156 results on '"Nielsen, Morten Muhlig"'
Search Results
2. Transcriptome-wide profiles of circular RNA and RNA-binding protein interactions reveal effects on circular RNA biogenesis and cancer pathway expression
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Okholm, Trine Line Hauge, Sathe, Shashank, Park, Samuel S, Kamstrup, Andreas Bjerregaard, Rasmussen, Asta Mannstaedt, Shankar, Archana, Chua, Zong Ming, Fristrup, Niels, Nielsen, Morten Muhlig, Vang, Søren, Dyrskjøt, Lars, Aigner, Stefan, Damgaard, Christian Kroun, Yeo, Gene W, and Pedersen, Jakob Skou
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Biological Sciences ,Bioinformatics and Computational Biology ,Genetics ,Human Genome ,Urologic Diseases ,Biotechnology ,Cancer ,2.1 Biological and endogenous factors ,Aetiology ,Binding Sites ,Carcinogenesis ,Carrier Proteins ,Exons ,Gene Expression Regulation ,Neoplastic ,Hep G2 Cells ,Humans ,Introns ,K562 Cells ,Neoplasms ,RNA ,RNA ,Circular ,RNA-Binding Proteins ,Trans-Activators ,Transcriptome ,Urinary Bladder Neoplasms ,Circular RNAs ,RNA-binding proteins ,RBP sponges ,circCDYL ,Bladder cancer ,Tumorigenesis ,Clinical Sciences - Abstract
BackgroundCircular RNAs (circRNAs) are stable, often highly expressed RNA transcripts with potential to modulate other regulatory RNAs. A few circRNAs have been shown to bind RNA-binding proteins (RBPs); however, little is known about the prevalence and distribution of these interactions in different biological contexts.MethodsWe conduct an extensive screen of circRNA-RBP interactions in the ENCODE cell lines HepG2 and K562. We profile circRNAs in deep-sequenced total RNA samples and analyze circRNA-RBP interactions using a large set of eCLIP data with binding sites of 150 RBPs. We validate interactions for select circRNAs and RBPs by performing RNA immunoprecipitation and functionally characterize our most interesting candidates by conducting knockdown studies followed by RNA-Seq.ResultsWe generate a comprehensive catalog of circRNA-RBP interactions in HepG2 and K562 cells. We show that KHSRP binding sites are enriched in flanking introns of circRNAs and that KHSRP depletion affects circRNA biogenesis. We identify circRNAs that are highly covered by RBP binding sites and experimentally validate individual circRNA-RBP interactions. We show that circCDYL, a highly expressed circRNA with clinical and functional implications in bladder cancer, is almost completely covered with GRWD1 binding sites in HepG2 cells, and that circCDYL depletion counteracts the effect of GRWD1 depletion. Furthermore, we confirm interactions between circCDYL and RBPs in bladder cancer cells and demonstrate that circCDYL depletion affects hallmarks of cancer and perturbs the expression of key cancer genes, e.g., TP53. Finally, we show that elevated levels of circCDYL are associated with overall survival of bladder cancer patients.ConclusionsOur study demonstrates transcriptome-wide and cell-type-specific circRNA-RBP interactions that could play important regulatory roles in tumorigenesis.
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- 2020
3. Analyses of non-coding somatic drivers in 2,658 cancer whole genomes.
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Rheinbay, Esther, Nielsen, Morten Muhlig, Abascal, Federico, Wala, Jeremiah A, Shapira, Ofer, Tiao, Grace, Hornshøj, Henrik, Hess, Julian M, Juul, Randi Istrup, Lin, Ziao, Feuerbach, Lars, Sabarinathan, Radhakrishnan, Madsen, Tobias, Kim, Jaegil, Mularoni, Loris, Shuai, Shimin, Lanzós, Andrés, Herrmann, Carl, Maruvka, Yosef E, Shen, Ciyue, Amin, Samirkumar B, Bandopadhayay, Pratiti, Bertl, Johanna, Boroevich, Keith A, Busanovich, John, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Craft, David, Dhingra, Priyanka, Diamanti, Klev, Fonseca, Nuno A, Gonzalez-Perez, Abel, Guo, Qianyun, Hamilton, Mark P, Haradhvala, Nicholas J, Hong, Chen, Isaev, Keren, Johnson, Todd A, Juul, Malene, Kahles, Andre, Kahraman, Abdullah, Kim, Youngwook, Komorowski, Jan, Kumar, Kiran, Kumar, Sushant, Lee, Donghoon, Lehmann, Kjong-Van, Li, Yilong, Liu, Eric Minwei, Lochovsky, Lucas, Park, Keunchil, Pich, Oriol, Roberts, Nicola D, Saksena, Gordon, Schumacher, Steven E, Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stewart, Chip, Tamborero, David, Tubio, Jose MC, Umer, Husen M, Uusküla-Reimand, Liis, Wadelius, Claes, Wadi, Lina, Yao, Xiaotong, Zhang, Cheng-Zhong, Zhang, Jing, Haber, James E, Hobolth, Asger, Imielinski, Marcin, Kellis, Manolis, Lawrence, Michael S, von Mering, Christian, Nakagawa, Hidewaki, Raphael, Benjamin J, Rubin, Mark A, Sander, Chris, Stein, Lincoln D, Stuart, Joshua M, Tsunoda, Tatsuhiko, Wheeler, David A, Johnson, Rory, Reimand, Jüri, Gerstein, Mark, Khurana, Ekta, Campbell, Peter J, López-Bigas, Núria, PCAWG Drivers and Functional Interpretation Working Group, PCAWG Structural Variation Working Group, Weischenfeldt, Joachim, Beroukhim, Rameen, Martincorena, Iñigo, Pedersen, Jakob Skou, Getz, Gad, and PCAWG Consortium
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PCAWG Drivers and Functional Interpretation Working Group ,PCAWG Structural Variation Working Group ,PCAWG Consortium ,Humans ,Neoplasms ,Gene Expression Regulation ,Neoplastic ,Mutation ,Genome ,Human ,Databases ,Genetic ,DNA Breaks ,INDEL Mutation ,Genome-Wide Association Study ,Gene Expression Regulation ,Neoplastic ,Genome ,Human ,Databases ,Genetic ,General Science & Technology - Abstract
The discovery of drivers of cancer has traditionally focused on protein-coding genes1-4. Here we present analyses of driver point mutations and structural variants in non-coding regions across 2,658 genomes from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium5 of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). For point mutations, we developed a statistically rigorous strategy for combining significance levels from multiple methods of driver discovery that overcomes the limitations of individual methods. For structural variants, we present two methods of driver discovery, and identify regions that are significantly affected by recurrent breakpoints and recurrent somatic juxtapositions. Our analyses confirm previously reported drivers6,7, raise doubts about others and identify novel candidates, including point mutations in the 5' region of TP53, in the 3' untranslated regions of NFKBIZ and TOB1, focal deletions in BRD4 and rearrangements in the loci of AKR1C genes. We show that although point mutations and structural variants that drive cancer are less frequent in non-coding genes and regulatory sequences than in protein-coding genes, additional examples of these drivers will be found as more cancer genomes become available.
