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2. Roflumilast inhibits tumor growth and migration in STK11/LKB1 deficient pancreatic cancer

Author

Zhang, Shuman, Yun, Duo, Yang, Hao, Eckstein, Markus, Elbait, Gihan Daw, Zhou, Yaxing, Lu, Yanxi, Yang, Hai, Zhang, Jinping, Dörflein, Isabella, Britzen-Laurent, Nathalie, Pfeffer, Susanne, Stemmler, Marc P., Dahl, Andreas, Mukhopadhyay, Debabrata, Chang, David, He, Hang, Zeng, Siyuan, Lan, Bin, Frey, Benjamin, Hampel, Chuanpit, Lentsch, Eva, Gollavilli, Paradesi Naidu, Büttner, Christian, Ekici, Arif B., Biankin, Andrew, Schneider-Stock, Regine, Ceppi, Paolo, Grützmann, Robert, and Pilarsky, Christian

Published
2024
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4. Mutated IKZF1 is an independent marker of adverse risk in acute myeloid leukemia

Author

Eckardt, Jan-Niklas, Stasik, Sebastian, Röllig, Christoph, Petzold, Andreas, Sauer, Tim, Scholl, Sebastian, Hochhaus, Andreas, Crysandt, Martina, Brümmendorf, Tim H., Naumann, Ralph, Steffen, Björn, Kunzmann, Volker, Einsele, Hermann, Schaich, Markus, Burchert, Andreas, Neubauer, Andreas, Schäfer-Eckart, Kerstin, Schliemann, Christoph, Krause, Stefan W., Herbst, Regina, Hänel, Mathias, Hanoun, Maher, Kaiser, Ulrich, Kaufmann, Martin, Rácil, Zdenek, Mayer, Jiri, Oelschlägel, Uta, Berdel, Wolfgang E., Ehninger, Gerhard, Serve, Hubert, Müller-Tidow, Carsten, Platzbecker, Uwe, Baldus, Claudia D., Dahl, Andreas, Schetelig, Johannes, Bornhäuser, Martin, Middeke, Jan Moritz, and Thiede, Christian

Published
2023
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5. Museomics help resolving the phylogeny of snowfinches (Aves, Passeridae, Montifringilla and allies)

Author

Islam, Safiqul, Peart, Claire, Kehlmaier, Christian, Sun, Yue-Hua, Lei, Fumin, Dahl, Andreas, Klemroth, Sylvia, Alexopoulou, Dimitra, del Mar Delgado, Maria, Laiolo, Paola, Carlos Illera, Juan, Dirren, Sebastian, Hille, Sabine, Lkhagvasuren, Davaa, Töpfer, Till, Kaiser, Martin, Gebauer, Axel, Martens, Jochen, Paetzold, Claudia, and Päckert, Martin

Published
2024
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19. Targeting cardiomyocyte ADAM10 ectodomain shedding promotes survival early after myocardial infarction

Author

Klapproth, Erik, Witt, Anke, Klose, Pauline, Wiedemann, Johanna, Vavilthota, Nikitha, Künzel, Stephan R., Kämmerer, Susanne, Günscht, Mario, Sprott, David, Lesche, Mathias, Rost, Fabian, Dahl, Andreas, Rauch, Erik, Kattner, Lars, Weber, Silvio, Mirtschink, Peter, Kopaliani, Irakli, Guan, Kaomei, Lorenz, Kristina, Saftig, Paul, Wagner, Michael, and El-Armouche, Ali

Published
2022
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21. Multi-omics profiling of living human pancreatic islet donors reveals heterogeneous beta cell trajectories towards type 2 diabetes

Author

Wigger, Leonore, Barovic, Marko, Brunner, Andreas-David, Marzetta, Flavia, Schöniger, Eyke, Mehl, Florence, Kipke, Nicole, Friedland, Daniela, Burdet, Frederic, Kessler, Camille, Lesche, Mathias, Thorens, Bernard, Bonifacio, Ezio, Legido-Quigley, Cristina, Barbier Saint Hilaire, Pierre, Delerive, Philippe, Dahl, Andreas, Klose, Christian, Gerl, Mathias J., Simons, Kai, Aust, Daniela, Weitz, Jürgen, Distler, Marius, Schulte, Anke M., Mann, Matthias, Ibberson, Mark, and Solimena, Michele

Published
2021
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25. Individual differences in internalizing symptoms in late childhood: A variance decomposition into cortical thickness, genetic and environmental differences.

