InVivo and In Vitro.

Author

Saborowski, Anna, Wolff, Katharina, Spielberg, Steffi, Beer, Benedikt, Hartleben, Björn, Erlangga, Zulrahman, Becker, Diana, Dow, Lukas E., Marhenke, Silke, Woller, Norman, Unger, Kristian, Schirmacher, Peter, Manns, Michael P., Marquardt, Jens U., Vogel, Arndt, and Saborowski, Michael

Subjects
LIVER cancer, ORGANOIDS, LABORATORY mice
Abstract

The rising incidence of cholangiocarcinoma (CCA) coupled with a low 5‐year survival rate that remains below 10% delineates the urgent need for more effective treatment strategies. Although several recent studies provided detailed information on the genetic landscape of this fatal malignancy, versatile model systems to functionally dissect the immediate clinical relevance of the identified genetic alterations are still missing. To enhance our understanding of CCA pathophysiology and facilitate rapid functional annotation of putative CCA driver and tumor maintenance genes, we developed a tractable murine CCA model by combining the cyclization recombination (Cre)‐lox system, RNA interference, and clustered regularly interspaced short palindromic repeats/CRISPR associated protein 9 (CRISPR/Cas9) technology with liver organoids, followed by subsequent transplantation into immunocompetent, syngeneic mice. Histologically, resulting tumors displayed cytokeratin 19–positive ductal structures surrounded by a desmoplastic stroma—hallmark features of human CCAs. Despite their initial biliary phenotype in vitro, organoids retained the plasticity to induce a broader differentiation spectrum of primary liver cancers following transplantation into recipient mice, depending on their genetic context. Thus, the organoid system combines the advantage of using nontransformed, premalignant cells to recapitulate liver tumorigenesis as a multistep process, with the advantage of a reproducible and expandable cell culture system that abrogates the need for recurrent isolations of primary cells. Conclusion: Genetically modified liver organoids are able to transform into histologically accurate CCAs. Depending on the oncogenic context, they are also able to give rise to liver cancers that show features of hepatocellular carcinomas. The model can be used to functionally explore candidate cancer genes of primary liver cancers in immunocompetent animals and evaluate novel treatment regimens. Genetically modified liver organoids are able to transform into histologically accurate cholangiocarcinomas. Depending on the oncogenic context, they are also able to give rise to liver cancers that show features of hepatocellular carcinomas. This organoid‐based model can be used to functionally explore candidate cancer genes of primary liver cancers in immunocompetent animals and evaluate novel treatment regimens. [ABSTRACT FROM AUTHOR]

Published
2019
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157. Natural Cubic Spline Regression Modeling Followed by Dynamic Network Reconstruction for the Identification of Radiation-Sensitivity Gene Association Networks from Time-Course Transcriptome Data

Author

Michna, Agata, primary, Braselmann, Herbert, additional, Selmansberger, Martin, additional, Dietz, Anne, additional, Hess, Julia, additional, Gomolka, Maria, additional, Hornhardt, Sabine, additional, Blüthgen, Nils, additional, Zitzelsberger, Horst, additional, and Unger, Kristian, additional

Published
2016
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158. Dual Role of the Adaptive Immune System in Liver Injury and Hepatocellular Carcinoma Development

Author

Endig, Jessica, primary, Buitrago-Molina, Laura Elisa, additional, Marhenke, Silke, additional, Reisinger, Florian, additional, Saborowski, Anna, additional, Schütt, Jutta, additional, Limbourg, Florian, additional, Könecke, Christian, additional, Schreder, Alina, additional, Michael, Alina, additional, Misslitz, Ana Clara, additional, Healy, Marc Eammonn, additional, Geffers, Robert, additional, Clavel, Thomas, additional, Haller, Dirk, additional, Unger, Kristian, additional, Finegold, Milton, additional, Weber, Achim, additional, Manns, Michael P., additional, Longerich, Thomas, additional, Heikenwälder, Mathias, additional, and Vogel, Arndt, additional