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- 2020
4. circHIPK3 nucleates IGF2BP2 and functions as a competing endogenous RNA
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Hauge Okholm, Trine Line, primary, Kamstrup, Andreas Bjerregaard, additional, Nielsen, Morten Muhlig, additional, Hollensen, Anne Kruse, additional, Graversgaard, Mette Laugesen, additional, Sørensen, Matilde Helbo, additional, Kristensen, Lasse Sommer, additional, Vang, Søren, additional, Park, Samuel S., additional, Yeo, Gene W., additional, Dyrskjøt, Lars, additional, Kjems, Jørgen, additional, Pedersen, Jakob Skou, additional, and Damgaard, Christian Kroun, additional
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- 2024
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5. Author response: circHIPK3 nucleates IGF2BP2 and functions as a competing endogenous RNA
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Hauge Okholm, Trine Line, primary, Kamstrup, Andreas Bjerregaard, additional, Nielsen, Morten Muhlig, additional, Hollensen, Anne Kruse, additional, Graversgaard, Mette Laugesen, additional, Sørensen, Matilde Helbo, additional, Kristensen, Lasse Sommer, additional, Vang, Søren, additional, Park, Samuel S., additional, Yeo, Gene W., additional, Dyrskjøt, Lars, additional, Kjems, Jørgen, additional, Pedersen, Jakob Skou, additional, and Damgaard, Christian Kroun, additional
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- 2024
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6. circHIPK3 nucleates IGF2BP2 and functions as a competing endogenous RNA.
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Hauge Okholm, Trine Line, Kamstrup, Andreas Bjerregaard, Nielsen, Morten Muhlig, Hollensen, Anne Kruse, Graversgaard, Mette Laugesen, Sørensen, Matilde Helbo, Kristensen, Lasse Sommer, Vang, Søren, Park, Samuel S., Yeo, Eugene, Dyrskjøt, Lars, Kjems, Jørgen, Pedersen, Jakob Skou, and Damgaard, Christian Kroun
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- 2024
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7. Author Response: circHIPK3 nucleates IGF2BP2 and functions as a competing endogenous RNA
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Okholm, Trine Line Hauge, primary, Kamstrup, Andreas Bjerregaard, additional, Nielsen, Morten Muhlig, additional, Hollensen, Anne Kruse, additional, Graversgaard, Mette Laugesen, additional, Sørensen, Matilde Helbo, additional, Kristensen, Lasse Sommer, additional, Vang, Søren, additional, Park, Samuel S., additional, Yeo, Gene W., additional, Dyrskjøt, Lars, additional, Kjems, Jørgen, additional, Pedersen, Jakob Skou, additional, and Damgaard, Christian Kroun, additional
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- 2024
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8. circHIPK3 nucleates IGF2BP2 and functions as a competing endogenous RNA
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Okholm, Trine Line Hauge, primary, Kamstrup, Andreas Bjerregaard, additional, Nielsen, Morten Muhlig, additional, Hollensen, Anne Kruse, additional, Graversgaard, Mette Laugesen, additional, Kristensen, Lasse Sommer, additional, Vang, Søren, additional, Park, Samuel S., additional, Yeo, Gene W., additional, Dyrskjøt, Lars, additional, Kjems, Jørgen, additional, Pedersen, Jakob Skou, additional, and Damgaard, Christian Kroun, additional
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- 2024
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9. Author Correction: Analyses of non-coding somatic drivers in 2,658 cancer whole genomes
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Rheinbay, Esther, Nielsen, Morten Muhlig, Abascal, Federico, Wala, Jeremiah A., Shapira, Ofer, Tiao, Grace, Hornshøj, Henrik, Hess, Julian M., Juul, Randi Istrup, Lin, Ziao, Feuerbach, Lars, Sabarinathan, Radhakrishnan, Madsen, Tobias, Kim, Jaegil, Mularoni, Loris, Shuai, Shimin, Lanzós, Andrés, Herrmann, Carl, Maruvka, Yosef E., Shen, Ciyue, Amin, Samirkumar B., Bandopadhayay, Pratiti, Bertl, Johanna, Boroevich, Keith A., Busanovich, John, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Craft, David, Dhingra, Priyanka, Diamanti, Klev, Fonseca, Nuno A., Gonzalez-Perez, Abel, Guo, Qianyun, Hamilton, Mark P., Haradhvala, Nicholas J., Hong, Chen, Isaev, Keren, Johnson, Todd A., Juul, Malene, Kahles, Andre, Kahraman, Abdullah, Kim, Youngwook, Komorowski, Jan, Kumar, Kiran, Kumar, Sushant, Lee, Donghoon, Lehmann, Kjong-Van, Li, Yilong, Liu, Eric Minwei, Lochovsky, Lucas, Park, Keunchil, Pich, Oriol, Roberts, Nicola D., Saksena, Gordon, Schumacher, Steven E., Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stewart, Chip, Tamborero, David, Tubio, Jose M. C., Umer, Husen M., Uusküla-Reimand, Liis, Wadelius, Claes, Wadi, Lina, Yao, Xiaotong, Zhang, Cheng-Zhong, Zhang, Jing, Haber, James E., Hobolth, Asger, Imielinski, Marcin, Kellis, Manolis, Lawrence, Michael S., von Mering, Christian, Nakagawa, Hidewaki, Raphael, Benjamin J., Rubin, Mark A., Sander, Chris, Stein, Lincoln D., Stuart, Joshua M., Tsunoda, Tatsuhiko, Wheeler, David A., Johnson, Rory, Reimand, Jüri, Gerstein, Mark, Khurana, Ekta, Campbell, Peter J., López-Bigas, Núria, Weischenfeldt, Joachim, Beroukhim, Rameen, Martincorena, Iñigo, Pedersen, Jakob Skou, and Getz, Gad
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- 2023
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10. Secukinumab and Dead Sea Climatotherapy Impact Resolved Psoriasis Skin Differently Potentially Affecting Disease Memory.