Author

Tandberg, Anneli D., Dahl, Andreas, Norbom, Linn B., Westlye, Lars T., Ystrom, Eivind, Tamnes, Christian K., and Eilertsen, Espen M.

Abstract

Research Highlights The brain undergoes extensive development during late childhood and early adolescence. Cortical thinning is a prominent feature of this development, and some researchers have suggested that differences in cortical thickness may be related to internalizing symptoms, which typically increase during the same period. However, research has yielded inconclusive results. We utilized a new method that estimates the combined effect of individual differences in vertex‐wise cortical thickness on internalizing symptoms. This approach allows for many small effects to be distributed across the cortex and avoids the necessity of correcting for multiple tests. Using a sample of 8763 children aged 8.9 to 11.1 from the ABCD study, we decomposed the total variation in caregiver‐reported internalizing symptoms into differences in cortical thickness, additive genetics, and shared family environmental factors and unique environmental factors. Our results indicated that individual differences in cortical thickness accounted for less than 0.5% of the variation in internalizing symptoms. In contrast, the analysis revealed a substantial effect of additive genetics and family environmental factors on the different components of internalizing symptoms, ranging from 06% to 48% and from 0% to 34%, respectively. Overall, while this study found a minimal association between cortical thickness and internalizing symptoms, additive genetics, and familial environmental factors appear to be of importance for describing differences in internalizing symptoms in late childhood. We utilized a new method for modelling the total contribution of vertex‐wise individual differences in cortical thickness to internalizing symptoms in late childhood. The total contribution of individual differences in cortical thickness accounted for <0.5% of the variance in internalizing symptoms. Additive genetics and shared family environmental variation accounted for 17% and 34% of the variance in internalizing symptoms, respectively. Our results suggest that cortical thickness is not an important indicator for internalizing symptoms in childhood, whereas genetic and environmental differences have a substantial impact. [ABSTRACT FROM AUTHOR]

Published
2024
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31. BRAF and MEK inhibitor combinations induce potent molecular and immunological effects in NRAS‐mutant melanoma cells: Insights into mode of action and resistance mechanisms.

Author

Dinter, Lisa, Karitzky, Paula C., Schulz, Alexander, Wurm, Alexander A., Mehnert, Marie‐Christin, Sergon, Mildred, Tunger, Antje, Lesche, Mathias, Wehner, Rebekka, Müller, Anja, Käubler, Theresa, Niessner, Heike, Dahl, Andreas, Beissert, Stefan, Schmitz, Marc, Meier, Friedegund, Seliger, Barbara, and Westphal, Dana

Subjects
MITOGEN-activated protein kinases, BRAF genes, MELANOMA, PROTEIN kinases, IPILIMUMAB, GENE expression
Abstract

About 25% of melanoma harbor activating NRAS mutations, which are associated with aggressive disease therefore requiring a rapid antitumor intervention. However, no efficient targeted therapy options are currently available for patients with NRAS‐mutant melanoma. MEK inhibitors (MEKi) appear to display a moderate antitumor activity and also immunological effects in NRAS‐mutant melanoma, providing an ideal backbone for combination treatments. In our study, the MEKi binimetinib, cobimetinib and trametinib combined with the BRAF inhibitors (BRAFi) encorafenib, vemurafenib and dabrafenib were investigated for their ability to inhibit proliferation, induce apoptosis and alter the expression of immune modulatory molecules in sensitive NRAS‐mutant melanoma cells using two‐ and three‐dimensional cell culture models as well as RNA sequencing analyses. Furthermore, NRAS‐mutant melanoma cells resistant to the three BRAFi/MEKi combinations were established to characterize the mechanisms contributing to their resistance. All BRAFi induced a stress response in the sensitive NRAS‐mutant melanoma cells thereby significantly enhancing the antiproliferative and proapoptotic activity of the MEKi analyzed. Furthermore, BRAFi/MEKi combinations upregulated immune relevant molecules, such as ICOS‐L, components of antigen‐presenting machinery and the "don't eat me signal" molecule CD47 in the melanoma cells. The BRAFi/MEKi‐resistant, NRAS‐mutant melanoma cells counteracted the molecular and immunological effects of BRAFi/MEKi by upregulating downstream mitogen‐activated protein kinase pathway molecules, inhibiting apoptosis and promoting immune escape mechanisms. Together, our study reveals potent molecular and immunological effects of BRAFi/MEKi in sensitive NRAS‐mutant melanoma cells that may be exploited in new combinational treatment strategies for patients with NRAS‐mutant melanoma. [ABSTRACT FROM AUTHOR]