Published
2016
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160. A Critical Evaluation of the PAXgene Tissue Fixation System

Author

Mathieson, William, primary, Marcon, Nathalie, additional, Antunes, Laurent, additional, Ashford, David A., additional, Betsou, Fay, additional, Frasquilho, Sonia G., additional, Kofanova, Olga A., additional, McKay, Siobhan C., additional, Pericleous, Stephan, additional, Smith, Colleen, additional, Unger, Kristian M., additional, Zeller, Constanze, additional, and Thomas, Geraldine A., additional

Published
2016
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161. A 4-miRNA signature predicts the therapeutic outcome of glioblastoma

Author

Niyazi, Maximilian, primary, Pitea, Adriana, additional, Mittelbronn, Michel, additional, Steinbach, Joachim, additional, Sticht, Carsten, additional, Zehentmayr, Franz, additional, Piehlmaier, Daniel, additional, Zitzelsberger, Horst, additional, Ganswindt, Ute, additional, Rödel, Claus, additional, Lauber, Kirsten, additional, Belka, Claus, additional, and Unger, Kristian, additional

Published
2016
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162. Depletion of Histone Demethylase Jarid1A Resulting in Histone Hyperacetylation and Radiation Sensitivity Does Not Affect DNA Double-Strand Break Repair

Author

Penterling, Corina, primary, Drexler, Guido A., additional, Böhland, Claudia, additional, Stamp, Ramona, additional, Wilke, Christina, additional, Braselmann, Herbert, additional, Caldwell, Randolph B., additional, Reindl, Judith, additional, Girst, Stefanie, additional, Greubel, Christoph, additional, Siebenwirth, Christian, additional, Mansour, Wael Y., additional, Borgmann, Kerstin, additional, Dollinger, Günther, additional, Unger, Kristian, additional, and Friedl, Anna A., additional

Published
2016
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163. Differential Response and Priming Dose Effect on the Proteome of Human Fibroblast and Stem Cells Induced by Exposure to Low Doses of Ionizing Radiation

Author

Hauptmann, Monika, primary, Haghdoost, Siamak, additional, Gomolka, Maria, additional, Sarioglu, Hakan, additional, Ueffing, Marius, additional, Dietz, Anne, additional, Kulka, Ulrike, additional, Unger, Kristian, additional, Babini, Gabriele, additional, Harms-Ringdahl, Mats, additional, Ottolenghi, Andrea, additional, and Hornhardt, Sabine, additional

Published
2016
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166. Ectopic lymphoid structures function as microniches for tumor progenitor cells in hepatocellular carcinoma

Author

Finkin, Shlomi, primary, Yuan, Detian, additional, Stein, Ilan, additional, Taniguchi, Koji, additional, Weber, Achim, additional, Unger, Kristian, additional, Browning, Jeffrey L, additional, Goossens, Nicolas, additional, Nakagawa, Shigeki, additional, Gunasekaran, Ganesh, additional, Schwartz, Myron E, additional, Kobayashi, Masahiro, additional, Kumada, Hiromitsu, additional, Berger, Michael, additional, Pappo, Orit, additional, Rajewsky, Klaus, additional, Hoshida, Yujin, additional, Karin, Michael, additional, Heikenwalder, Mathias, additional, Ben-Neriah, Yinon, additional, and Pikarsky, Eli, additional

Published
2015
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168. CRISPR/Cas9 somatic multiplex-mutagenesis for high-throughput functional cancer genomics in mice