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Emmanuel, Thomas, Ignatov, Borislav, Bertelsen, Trine, Litman, Thomas, Nielsen, Morten Muhlig, Brent, Mikkel Bo, Touborg, Toke, Rønsholdt, Anders Benjamin, Petersen, Annita, Boye, Mette, Kaaber, Ida, Sortebech, Daniel, Lybæk, Dorte, Steiniche, Torben, Bregnhøj, Anne, Eidsmo, Liv, Iversen, Lars, and Johansen, Claus
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END of treatment ,PSORIASIS ,DISEASE duration ,DISEASE relapse ,IMMUNOHISTOCHEMISTRY ,SKIN ,IODINE isotopes - Abstract
Secukinumab and Dead Sea treatment result in clear skin for many psoriasis patients, through distinct mechanisms. However, recurrence in the same areas after treatments suggests the existence of a molecular scar. We aimed to compare the molecular and genetic differences in psoriasis patients who achieved complete response from secukinumab and Dead Sea climatotherapy treatments. We performed quantitative immunohistochemical and transcriptomic analysis, in addition to digital spatial profiling of skin punch biopsies. Histologically, both treatments resulted in a normalization of the lesional skin to a level resembling nonlesional skin. Interestingly, the transcriptome was not normalized by either treatments. We revealed 479 differentially expressed genes between secukinumab and Dead Sea climatotherapy at the end of treatment, with a psoriasis panel identifying SERPINB4, SERPINB13, IL36G, IL36RN, and AKR1B10 as upregulated in Dead Sea climatotherapy compared with secukinumab. Using digital spatial profiling, pan-RAS was observed to be differentially expressed in the microenvironment surrounding CD103
+ cells, and IDO1 was differentially expressed in the dermis when comparing the two treatments. The differences observed between secukinumab and Dead Sea climatotherapy suggest the presence of a molecular scar, which may stem from mechanistically different pathways and potentially contribute to disease recurrence. This may be important for determining treatment response duration and disease memory. [ABSTRACT FROM AUTHOR]- Published
- 2024
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11. miRNA activity inferred from single cell mRNA expression
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Nielsen, Morten Muhlig and Pedersen, Jakob Skou
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- 2021
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12. The landscape and driver potential of site-specific hotspots across cancer genomes
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Juul, Randi Istrup, Nielsen, Morten Muhlig, Juul, Malene, Feuerbach, Lars, and Pedersen, Jakob Skou
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- 2021
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13. APD-Containing Cyclolipodepsipeptides Target Mitochondrial Function in Hypoxic Cancer Cells
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Jacobsen, Kristian Mark, Villadsen, Nikolaj Lilholm, Tørring, Thomas, Nielsen, Camilla Bak, Salomón, Trine, Nielsen, Morten Muhlig, Tsakos, Michail, Sibbersen, Christian, Scavenius, Carsten, Nielsen, Rikke, Christensen, Erik Ilsø, Guerra, Paula Fernandez, Bross, Peter, Pedersen, Jakob Skou, Enghild, Jan Johannes, Johannsen, Mogens, Frøkiær, Jørgen, Overgaard, Jens, Horsman, Michael R., Busk, Morten, and Poulsen, Thomas B.
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- 2018
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14. circHIPK3 nucleates IGF2BP2 and functions as a competing endogenous RNA
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Okholm, Trine Line Hauge, primary, Kamstrup, Andreas Bjerregaard, additional, Nielsen, Morten Muhlig, additional, Hollensen, Anne Kruse, additional, Graversgaard, Mette Laugesen, additional, Kristensen, Lasse Sommer, additional, Vang, Soren, additional, Park, Samuel S., additional, Yeo, Gene W., additional, Dyrskjot, Lars, additional, Kjems, Jorgen, additional, Pedersen, Jakob Skou, additional, and Damgaard, Christian Kroun, additional
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- 2023
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15. Epigenetic Silencing of LRP2 Is Associated with Dedifferentiation and Poor Survival in Multiple Solid Tumor Types
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Rasmussen, Martin Q., primary, Tindbæk, Gitte, additional, Nielsen, Morten Muhlig, additional, Merrild, Camilla, additional, Steiniche, Torben, additional, Pedersen, Jakob Skou, additional, Moestrup, Søren K., additional, Degn, Søren E., additional, and Madsen, Mette, additional
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- 2023
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16. Erratum:Author Correction: Analyses of non-coding somatic drivers in 2,658 cancer whole genomes (Nature (2020) 578 7793 (102-111))
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Rheinbay, Esther, Nielsen, Morten Muhlig, Abascal, Federico, Wala, Jeremiah A, Shapira, Ofer, Tiao, Grace, Hornshøj, Henrik, Hess, Julian M, Juul, Randi Istrup, Lin, Ziao, Feuerbach, Lars, Sabarinathan, Radhakrishnan, Madsen, Tobias, Kim, Jaegil, Mularoni, Loris, Shuai, Shimin, Lanzós, Andrés, Herrmann, Carl, Maruvka, Yosef E, Shen, Ciyue, Amin, Samirkumar B, Bandopadhayay, Pratiti, Bertl, Johanna, and Boroevich, Keith A
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- 2023
17. A deep learning system accurately classifies primary and metastatic cancers using passenger mutation patterns