Published
2024
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32. Parental education and income are linked to offspring cortical brain structure and psychopathology at 9–11 years.

Author

Norbom, Linn B., Rokicki, Jaroslav, Eilertsen, Espen M., Wiker, Thea, Hanson, Jamie, Dahl, Andreas, Alnæs, Dag, Fernández‐Cabello, Sara, Beck, Dani, Agartz, Ingrid, Andreassen, Ole A., Westlye, Lars T., and Tamnes, Christian K.

Subjects
BRAIN anatomy, INCOME, PATHOLOGICAL psychology, INDEPENDENT component analysis, POOR families
Abstract

Background: A child's socioeconomic environment can shape central aspects of their life, including vulnerability to mental disorders. Negative environmental influences in youth may interfere with the extensive and dynamic brain development occurring at this time. Indeed, there are numerous yet diverging reports of associations between parental socioeconomic status (SES) and child cortical brain morphometry. Most of these studies have used single metric‐ or unimodal analyses of standard cortical morphometry that downplay the probable scenario where numerous biological pathways in sum account for SES‐related cortical differences in youth. Methods: To comprehensively capture such variability, using data from 9758 children aged 8.9–11.1 years from the ABCD Study®, we employed linked independent component analysis (LICA) and fused vertex‐wise cortical thickness, surface area, curvature and grey‐/white‐matter contrast (GWC). LICA revealed 70 uni‐ and multimodal components. We then assessed the linear relationships between parental education, parental income and each of the cortical components, controlling for age, sex, genetic ancestry, and family relatedness. We also assessed whether cortical structure moderated the negative relationships between parental SES and child general psychopathology. Results: Parental education and income were both associated with larger surface area and higher GWC globally, in addition to local increases in surface area and to a lesser extent bidirectional GWC and cortical thickness patterns. The negative relation between parental income and child psychopathology were attenuated in children with a multimodal pattern of larger frontal‐ and smaller occipital surface area, and lower medial occipital thickness and GWC. Conclusion: Structural brain MRI is sensitive to SES diversity in childhood, with GWC emerging as a particularly relevant marker together with surface area. In low‐income families, having a more developed cortex across MRI metrics, appears beneficial for mental health. [ABSTRACT FROM AUTHOR]

Published
2024
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33. CD38 promotes hematopoietic stem cell dormancy.

Author

Ibneeva, Liliia, Singh, Sumeet Pal, Sinha, Anupam, Eski, Sema Elif, Wehner, Rebekka, Rupp, Luise, Kovtun, Iryna, Pérez-Valencia, Juan Alberto, Gerbaulet, Alexander, Reinhardt, Susanne, Wobus, Manja, von Bonin, Malte, Sancho, Jaime, Lund, Frances, Dahl, Andreas, Schmitz, Marc, Bornhäuser, Martin, Chavakis, Triantafyllos, Wielockx, Ben, and Grinenko, Tatyana

Subjects
HEMATOPOIETIC stem cells, CD38 antigen, ADENOSINE diphosphate ribose, STEM cell transplantation, TRANSCRIPTION factors
Abstract