Author

Weber, Julia, primary, Öllinger, Rupert, additional, Friedrich, Mathias, additional, Ehmer, Ursula, additional, Barenboim, Maxim, additional, Steiger, Katja, additional, Heid, Irina, additional, Mueller, Sebastian, additional, Maresch, Roman, additional, Engleitner, Thomas, additional, Gross, Nina, additional, Geumann, Ulf, additional, Fu, Beiyuan, additional, Segler, Angela, additional, Yuan, Detian, additional, Lange, Sebastian, additional, Strong, Alexander, additional, de la Rosa, Jorge, additional, Esposito, Irene, additional, Liu, Pentao, additional, Cadiñanos, Juan, additional, Vassiliou, George S., additional, Schmid, Roland M., additional, Schneider, Günter, additional, Unger, Kristian, additional, Yang, Fengtang, additional, Braren, Rickmer, additional, Heikenwälder, Mathias, additional, Varela, Ignacio, additional, Saur, Dieter, additional, Bradley, Allan, additional, and Rad, Roland, additional

Published
2015
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169. Molekulare Muster von strahlungsbedingtem Brustkrebs.

Author

Unger, Kristian and Zitzelsberger, Horst

Abstract

Breast cancer is the most prevalent malignant disease in women. Amongst other risk factors such as age, life style, genetic factors and hormone status, exposure to ionizing irradiation is a known risk factor. Markers of radiation-associated breast cancer have been now identified at the DNA-, miRNA- and protein levels providing the starting point for the identification and personalized treatment of secondary, radiation-induced breast cancer. [ABSTRACT FROM AUTHOR]

Published
2019
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170. A genomic copy number signature predicts radiation exposure in post‐Chernobyl breast cancer.

Author

Wilke, Christina M., Braselmann, Herbert, Hess, Julia, Klymenko, Sergiy V., Chumak, Vadim V., Zakhartseva, Liubov M., Bakhanova, Elena V., Walch, Axel K., Selmansberger, Martin, Samaga, Daniel, Weber, Peter, Schneider, Ludmila, Fend, Falko, Bösmüller, Hans C., Zitzelsberger, Horst, and Unger, Kristian

Abstract

Breast cancer is the second leading cause of cancer death among women worldwide and besides life style, age and genetic risk factors, exposure to ionizing radiation is known to increase the risk for breast cancer. Further, DNA copy number alterations (CNAs), which can result from radiation‐induced double‐strand breaks, are frequently occurring in breast cancer cells. We set out to identify a signature of CNAs discriminating breast cancers from radiation‐exposed and non‐exposed female patients. We analyzed resected breast cancer tissues from 68 exposed female Chernobyl clean‐up workers and evacuees and 68 matched non‐exposed control patients for CNAs by array comparative genomic hybridization analysis (aCGH). Using a stepwise forward–backward selection approach a non‐complex CNA signature, that is, less than ten features, was identified in the training data set, which could be subsequently validated in the validation data set (p value < 0.05). The signature consisted of nine copy number regions located on chromosomal bands 7q11.22‐11.23, 7q21.3, 16q24.3, 17q21.31, 20p11.23‐11.21, 1p21.1, 2q35, 2q35, 6p22.2. The signature was independent of any clinical characteristics of the patients. In all, we identified a CNA signature that has the potential to allow identification of radiation‐associated breast cancer at the individual level. [ABSTRACT FROM AUTHOR]

Published
2018
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171. Lifetime study in mice after acute low-dose ionizing radiation: a multifactorial study with special focus on cataract risk.

Author

Dalke, Claudia, Neff, Frauke, Bains, Savneet Kaur, Bright, Scott, Lord, Deborah, Reitmeir, Peter, Rößler, Ute, Samaga, Daniel, Unger, Kristian, Braselmann, Herbert, Wagner, Florian, Greiter, Matthias, Gomolka, Maria, Hornhardt, Sabine, Kunze, Sarah, Kempf, Stefan J., Garrett, Lillian, Hölter, Sabine M., Wurst, Wolfgang, and Rosemann, Michael