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Jiao, Wei, Atwal, Gurnit, Polak, Paz, Karlic, Rosa, Cuppen, Edwin, Al-Shahrour, Fatima, Bailey, Peter J, Biankin, Andrew V, Boutros, Paul C, Campbell, Peter J, Chang, David K, Cooke, Susanna L, Deshpande, Vikram, Faltas, Bishoy M, Faquin, William C, Garraway, Levi, Getz, Gad, Grimmond, Sean M, Haider, Syed, Hoadley, Katherine A, Kaiser, Vera B, Kato, Mamoru, Kübler, Kirsten, Lazar, Alexander J, Li, Constance H, Louis, David N, Margolin, Adam, Martin, Sancha, Nahal-Bose, Hardeep K, Nielsen, G Petur, Nik-Zainal, Serena, Omberg, Larsson, P’ng, Christine, Perry, Marc D, Rheinbay, Esther, Rubin, Mark A, Semple, Colin A, Sgroi, Dennis C, Shibata, Tatsuhiro, Siebert, Reiner, Smith, Jaclyn, Stein, Lincoln D, Stobbe, Miranda D, Sun, Ren X, Thai, Kevin, Wright, Derek W, Wu, Chin-Lee, Yuan, Ke, Zhang, Junjun, Danyi, Alexandra, de Ridder, Jeroen, van Herpen, Carla, Lolkema, Martijn P, Steeghs, Neeltje, Morris, Quaid D, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Akdemir, Kadir C, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Alvarez, Eva G, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, Arihiro, Koji, Ariizumi, Shun-ichi, Armenia, Joshua, Arnould, Laurent, Asa, Sylvia, Assenov, Yassen, Aukema, Sietse, Auman, J Todd, Aure, Miriam RR, Awadalla, Philip, Aymerich, Marta, Bader, Gary D, Baez-Ortega, Adrian, Bailey, Matthew H, Balasundaram, Miruna, Balu, Saianand, Bandopadhayay, Pratiti, Banks, Rosamonde E, Barbi, Stefano, Barbour, Andrew P, Barenboim, Jonathan, Barnholtz-Sloan, Jill, Barr, Hugh, Barrera, Elisabet, Bartlett, John, Bartolome, Javier, Bassi, Claudio, Bathe, Oliver F, Baumhoer, Daniel, Bavi, Prashant, Baylin, Stephen B, Bazant, Wojciech, Beardsmore, Duncan, Beck, Timothy A, Behjati, Sam, Behren, Andreas, Niu, Beifang, Bell, Cindy, Beltran, Sergi, Benz, Christopher, Berchuck, Andrew, Bergmann, Anke K, Bergstrom, Erik N, Berman, Benjamin P, Berney, Daniel M, Bernhart, Stephan H, Beroukhim, Rameen, Berrios, Mario, Bersani, Samantha, Bertl, Johanna, Betancourt, Miguel, Bhandari, Vinayak, Bhosle, Shriram G, Bieg, Matthias, Bigner, Darell, Binder, Hans, Birney, Ewan, Birrer, Michael, Biswas, Nidhan K, Bjerkehagen, Bodil, Bodenheimer, Tom, Boice, Lori, Bonizzato, Giada, De Bono, Johann S, Boot, Arnoud, Bootwalla, Moiz S, Borg, Ake, Borkhardt, Arndt, Boroevich, Keith A, Borozan, Ivan, Borst, Christoph, Bosenberg, Marcus, Bosio, Mattia, Boultwood, Jacqueline, Bourque, Guillaume, Bova, G Steven, Bowen, David T, Bowlby, Reanne, Bowtell, David DL, Boyault, Sandrine, Boyce, Rich, Boyd, Jeffrey, Brazma, Alvis, Brennan, Paul, Brewer, Daniel S, Brinkman, Arie B, Bristow, Robert G, Broaddus, Russell R, Brock, Jane E, Brock, Malcolm, Broeks, Annegien, Brooks, Angela N, Brooks, Denise, Brors, Benedikt, Brunak, Søren, Bruxner, Timothy JC, Bruzos, Alicia L, Buchanan, Alex, Buchhalter, Ivo, Buchholz, Christiane, Bullman, Susan, Burke, Hazel, Burkhardt, Birgit, Burns, Kathleen H, Busanovich, John, Bustamante, Carlos D, Butler, Adam P, Butte, Atul J, Byrne, Niall J, Børresen-Dale, Anne-Lise, Caesar-Johnson, Samantha J, Cafferkey, Andy, Cahill, Declan, Calabrese, Claudia, Caldas, Carlos, Calvo, Fabien, Camacho, Niedzica, Campo, Elias, Cantù, Cinzia, Cao, Shaolong, Carey, Thomas E, Carlevaro-Fita, Joana, Carlsen, Rebecca, Cataldo, Ivana, Cazzola, Mario, Cebon, Jonathan, Cerfolio, Robert, Chadwick, Dianne E, Chakravarty, Dimple, Chalmers, Don, Chan, Calvin Wing Yiu, Chan, Kin, Chan-Seng-Yue, Michelle, Chandan, Vishal S, Chanock, Stephen J, Chantrill, Lorraine A, Chateigner, Aurélien, Chatterjee, Nilanjan, Chayama, Kazuaki, Chen, Hsiao-Wei, Chen, Jieming, Chen, Ken, Chen, Yiwen, Chen, Zhaohong, Cherniack, Andrew D, Chien, Jeremy, Chiew, Yoke-Eng, Chin, Suet-Feung, Cho, Juok, Cho, Sunghoon, Choi, Jung Kyoon, Choi, Wan, Chomienne, Christine, Chong, Zechen, Choo, Su Pin, Chou, Angela, Christ, Angelika N, Christie, Elizabeth L, Chuah, Eric, Cibulskis, Carrie, Cibulskis, Kristian, Cingarlini, Sara, Clapham, Peter, Claviez, Alexander, Cleary, Sean, Cloonan, Nicole, Cmero, Marek, Collins, Colin C, Connor, Ashton A, Cooper, Colin S, Cope, Leslie, Corbo, Vincenzo, Cordes, Matthew G, Cordner, Stephen M, Cortés-Ciriano, Isidro, Covington, Kyle, Cowin, Prue A, Craft, Brian, Craft, David, Creighton, Chad J, Cun, Yupeng, Curley, Erin, Cutcutache, Ioana, Czajka, Karolina, Czerniak, Bogdan, Dagg, Rebecca A, Danilova, Ludmila, Davi, Maria Vittoria, Davidson, Natalie R, Davies, Helen, Davis, Ian J, Davis-Dusenbery, Brandi N, Dawson, Kevin J, De La Vega, Francisco M, De Paoli-Iseppi, Ricardo, Defreitas, Timothy, Dei Tos, Angelo P, Delaneau, Olivier, Demchok, John A, Demeulemeester, Jonas, Demidov, German M, Demircioğlu, Deniz, Dennis, Nening M, Denroche, Robert E, Dentro, Stefan C, Desai, Nikita, Deshwar, Amit G, Desmedt, Christine, Deu-Pons, Jordi, Dhalla, Noreen, Dhani, Neesha C, Dhingra, Priyanka, Dhir, Rajiv, DiBiase, Anthony, Diamanti, Klev, Ding, Li, Ding, Shuai, Dinh, Huy Q, Dirix, Luc, Doddapaneni, HarshaVardhan, Donmez, Nilgun, Dow, Michelle T, Drapkin, Ronny, Drechsel, Oliver, Drews, Ruben M, Serge, Serge, Dudderidge, Tim, Dueso-Barroso, Ana, Dunford, Andrew J, Dunn, Michael, Dursi, Lewis Jonathan, Duthie, Fraser R, Dutton-Regester, Ken, Eagles, Jenna, Easton, Douglas F, Edmonds, Stuart, Edwards, Paul A, Edwards, Sandra E, Eeles, Rosalind A, Ehinger, Anna, Eils, Juergen, Eils, Roland, El-Naggar, Adel, Eldridge, Matthew, Ellrott, Kyle, Erkek, Serap, Escaramis, Georgia, Espiritu, Shadrielle