A subpopulation of deeply quiescent, so-called dormant hematopoietic stem cells (dHSCs) resides at the top of the hematopoietic hierarchy and serves as a reserve pool for HSCs. The state of dormancy protects the HSC pool from exhaustion throughout life; however, excessive dormancy may prevent an efficient response to hematological stresses. Despite the significance of dHSCs, the mechanisms maintaining their dormancy remain elusive. Here, we identify CD38 as a novel and broadly applicable surface marker for the enrichment of murine dHSCs. We demonstrate that cyclic adenosine diphosphate ribose (cADPR), the product of CD38 cyclase activity, regulates the expression of the transcription factor c-Fos by increasing the release of Ca2+ from the endoplasmic reticulum (ER). Subsequently, we uncover that c-Fos induces the expression of the cell cycle inhibitor p57Kip2 to drive HSC dormancy. Moreover, we found that CD38 ecto-enzymatic activity at the neighboring CD38-positive cells can promote human HSC quiescence. Together, CD38/cADPR/Ca2+/c-Fos/p57Kip2 axis maintains HSC dormancy. Pharmacological manipulations of this pathway can provide new strategies to improve the success of stem cell transplantation and blood regeneration after injury or disease. Dormant hematopoietic stem cells (dHSC) represent a stem cell reserve that is important for hematopoiesis throughout life. In this study, CD38 is identified as a surface marker and novel regulator of mouse HSCs that promotes their dormancy. Interestingly, while human HSCs lack CD38 expression, CD38 expression in neighboring cells similarly promotes human HSC quiescence. [ABSTRACT FROM AUTHOR]

Published
2024
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40. Systems biology of the IMIDIA biobank from organ donors and pancreatectomised patients defines a novel transcriptomic signature of islets from individuals with type 2 diabetes

Author

Solimena, Michele, Schulte, Anke M., Marselli, Lorella, Ehehalt, Florian, Richter, Daniela, Kleeberg, Manuela, Mziaut, Hassan, Knoch, Klaus-Peter, Parnis, Julia, Bugliani, Marco, Siddiq, Afshan, Jörns, Anne, Burdet, Frédéric, Liechti, Robin, Suleiman, Mara, Margerie, Daniel, Syed, Farooq, Distler, Marius, Grützmann, Robert, Petretto, Enrico, Moreno-Moral, Aida, Wegbrod, Carolin, Sönmez, Anke, Pfriem, Katja, Friedrich, Anne, Meinel, Jörn, Wollheim, Claes B., Baretton, Gustavo B., Scharfmann, Raphael, Nogoceke, Everson, Bonifacio, Ezio, Sturm, Dorothée, Meyer-Puttlitz, Birgit, Boggi, Ugo, Saeger, Hans-Detlev, Filipponi, Franco, Lesche, Mathias, Meda, Paolo, Dahl, Andreas, Wigger, Leonore, Xenarios, Ioannis, Falchi, Mario, Thorens, Bernard, Weitz, Jürgen, Bokvist, Krister, Lenzen, Sigurd, Rutter, Guy A., Froguel, Philippe, von Bülow, Manon, Ibberson, Mark, and Marchetti, Piero

Published
2017
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41. Succinate mediates inflammation-induced adrenocortical dysfunction.

Author

Mateska, Ivona, Witt, Anke, Hagag, Eman, Sinha, Anupam, Yilmaz, Canelif, Thanou, Evangelia, Sun, Na, Kolliniati, Ourania, Patschin, Maria, Abdelmegeed, Heba, Henneicke, Holger, Kanczkowski, Waldemar, Wielockx, Ben, Tsatsanis, Christos, Dahl, Andreas, Walch, Axel Karl, Ka Wan Li, Peitzsch, Mirko, Chavakis, Triantafyllos, and Alexaki, Vasileia Ismini

Published
2023
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42. Epigenomic map of human liver reveals principles of zonated morphogenic and metabolic control

Author

Brosch, Mario, Kattler, Kathrin, Herrmann, Alexander, von Schönfels, Witigo, Nordström, Karl, Seehofer, Daniel, Damm, Georg, Becker, Thomas, Zeissig, Sebastian, Nehring, Sophie, Reichel, Fabian, Moser, Vincent, Thangapandi, Raghavan Veera, Stickel, Felix, Baretton, Gustavo, Röcken, Christoph, Muders, Michael, Matz-Soja, Madlen, Krawczak, Michael, Gasparoni, Gilles, Hartmann, Hella, Dahl, Andreas, Schafmayer, Clemens, Walter, Jörn, and Hampe, Jochen

Published
2018
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45. Large-scale analysis of structural brain asymmetries in schizophrenia via the ENIGMA consortium.