Abstract

Because of the increasing application of ionizing radiation in medicine, quantitative data on effects of low-dose radiation are needed to optimize radiation protection, particularly with respect to cataract development. Using mice as mammalian animal model, we applied a single dose of 0, 0.063, 0.125 and 0.5 Gy at 10 weeks of age, determined lens opacities for up to 2 years and compared it with overall survival, cytogenetic alterations and cancer development. The highest dose was significantly associated with increased body weight and reduced survival rate. Chromosomal aberrations in bone marrow cells showed a dose-dependent increase 12 months after irradiation. Pathological screening indicated a dose-dependent risk for several types of tumors. Scheimpflug imaging of the lens revealed a significant dose-dependent effect of 1% of lens opacity. Comparison of different biological end points demonstrated long-term effects of low-dose irradiation for several biological end points. [ABSTRACT FROM AUTHOR]

Published
2018
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172. Expression of mi RNA-26b-5p and its target TRPS1 is associated with radiation exposure in post- Chernobyl breast cancer.

Author

Wilke, Christina M., Hess, Julia, Klymenko, Sergiy V., Chumak, Vadim V., Zakhartseva, Liubov M., Bakhanova, Elena V., Feuchtinger, Annette, Walch, Axel K., Selmansberger, Martin, Braselmann, Herbert, Schneider, Ludmila, Pitea, Adriana, Steinhilber, Julia, Fend, Falko, Bösmüller, Hans C., Zitzelsberger, Horst, and Unger, Kristian

Abstract

Ionizing radiation is a well-recognized risk factor for the development of breast cancer. However, it is unknown whether radiation-specific molecular oncogenic mechanisms exist. We investigated post-Chernobyl breast cancers from radiation-exposed female clean-up workers and nonexposed controls for molecular changes. Radiation-associated alterations identified in the discovery cohort ( n = 38) were subsequently validated in a second cohort ( n = 39). Increased expression of hsa-miR-26b-5p was associated with radiation exposure in both of the cohorts. Moreover, downregulation of the TRPS1 protein, which is a transcriptional target of hsa-miR-26b-5p, was associated with radiation exposure. As TRPS1 overexpression is common in sporadic breast cancer, its observed downregulation in radiation-associated breast cancer warrants clarification of the specific functional role of TRPS1 in the radiation context. For this purpose, the impact of TRPS1 on the transcriptome was characterized in two radiation-transformed breast cell culture models after siRNA-knockdown. Deregulated genes upon TRPS1 knockdown were associated with DNA-repair, cell cycle, mitosis, cell migration, angiogenesis and EMT pathways. Furthermore, we identified the interaction partners of TRPS1 from the transcriptomic correlation networks derived from gene expression data on radiation-transformed breast cell culture models and sporadic breast cancer tissues provided by the TCGA database. The genes correlating with TRPS1 in the radiation-transformed breast cell lines were primarily linked to DNA damage response and chromosome segregation, while the transcriptional interaction partners in the sporadic breast cancers were mostly associated with apoptosis. Thus, upregulation of hsa-miR-26b-5p and downregulation of TRPS1 in radiation-associated breast cancer tissue samples suggests these molecules representing radiation markers in breast cancer. [ABSTRACT FROM AUTHOR]

Published
2018
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173. Platelet GPIbα is a mediator and potential interventional target for NASH and subsequent liver cancer