MG, Estivill, Xavier, Etemadmoghadam, Dariush, Eyfjord, Jorunn E, Fan, Daiming, Fan, Yu, Farcas, Claudiu, Fassan, Matteo, Fatima, Aquila, Favero, Francesco, Fayzullaev, Nodirjon, Felau, Ina, Fereday, Sian, Ferguson, Martin L, Ferretti, Vincent, Feuerbach, Lars, Field, Matthew A, Fink, J Lynn, Finocchiaro, Gaetano, Fisher, Cyril, Fittall, Matthew W, Fitzgerald, Anna, Fitzgerald, Rebecca C, Flanagan, Adrienne M, Fleshner, Neil E, Flicek, Paul, Foekens, John A, Fong, Kwun M, Fonseca, Nuno A, Foster, Christopher S, Fox, Natalie S, Fraser, Michael, Frazer, Scott, Frenkel-Morgenstern, Milana, Friedman, William, Frigola, Joan, Fronick, Catrina C, Fujimoto, Akihiro, Fujita, Masashi, Fukayama, Masashi, Fulton, Lucinda A, Fulton, Robert S, Furuta, Mayuko, Futreal, P Andrew, Füllgrabe, Anja, Gabriel, Stacey B, Gallinger, Steven, Gambacorti-Passerini, Carlo, Gao, Jianjiong, Gao, Shengjie, Garred, Øystein, Garrison, Erik, Garsed, Dale W, Gehlenborg, Nils, Gelpi, Josep LL, George, Joshy, Gerhard, Daniela S, Gerhauser, Clarissa, Gershenwald, Jeffrey E, Gerstein, Mark, Gerstung, Moritz, Ghori, Mohammed, Ghossein, Ronald, Giama, Nasra H, Gibbs, Richard A, Gibson, Bob, Gill, Anthony J, Gill, Pelvender, Giri, Dilip D, Glodzik, Dominik, Gnanapragasam, Vincent J, Goebler, Maria Elisabeth, Goldman, Mary J, Gomez, Carmen, Gonzalez, Santiago, Gonzalez-Perez, Abel, Gordenin, Dmitry A, Gossage, James, Gotoh, Kunihito, Govindan, Ramaswamy, Grabau, Dorthe, Graham, Janet S, Grant, Robert C, Green, Anthony R, Green, Eric, Greger, Liliana, Grehan, Nicola, Grimaldi, Sonia, Grossman, Robert L, Grundhoff, Adam, Gundem, Gunes, Guo, Qianyun, Gupta, Manaswi, Gupta, Shailja, Gut, Ivo G, Gut, Marta, Göke, Jonathan, Ha, Gavin, Haake, Andrea, Haan, David, Haas, Siegfried, Haase, Kerstin, Haber, James E, Habermann, Nina, Hach, Faraz, Hama, Natsuko, Hamdy, Freddie C, Hamilton, Anne, Hamilton, Mark P, Han, Leng, Hanna, George B, Hansmann, Martin, Haradhvala, Nicholas J, Harismendy, Olivier, Harliwong, Ivon, Harmanci, Arif O, Harrington, Eoghan, Hasegawa, Takanori, Haussler, David, Hawkins, Steve, Hayami, Shinya, Hayashi, Shuto, Hayes, D Neil, Hayes, 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Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
In cancer, the primary tumour’s organ of origin and histopathology are the strongest determinants of its clinical behaviour, but in 3% of cases a patient presents with a metastatic tumour and no obvious primary. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we train a deep learning classifier to predict cancer type based on patterns of somatic passenger mutations detected in whole genome sequencing (WGS) of 2606 tumours representing 24 common cancer types produced by the PCAWG Consortium. Our classifier achieves an accuracy of 91% on held-out tumor samples and 88% and 83% respectively on independent primary and metastatic samples, roughly double the accuracy of trained pathologists when presented with a metastatic tumour without knowledge of the primary. Surprisingly, adding information on driver mutations reduced accuracy. Our results have clinical applicability, underscore how patterns of somatic passenger mutations encode the state of the cell of origin, and can inform future strategies to detect the source of circulating tumour DNA.
- Published
- 2023
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18. Combined burden and functional impact tests for cancer driver discovery using DriverPower
- Author
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Shuai, Shimin, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Bandopadhayay, Pratiti, Barenboim, Jonathan, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Brunak, Søren, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Dhingra, Priyanka, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Getz, Gad, Guo, Qianyun, Gut, Ivo G, Haan, David, Hamilton, Mark P, Haradhvala, Nicholas J, Harmanci, Arif O, Helmy, Mohamed, Herrmann, Carl, Hess, Julian M, Hobolth, Asger, Hodzic, Ermin, Hong, Chen, Hornshøj, Henrik, Isaev, Keren, Izarzugaza, Jose MG, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kahraman, Abdullah, Kellis, Manolis, Khurana, Ekta, Kim, Jaegil, Kim, Jong K, Kim, Youngwook, Komorowski, Jan, Korbel, Jan O, Kumar, Sushant, Lanzós, Andrés, Larsson, Erik, Lawrence, Michael 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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
The discovery of driver mutations is one of the key motivations for cancer genome sequencing. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we describe DriverPower, a software package that uses mutational burden and functional impact evidence to identify driver mutations in coding and non-coding sites within cancer whole genomes. Using a total of 1373 genomic features derived from public sources, DriverPower’s background mutation model explains up to 93% of the regional variance in the mutation rate across multiple tumour types. By incorporating functional impact scores, we are able to further increase the accuracy of driver discovery. Testing across a collection of 2583 cancer genomes from the PCAWG project, DriverPower identifies 217 coding and 95 non-coding driver candidates. Comparing to six published methods used by the PCAWG Drivers and Functional Interpretation Working Group, DriverPower has the highest F1 score for both coding and non-coding driver discovery. This demonstrates that DriverPower is an effective framework for computational driver discovery.