Author

Schijven, Dick, Postema, Merel C., Fukunaga, Masaki, Matsumoto, Junya, Miura, Kenichiro, de Zwarte, Sonja M. C., van Haren, Neeltje E. M., Cahn, Wiepke, Hulshoff Pol, Hilleke E., Kahn, René S., Ayesa-Arriola, Rosa, Ortiz-García de la Foz, Víctor, Tordesillas-Gutierrez, Diana, Vázquez-Bourgon, Javier, Crespo-Facorro, Benedicto, Alnæs, Dag, Dahl, Andreas, Westlye, Lars T., Agartz, Ingrid, and Andreassen, Ole A.

Subjects
PEOPLE with schizophrenia, BRAIN function localization, CONSORTIA, SCHIZOPHRENIA, TEMPORAL lobe, CINGULATE cortex
Abstract

Left–right asymmetry is an important organizing feature of the healthy brain that may be altered in schizophrenia, but most studies have used relatively small samples and heterogeneous approaches, resulting in equivocal findings. We carried out the largest case–control study of structural brain asymmetries in schizophrenia, with MRI data from 5,080 affected individuals and 6,015 controls across 46 datasets, using a single image analysis protocol. Asymmetry indexes were calculated for global and regional cortical thickness, surface area, and subcortical volume measures. Differences of asymmetry were calculated between affected individuals and controls per dataset, and effect sizes were meta-analyzed across datasets. Small average case–control differences were observed for thickness asymmetries of the rostral anterior cingulate and the middle temporal gyrus, both driven by thinner left-hemispheric cortices in schizophrenia. Analyses of these asymmetries with respect to the use of antipsychotic medication and other clinical variables did not show any significant associations. Assessment of age-and sex-specific effects revealed a stronger average leftward asymmetry of pallidum volume between older cases and controls. Case–control differences in a multivariate context were assessed in a subset of the data (N = 2,029), which revealed that 7% of the variance across all structural asymmetries was explained by case–control status. Subtle case–control differences of brain macrostructural asymmetry may reflect differences at the molecular, cytoarchitectonic, or circuit levels that have functional relevance for the disorder. Reduced left middle temporal cortical thickness is consistent with altered left-hemisphere language network organization in schizophrenia. [ABSTRACT FROM AUTHOR]

Published
2023
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48. The histone demethylase UTX regulates stem cell migration and hematopoiesis

Author

Thieme, Sebastian, Gyárfás, Tobias, Richter, Cornelia, Özhan, Günes, Fu, Jun, Alexopoulou, Dimitra, Muders, Michael H., Michalk, Irene, Jakob, Christiane, Dahl, Andreas, Klink, Barbara, Bandoła, Joanna, Bachmann, Michael, Schröck, Evelin, Buchholz, Frank, Stewart, A. Francis, Weidinger, Gilbert, Anastassiadis, Konstantinos, and Brenner, Sebastian

Published
2013
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49. Analysis of Electric Field Stimulation in Blue Light Stressed 661W Cells.

Author

Bola, Sharanya, Subramanian, Pallavi, Calzia, Daniela, Dahl, Andreas, Panfoli, Isabella, Funk, Richard H. W., and Roehlecke, Cora

Subjects
ELECTRIC fields, BLUE light, UNFOLDED protein response, RETINAL injuries, GENETIC testing, ELECTRIC stimulation
Abstract

Though electrical stimulation is used as a therapeutic approach to treat retinal and spinal injuries, many protective mechanisms at cellular level have not been elucidated. We performed a detailed analysis of cellular events in blue light (Li) stressed 661W cells, which were subjected to direct current electric field (EF) stimulation. Our findings revealed that EF stimulation induced protective effects in 661W cells from Li-induced stress by multiple defense mechanisms, such as increase in mitochondrial activity, gain in mitochondrial potential, increase in superoxide levels, and the activation of unfolded protein response (UPR) pathways, all leading to an enhanced cell viability and decreased DNA damage. Here, our genetic screen results revealed the UPR pathway to be a promising target to ameliorate Li-induced stress by EF stimulation. Thus, our study is important for a knowledgeable transfer of EF stimulation into clinical application. [ABSTRACT FROM AUTHOR]

Published
2023
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