Author

Malehmir, Mohsen, Pfister, Dominik, Gallage, Suchira, Szydlowska, Marta, Inverso, Donato, Kotsiliti, Elena, Leone, Valentina, Peiseler, Moritz, Surewaard, Bas G. J., Rath, Dominik, Ali, Adnan, Wolf, Monika Julia, Drescher, Hannah, Healy, Marc E., Dauch, Daniel, Kroy, Daniela, Krenkel, Oliver, Kohlhepp, Marlene, Engleitner, Thomas, Olkus, Alexander, Sijmonsma, Tjeerd, Volz, Julia, Deppermann, Carsten, Stegner, David, Helbling, Patrick, Nombela-Arrieta, César, Rafiei, Anahita, Hinterleitner, Martina, Rall, Marcel, Baku, Florian, Borst, Oliver, Wilson, Caroline L., Leslie, Jack, O’Connor, Tracy, Weston, Christopher J., Chauhan, Abhishek, Adams, David H., Sheriff, Lozan, Teijeiro, Ana, Prinz, Marco, Bogeska, Ruzhica, Anstee, Natasha, Bongers, Malte N., Notohamiprodjo, Mike, Geisler, Tobias, Withers, Dominic J., Ware, Jerry, Mann, Derek A., Augustin, Hellmut G., Vegiopoulos, Alexandros, Milsom, Michael D., Rose, Adam J., Lalor, Patricia F., Llovet, Josep M., Pinyol, Roser, Tacke, Frank, Rad, Roland, Matter, Matthias, Djouder, Nabil, Kubes, Paul, Knolle, Percy A., Unger, Kristian, Zender, Lars, Nieswandt, Bernhard, Gawaz, Meinrad, Weber, Achim, and Heikenwalder, Mathias

Abstract

Non-alcoholic fatty liver disease ranges from steatosis to non-alcoholic steatohepatitis (NASH), potentially progressing to cirrhosis and hepatocellular carcinoma (HCC). Here, we show that platelet number, platelet activation and platelet aggregation are increased in NASH but not in steatosis or insulin resistance. Antiplatelet therapy (APT; aspirin/clopidogrel, ticagrelor) but not nonsteroidal anti-inflammatory drug (NSAID) treatment with sulindac prevented NASH and subsequent HCC development. Intravital microscopy showed that liver colonization by platelets depended primarily on Kupffer cells at early and late stages of NASH, involving hyaluronan-CD44 binding. APT reduced intrahepatic platelet accumulation and the frequency of platelet–immune cell interaction, thereby limiting hepatic immune cell trafficking. Consequently, intrahepatic cytokine and chemokine release, macrovesicular steatosis and liver damage were attenuated. Platelet cargo, platelet adhesion and platelet activation but not platelet aggregation were identified as pivotal for NASH and subsequent hepatocarcinogenesis. In particular, platelet-derived GPIbα proved critical for development of NASH and subsequent HCC, independent of its reported cognate ligands vWF, P-selectin or Mac-1, offering a potential target against NASH.

Published
2019
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174. Model Matters: Differences in Orthotopic Rat Hepatocellular Carcinoma Physiology Determine Therapy Response to Sorafenib

Author

Groß, Claudia, primary, Steiger, Katja, additional, Sayyed, Sufyan, additional, Heid, Irina, additional, Feuchtinger, Annette, additional, Walch, Axel, additional, Heß, Julia, additional, Unger, Kristian, additional, Zitzelsberger, Horst, additional, Settles, Marcus, additional, Schlitter, Anna Melissa, additional, Dworniczak, Juliane, additional, Altomonte, Jennifer, additional, Ebert, Oliver, additional, Schwaiger, Markus, additional, Rummeny, Ernst, additional, Steingötter, Andreas, additional, Esposito, Irene, additional, and Braren, Rickmer, additional

Published
2015
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177. Association of Radiation-Induced Genes with Noncancer Chronic Diseases in Mayak Workers Occupationally Exposed to Prolonged Radiation

Author

Abend, Michael, primary, Azizova, Tamara, additional, Müller, Kerstin, additional, Dörr, Harald, additional, Doucha-Senf, Sven, additional, Kreppel, Helmut, additional, Rusinova, Galina, additional, Glazkova, Irina, additional, Vyazovskaya, Natalia, additional, Unger, Kristian, additional, Braselmann, Herbert, additional, and Meineke, Viktor, additional

Published
2015
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178. Metabolic Activation of Intrahepatic CD8+ T Cells and NKT Cells Causes Nonalcoholic Steatohepatitis and Liver Cancer via Cross-Talk with Hepatocytes