- Published
- 2023
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19. Integrative pathway enrichment analysis of multivariate omics data
- Author
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Paczkowska, Marta, Barenboim, Jonathan, Sintupisut, Nardnisa, Fox, Natalie S, Zhu, Helen, Abd-Rabbo, Diala, Mee, Miles W, Boutros, Paul C, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Brunak, Søren, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Dhingra, Priyanka, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Getz, Gad, Gonzalez-Perez, Abel, Guo, Qianyun, Gut, Ivo G, Haan, David, Hamilton, Mark P, Haradhvala, Nicholas J, Harmanci, Arif O, Helmy, Mohamed, Herrmann, Carl, Hess, Julian M, Hobolth, Asger, Hodzic, Ermin, Hong, Chen, Hornshøj, Henrik, Isaev, Keren, Izarzugaza, Jose MG, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kahraman, Abdullah, Kellis, Manolis, Khurana, Ekta, Kim, Jaegil, Kim, Jong K, Kim, 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Vijver, Marc J, and Veer, L van’t
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
Multi-omics datasets represent distinct aspects of the central dogma of molecular biology. Such high-dimensional molecular profiles pose challenges to data interpretation and hypothesis generation. ActivePathways is an integrative method that discovers significantly enriched pathways across multiple datasets using statistical data fusion, rationalizes contributing evidence and highlights associated genes. As part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumor types, we integrated genes with coding and non-coding mutations and revealed frequently mutated pathways and additional cancer genes with infrequent mutations. We also analyzed prognostic molecular pathways by integrating genomic and transcriptomic features of 1780 breast cancers and highlighted associations with immune response and anti-apoptotic signaling. Integration of ChIP-seq and RNA-seq data for master regulators of the Hippo pathway across normal human tissues identified processes of tissue regeneration and stem cell regulation. ActivePathways is a versatile method that improves systems-level understanding of cellular organization in health and disease through integration of multiple molecular datasets and pathway annotations.
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- 2023
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20. Pathway and network analysis of more than 2500 whole cancer genomes
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
The catalog of cancer driver mutations in protein-coding genes has greatly expanded in the past decade. However, non-coding cancer driver mutations are less well-characterized and only a handful of recurrent non-coding mutations, most notably TERT promoter mutations, have been reported. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancer across 38 tumor types, we perform multi-faceted pathway and network analyses of non-coding mutations across 2583 whole cancer genomes from 27 tumor types compiled by the ICGC/TCGA PCAWG project that was motivated by the success of pathway and network analyses in prioritizing rare mutations in protein-coding genes. While few non-coding genomic elements are recurrently mutated in this cohort, we identify 93 genes harboring non-coding mutations that cluster into several modules of interacting proteins. Among these are promoter mutations associated with reduced mRNA expression in TP53, TLE4, and TCF4. We find that biological processes had variable proportions of coding and non-coding mutations, with chromatin remodeling and proliferation pathways altered primarily by coding mutations, while developmental pathways, including Wnt and Notch, altered by both coding and non-coding mutations. RNA splicing is primarily altered by non-coding mutations in this cohort, and samples containing non-coding mutations in well-known RNA splicing factors exhibit similar gene expression signatures as samples with coding mutations in these genes. These analyses contribute a new repertoire of possible cancer genes and mechanisms that are altered by non-coding mutations and offer insights into additional cancer vulnerabilities that can be investigated for potential therapeutic treatments.
- Published
- 2023
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21. Divergent mutational processes distinguish hypoxic and normoxic tumours
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Bhandari, Vinayak, Li, Constance H, Bristow, Robert G, Boutros, Paul C, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Akdemir, Kadir C, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Al-Shahrour, Fatima, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Alvarez, Eva G, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, Arihiro, Koji, Ariizumi, Shun-ichi, Armenia, Joshua, Arnould, Laurent, Asa, Sylvia, Assenov, Yassen, Atwal, Gurnit, Aukema, Sietse, Auman, J Todd, Aure, Miriam RR, Awadalla, Philip, Aymerich, Marta, Bader, Gary D, Baez-Ortega, Adrian, Bailey, Matthew H, Bailey, Peter J, Balasundaram, Miruna, Balu, Saianand, Bandopadhayay, Pratiti, Banks, Rosamonde E, 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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
Many primary tumours have low levels of molecular oxygen (hypoxia), and hypoxic tumours respond poorly to therapy. Pan-cancer molecular hallmarks of tumour hypoxia remain poorly understood, with limited comprehension of its associations with specific mutational processes, non-coding driver genes and evolutionary features. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we quantify hypoxia in 1188 tumours spanning 27 cancer types. Elevated hypoxia associates with increased mutational load across cancer types, irrespective of underlying mutational class. The proportion of mutations attributed to several mutational signatures of unknown aetiology directly associates with the level of hypoxia, suggesting underlying mutational processes for these signatures. At the gene level, driver mutations in TP53, MYC and PTEN are enriched in hypoxic tumours, and mutations in PTEN interact with hypoxia to direct tumour evolutionary trajectories. Overall, hypoxia plays a critical role in shaping the genomic and evolutionary landscapes of cancer.