Author

Wolf, Monika Julia, primary, Adili, Arlind, additional, Piotrowitz, Kira, additional, Abdullah, Zeinab, additional, Boege, Yannick, additional, Stemmer, Kerstin, additional, Ringelhan, Marc, additional, Simonavicius, Nicole, additional, Egger, Michèle, additional, Wohlleber, Dirk, additional, Lorentzen, Anna, additional, Einer, Claudia, additional, Schulz, Sabine, additional, Clavel, Thomas, additional, Protzer, Ulrike, additional, Thiele, Christoph, additional, Zischka, Hans, additional, Moch, Holger, additional, Tschöp, Matthias, additional, Tumanov, Alexei V., additional, Haller, Dirk, additional, Unger, Kristian, additional, Karin, Michael, additional, Kopf, Manfred, additional, Knolle, Percy, additional, Weber, Achim, additional, and Heikenwalder, Mathias, additional

Published
2014
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180. Genomic amplification of Fanconi anemia complementation group A (FancA) in head and neck squamous cell carcinoma (HNSCC): Cellular mechanisms of radioresistance and clinical relevance.

Author

Hess, Julia, Unger, Kristian, Orth, Michael, Schötz, Ulrike, Schüttrumpf, Lars, Zangen, Verena, Gimenez-Aznar, Igor, Michna, Agata, Schneider, Ludmila, Stamp, Ramona, Selmansberger, Martin, Braselmann, Herbert, Hieber, Ludwig, Drexler, Guido A., Kuger, Sebastian, Klein, Diana, Jendrossek, Verena, Friedl, Anna A., Belka, Claus, and Zitzelsberger, Horst

Subjects
*FANCONI'S anemia, *GENE amplification, *CHEMORADIOTHERAPY, *HEAD & neck cancer, *GENETIC overexpression, *DNA repair, *PROTEIN metabolism, *RNA metabolism, *CELL lines, *CELLULAR aging, *GENES, *GENETIC techniques, *HEAD tumors, *KERATINOCYTES, *MOLECULAR structure, *NECK tumors, *PROGNOSIS, *PROTEINS, *RADIATION, *RNA, *SQUAMOUS cell carcinoma, *TIME, *PHENOTYPES, *TREATMENT effectiveness, *OLIGONUCLEOTIDE arrays, *GENE expression profiling, *KAPLAN-Meier estimator, *GENOTYPES
Abstract

Radio (chemo) therapy is a crucial treatment modality for head and neck squamous cell carcinoma (HNSCC), but relapse is frequent, and the underlying mechanisms remain largely elusive. Therefore, novel biomarkers are urgently needed. Previously, we identified gains on 16q23-24 to be associated with amplification of the Fanconi anemia A (FancA) gene and to correlate with reduced progression-free survival after radiotherapy. Here, we analyzed the effects of FancA on radiation sensitivity in vitro, characterized the underlying mechanisms, and evaluated their clinical relevance. Silencing of FancA expression in HNSCC cell lines with genomic gains on 16q23-24 resulted in significantly impaired clonogenic survival upon irradiation. Conversely, overexpression of FancA in immortalized keratinocytes conferred increased survival accompanied by improved DNA repair, reduced accumulation of chromosomal translocations, but no hyperactivation of the FA/BRCA-pathway. Downregulation of interferon signaling as identified by microarray analyses, enforced irradiation-induced senescence, and elevated production of the senescence-associated secretory phenotype (SASP) appeared to be candidate mechanisms contributing to FancA-mediated radioresistance. Data of the TCGA HNSCC cohort confirmed the association of gains on 16q24.3 with FancA overexpression and impaired overall survival. Importantly, transcriptomic alterations similar to those observed upon FancA overexpression in vitro strengthened the clinical relevance. Overall, FancA amplification and overexpression appear to be crucial for radiotherapeutic failure in HNSCC. [ABSTRACT FROM AUTHOR]

Published
2017
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181. Independent Validation of Candidate Genes Identified after a Whole Genome Screening on Mayak Workers Exposed to Prolonged Occupational Radiation

Author

Abend, Michael, primary, Azizova, Tamara, additional, Müller, Kerstin, additional, Dörr, Harald, additional, Senf, Sven, additional, Kreppel, Helmut, additional, Rusinova, Galina, additional, Glazkova, Irina, additional, Vyazovskaya, Natalia, additional, Unger, Kristian, additional, and Meineke, Viktor, additional

Published
2014
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182. Anterior gradient protein 2 promotes survival, migration and invasion of papillary thyroid carcinoma cells

Author

Di Maro, Gennaro, primary, Salerno, Paolo, additional, Unger, Kristian, additional, Orlandella, Francesca Maria, additional, Monaco, Mario, additional, Chiappetta, Gennaro, additional, Thomas, Gerry, additional, Oczko-Wojciechowska, Malgorzata, additional, Masullo, Mariorosario, additional, Jarzab, Barbara, additional, Santoro, Massimo, additional, and Salvatore, Giuliana, additional

Published
2014
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185. Evolutionary routes and KRASdosage define pancreatic cancer phenotypes

Author

Mueller, Sebastian, Engleitner, Thomas, Maresch, Roman, Zukowska, Magdalena, Lange, Sebastian, Kaltenbacher, Thorsten, Konukiewitz, Björn, Öllinger, Rupert, Zwiebel, Maximilian, Strong, Alex, Yen, Hsi-Yu, Banerjee, Ruby, Louzada, Sandra, Fu, Beiyuan, Seidler, Barbara, Götzfried, Juliana, Schuck, Kathleen, Hassan, Zonera, Arbeiter, Andreas, Schönhuber, Nina, Klein, Sabine, Veltkamp, Christian, Friedrich, Mathias, Rad, Lena, Barenboim, Maxim, Ziegenhain, Christoph, Hess, Julia, Dovey, Oliver M., Eser, Stefan, Parekh, Swati, Constantino-Casas, Fernando, de la Rosa, Jorge, Sierra, Marta I., Fraga, Mario, Mayerle, Julia, Klöppel, Günter, Cadiñanos, Juan, Liu, Pentao, Vassiliou, George, Weichert, Wilko, Steiger, Katja, Enard, Wolfgang, Schmid, Roland M., Yang, Fengtang, Unger, Kristian, Schneider, Günter, Varela, Ignacio, Bradley, Allan, Saur, Dieter, and Rad, Roland

Abstract

The poor correlation of mutational landscapes with phenotypes limits our understanding of the pathogenesis and metastasis of pancreatic ductal adenocarcinoma (PDAC). Here we show that oncogenic dosage-variation has a critical role in PDAC biology and phenotypic diversification. We find an increase in gene dosage of mutant KRASin human PDAC precursors, which drives both early tumorigenesis and metastasis and thus rationalizes early PDAC dissemination. To overcome the limitations posed to gene dosage studies by the stromal richness of PDAC, we have developed large cell culture resources of metastatic mouse PDAC. Integration of cell culture genomes, transcriptomes and tumour phenotypes with functional studies and human data reveals additional widespread effects of oncogenic dosage variation on cell morphology and plasticity, histopathology and clinical outcome, with the highest KrasMUTlevels underlying aggressive undifferentiated phenotypes. We also identify alternative oncogenic gains (Myc, Yap1or Nfkb2), which collaborate with heterozygous KrasMUTin driving tumorigenesis, but have lower metastatic potential. Mechanistically, different oncogenic gains and dosages evolve along distinct evolutionary routes, licensed by defined allelic states and/or combinations of hallmark tumour suppressor alterations (Cdkn2a, Trp53, Tgfβ-pathway). Thus, evolutionary constraints and contingencies direct oncogenic dosage gain and variation along defined routes to drive the early progression of PDAC and shape its downstream biology. Our study uncovers universal principles of Ras-driven oncogenesis that have potential relevance beyond pancreatic cancer.