- Published
- 2023
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22. Genomic footprints of activated telomere maintenance mechanisms in cancer
- Author
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Staaf, Johan, Stadler, Peter F, Staib, Peter, Stark, Stefan G, Stebbings, Lucy, Stefánsson, Ólafur Andri, Stegle, Oliver, Stein, Lincoln D, Stenhouse, Alasdair, Stilgenbauer, Stephan, Stobbe, Miranda D, Stratton, Michael R, Stretch, Jonathan R, Struck, Adam J, Stuart, Joshua M, Stunnenberg, Henk G, Su, Hong, Su, Xiaoping, Sun, Ren X, Sungalee, Stephanie, Susak, Hana, Suzuki, Akihiro, Sweep, Fred, Szczepanowski, Monika, Sültmann, Holger, Yugawa, Takashi, Tam, Angela, Tamborero, David, Tan, Benita Kiat Tee, Tan, Donghui, Tan, Patrick, Tanaka, Hiroko, Taniguchi, Hirokazu, Tanskanen, Tomas J, Tarabichi, Maxime, Tarnuzzer, Roy, Tarpey, Patrick, Taschuk, Morgan L, Tatsuno, Kenji, Tavaré, Simon, Taylor, Darrin F, Taylor-Weiner, Amaro, Teague, Jon W, Teh, Bin Tean, Tembe, Varsha, Temes, Javier, Thai, Kevin, Thayer, Sarah P, Thiessen, Nina, Thomas, Gilles, Thomas, Sarah, Thompson, Alan, Thompson, Alastair M, Thompson, John FF, Thompson, R Houston, Thorne, Heather, Thorne, Leigh B, Thorogood, Adrian, Tiao, Grace, Tijanic, Nebojsa, Timms, Lee E, Tirabosco, Roberto, Tojo, Marta, Tommasi, Stefania, Toon, Christopher W, Toprak, Umut H, Tortora, Giampaolo, Tost, Jörg, Totoki, Yasushi, Townend, David, Traficante, Nadia, Treilleux, Isabelle, Trotta, Jean-Rémi, Trümper, Lorenz HP, Tsao, Ming, Tsunoda, Tatsuhiko, Tucker, Olga, Turkington, Richard, Turner, Daniel J, Tutt, Andrew, Ueno, Masaki, Ueno, Naoto T, Umbricht, Christopher, Umer, Husen M, Underwood, Timothy J, Urban, Lara, Urushidate, Tomoko, Ushiku, Tetsuo, Uusküla-Reimand, Liis, Valencia, Alfonso, Van Den Berg, David J, Van Laere, Steven, Van Loo, Peter, Van Meir, Erwin G, Van den Eynden, Gert G, Van der Kwast, Theodorus, Vasudev, Naveen, Vazquez, Miguel, Vedururu, Ravikiran, Veluvolu, Umadevi, Vembu, Shankar, Verbeke, Lieven PC, Vermeulen, Peter, Verrill, Clare, Viari, Alain, Vicente, David, Vicentini, Caterina, VijayRaghavan, K, Viksna, Juris, Vilain, Ricardo E, Vincent-Salomon, Anne, Visakorpi, Tapio, Voet, Douglas, Vyas, Paresh, Vázquez-García, Ignacio, Waddell, Nick M, Wadelius, Claes, Wadi, Lina, Wagener, Rabea, Wang, Jian, Wang, Jiayin, Wang, Linghua, Wang, Qi, Wang, Wenyi, Wang, Yumeng, Wang, Zhining, Waring, Paul M, Warnatz, Hans-Jörg, Warrell, Jonathan, Warren, Anne Y, Waszak, Sebastian M, Wedge, David C, Weichenhan, Dieter, Weinberger, Paul, Weinstein, John N, Weisenberger, Daniel J, Welch, Ian, Wendl, Michael C, Werner, Johannes, Whalley, Justin P, Wheeler, David A, Whitaker, Hayley C, Wigle, Dennis, Wilkerson, Matthew D, Williams, Ashley, Wilmott, James S, Wilson, Gavin W, Wilson, Julie M, Wilson, Richard K, Winterhoff, Boris, Wintersinger, Jeffrey A, Wiznerowicz, Maciej, Wolf, Stephan, Wong, Bernice H, Wong, Tina, Wong, Winghing, Woo, Youngchoon, Wood, Scott, Wouters, Bradly G, Wright, Adam J, Wright, Derek W, Wright, Mark H, Wu, Chin-Lee, Wu, Dai-Ying, Wu, Guanming, Wu, Jianmin, Wu, Kui, Wu, Yang, Wu, Zhenggang, Xi, Liu, Xia, Tian, Xiang, Qian, Xiao, Xiao, Xing, Rui, Xiong, Heng, Xu, Qinying, Xu, Yanxun, Xue, Hong, Yachida, Shinichi, Yakneen, Sergei, Yamaguchi, Rui, Yamaguchi, Takafumi N, Yamamoto, Masakazu, Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yousif, Fouad, Yu, Jun, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Ke, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Jing, Zhang, Junjun, Zhang, Xiuqing, Zhang, Xuanping, Zhang, Yan, Zhang, Zemin, Zhao, Zhongming, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Lihua, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian
- Subjects
Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
Cancers require telomere maintenance mechanisms for unlimited replicative potential. They achieve this through TERT activation or alternative telomere lengthening associated with ATRX or DAXX loss. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we dissect whole-genome sequencing data of over 2500 matched tumor-control samples from 36 different tumor types aggregated within the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium to characterize the genomic footprints of these mechanisms. While the telomere content of tumors with ATRX or DAXX mutations (ATRX/DAXXtrunc) is increased, tumors with TERT modifications show a moderate decrease of telomere content. One quarter of all tumor samples contain somatic integrations of telomeric sequences into non-telomeric DNA. This fraction is increased to 80% prevalence in ATRX/DAXXtrunc tumors, which carry an aberrant telomere variant repeat (TVR) distribution as another genomic marker. The latter feature includes enrichment or depletion of the previously undescribed singleton TVRs TTCGGG and TTTGGG, respectively. Our systematic analysis provides new insight into the recurrent genomic alterations associated with telomere maintenance mechanisms in cancer.
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- 2023
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23. Regmex: a statistical tool for exploring motifs in ranked sequence lists from genomics experiments
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Nielsen, Morten Muhlig, Tataru, Paula, Madsen, Tobias, Hobolth, Asger, and Pedersen, Jakob Skou
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- 2018
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24. DNA hypermethylation and differential gene expression associated with Klinefelter syndrome
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Skakkebæk, Anne, Nielsen, Morten Muhlig, Trolle, Christian, Vang, Søren, Hornshøj, Henrik, Hedegaard, Jakob, Wallentin, Mikkel, Bojesen, Anders, Hertz, Jens Michael, Fedder, Jens, Østergaard, John Rosendahl, Pedersen, Jakob Skou, and Gravholt, Claus Højbjerg
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- 2018
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- View/download PDF
25. A site specific model and analysis of the neutral somatic mutation rate in whole-genome cancer data
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Bertl, Johanna, Guo, Qianyun, Juul, Malene, Besenbacher, Søren, Nielsen, Morten Muhlig, Hornshøj, Henrik, Pedersen, Jakob Skou, and Hobolth, Asger
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- 2018
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26. Pan-cancer screen for mutations in non-coding elements with conservation and cancer specificity reveals correlations with expression and survival
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Hornshøj, Henrik, Nielsen, Morten Muhlig, Sinnott-Armstrong, Nicholas A., Świtnicki, Michał P., Juul, Malene, Madsen, Tobias, Sallari, Richard, Kellis, Manolis, Ørntoft, Torben, Hobolth, Asger, and Pedersen, Jakob Skou
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- 2018
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27. Circular RNA expression is abundant and correlated to aggressiveness in early-stage bladder cancer
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Okholm, Trine Line Hauge, Nielsen, Morten Muhlig, Hamilton, Mark P., Christensen, Lise-Lotte, Vang, Søren, Hedegaard, Jakob, Hansen, Thomas Birkballe, Kjems, Jørgen, Dyrskjøt, Lars, and Pedersen, Jakob Skou
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- 2017
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28. New Candidate Genes for Heat Resistance in Drosophila melanogaster Are Regulated by HSF
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Jensen, Louise Toft, Nielsen, Morten Muhlig, and Loeschcke, Volker
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- 2008
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29. Sequence dependencies and mutation rates of localized mutational processes in cancer
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Poulsgaard, Gustav Alexander, primary, Sørensen, Simon Grund, additional, Juul, Randi Istrup, additional, Nielsen, Morten Muhlig, additional, and Pedersen, Jakob Skou, additional
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- 2021
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30. PROLONGED ERYTHROPOIETIN TREATMENT DOES NOT IMPACT GENE EXPRESSION IN HUMAN SKELETAL MUSCLE
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CHRISTENSEN, BRITT, NELLEMANN, BIRGITTE, THORSEN, KASPER, NIELSEN, MORTEN MUHLIG, PEDERSEN, STEEN B., ORNSTRUP, MARIE JUUL, JØRGENSEN, JENS OTTO L., and JESSEN, NIELS
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- 2015
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31. Passenger mutations in 2500 cancer genomes: Overall molecular functional impact and consequences
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Kumar, Sushant, Warrell, Jonathan, Li, Shantao, McGillivray, Patrick D., Meyerson, William, Salichos, Leonidas, Harmanci, Arif, Martinez-Fundichely, Alexander, Chan, Calvin W.Y., Nielsen, Morten Muhlig, Lochovsky, Lucas, Zhang, Yan, Li, Xiaotong, Lou, Shaoke, Pedersen, Jakob Skou, Herrmann, Carl, Getz, Gad, Khurana, Ekta, and Gerstein, Mark B.