Published
2018
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187. RIP3 Inhibits Inflammatory Hepatocarcinogenesis but Promotes Cholestasis by Controlling Caspase-8- and JNK-Dependent Compensatory Cell Proliferation

Author

Vucur, Mihael, primary, Reisinger, Florian, additional, Gautheron, Jérémie, additional, Janssen, Joern, additional, Roderburg, Christoph, additional, Cardenas, David Vargas, additional, Kreggenwinkel, Karina, additional, Koppe, Christiane, additional, Hammerich, Linda, additional, Hakem, Razq, additional, Unger, Kristian, additional, Weber, Achim, additional, Gassler, Nikolaus, additional, Luedde, Mark, additional, Frey, Norbert, additional, Neumann, Ulf Peter, additional, Tacke, Frank, additional, Trautwein, Christian, additional, Heikenwalder, Mathias, additional, and Luedde, Tom, additional

Published
2013
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189. Novel candidate genes of thyroid tumourigenesis identified in Trk-T1 transgenic mice

Author

Heiliger, Katrin-Janine, primary, Hess, Julia, additional, Vitagliano, Donata, additional, Salerno, Paolo, additional, Braselmann, Herbert, additional, Salvatore, Giuliana, additional, Ugolini, Clara, additional, Summerer, Isolde, additional, Bogdanova, Tatjana, additional, Unger, Kristian, additional, Thomas, Gerry, additional, Santoro, Massimo, additional, and Zitzelsberger, Horst, additional

Published
2012
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190. S100-A10, thioredoxin, and S100-A6 as biomarkers of papillary thyroid carcinoma with lymph node metastasis identified by MALDI Imaging

Author

Nipp, Martin, primary, Elsner, Mareike, additional, Balluff, Benjamin, additional, Meding, Stephan, additional, Sarioglu, Hakan, additional, Ueffing, Marius, additional, Rauser, Sandra, additional, Unger, Kristian, additional, Höfler, Heinz, additional, Walch, Axel, additional, and Zitzelsberger, Horst, additional

Published
2011
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193. Novel gene rearrangements in transformed breast cells identified by high-resolution breakpoint analysis of chromosomal aberrations

Author

Unger, Kristian, primary, Wienberg, Johannes, additional, Riches, Andrew, additional, Hieber, Ludwig, additional, Walch, Axel, additional, Brown, Andreas, additional, O'Brien, Patricia C M, additional, Briscoe, Cäcilia, additional, Gray, Lindsey, additional, Rodriguez, Elke, additional, Jackl, Gerhard, additional, Knijnenburg, Jeroen, additional, Tallini, Giovanni, additional, Ferguson-Smith, Malcolm, additional, and Zitzelsberger, Horst, additional

Published
2010
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194. High resolution array-CGH analysis of single cells

Author

Fiegler, Heike, primary, Geigl, Jochen B., additional, Langer, Sabine, additional, Rigler, Diane, additional, Porter, Keith, additional, Unger, Kristian, additional, Carter, Nigel P., additional, and Speicher, Michael R., additional

Published
2006
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197. Heterogeneity in the Distribution ofRET/PTCRearrangements within Individual Post-Chernobyl Papillary Thyroid Carcinomas

Author

Unger, Kristian, primary, Zitzelsberger, Horst, additional, Salvatore, Giuliana, additional, Santoro, Massimo, additional, Bogdanova, Tatjana, additional, Braselmann, Herbert, additional, Kastner, Peter, additional, Zurnadzhy, Lyudmilla, additional, Tronko, Nikolay, additional, Hutzler, Peter, additional, and Thomas, Gerry, additional

Published
2004
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