- Subjects
Whole Genome Sequencing ,Genome, Human ,Neoplasms ,DNA Mutational Analysis ,Mutation ,Disease Progression ,Humans ,Genomics ,Article - Abstract
The dichotomous model of "drivers" and "passengers" in cancer posits that only a few mutations in a tumor strongly affect its progression, with the remaining ones being inconsequential. Here, we leveraged the comprehensive variant dataset from the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) project to demonstrate that-in addition to the dichotomy of high- and low-impact variants-there is a third group of medium-impact putative passengers. Moreover, we also found that molecular impact correlates with subclonal architecture (i.e., early versus late mutations), and different signatures encode for mutations with divergent impact. Furthermore, we adapted an additive-effects model from complex-trait studies to show that the aggregated effect of putative passengers, including undetected weak drivers, provides significant additional power (∼12% additive variance) for predicting cancerous phenotypes, beyond PCAWG-identified driver mutations. Finally, this framework allowed us to estimate the frequency of potential weak-driver mutations in PCAWG samples lacking any well-characterized driver alterations.
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- 2020
32. High-coverage whole-genome analysis of 1220 cancers reveals hundreds of genes deregulated by rearrangement-mediated cis-regulatory alterations
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Zhang, Yiqun, Chen, Fengju, Fonseca, Nuno A., He, Yao, Fujita, Masashi, Nakagawa, Hidewaki, Zhang, Zemin, Brazma, Alvis, Creighton, Chad J., Amin, Samirkumar B., Awadalla, Philip, Bailey, Peter J., Brooks, Angela N., Calabrese, Claudia, Chateigner, Aurélien, Cortés-Ciriano, Isidro, Craft, Brian, Craft, David, Davidson, Natalie R., Demircioğlu, Deniz, Erkek, Serap, Frenkel-Morgenstern, Milana, Goldman, Mary J., Greger, Liliana, Göke, Jonathan, Hoadley, Katherine A., Hou, Yong, Huska, Matthew R., Kahles, Andre, Khurana, Ekta, Kilpinen, Helena, Korbel, Jan O., Lamaze, Fabien C., Lehmann, Kjong-Van, Li, Chang, Li, Siliang, Li, Xiaobo, Li, Xinyue, Liu, Dongbing, Liu, Fenglin, Liu, Xingmin, Marin, Maximillian G., Markowski, Julia, Meyerson, Matthew, Nandi, Tannistha, Nielsen, Morten Muhlig, Ojesina, Akinyemi I., Ouellette, B. F. Francis, Pan-Hammarström, Qiang, Park, Peter J., Pedamallu, Chandra Sekhar, Pedersen, Jakob Skou, Perry, Marc D., Rätsch, Gunnar, Schwarz, Roland F., Shiraishi, Yuichi, Siebert, Reiner, Soulette, Cameron M., Stark, Stefan G., Stegle, Oliver, Su, Hong, Tan, Patrick, Teh, Bin Tean, Urban, Lara, Wang, Jian, Waszak, Sebastian M., Wu, Kui, Xiang, Qian, Xiong, Heng, Yakneen, Sergei, Yang, Huanming, Ye, Chen, Yung, Christina K., Zhang, Fan, Zhang, Junjun, Zhang, Xiuqing, Zheng, Liangtao, Zhu, Jingchun, Zhu, Shida, Akdemir, Kadir C., Alvarez, Eva G., Baez-Ortega, Adrian, Beroukhim, Rameen, Boutros, Paul C., Bowtell, David D. L., Brors, Benedikt, Burns, Kathleen H., Campbell, Peter J., Chan, Kin, Chen, Ken, Dueso-Barroso, Ana, Dunford, Andrew J., Edwards, Paul A., Estivill, Xavier, Etemadmoghadam, Dariush, Feuerbach, Lars, Fink, J. Lynn, Garsed, Dale W., Gerstein, Mark, Gordenin, Dmitry A., Haan, David, Haber, James E., Hess, Julian M., Hutter, Barbara, Imielinski, Marcin, Jones, David T. W., Ju, Young Seok, Kazanov, Marat D., Klimczak, Leszek J., Koh, Youngil, Kumar, Kiran, Lee, Eunjung Alice, Lee, Jake June-Koo, Li, Yilong, Lynch, Andy G., Macintyre, Geoff, Markowetz, Florian, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Miyano, Satoru, Navarro, Fabio C. P., Ossowski, Stephan, Pearson, John V., Puiggròs, Montserrat, Rippe, Karsten, Roberts, Nicola D., Roberts, Steven A., Rodriguez-Martin, Bernardo, Schumacher, Steven E., Scully, Ralph, Shackleton, Mark, Sidiropoulos, Nikos, Sieverling, Lina, Stewart, Chip, Torrents, David, Tubio, Jose M. C., Villasante, Izar, Waddell, Nicola, Wala, Jeremiah A., Weischenfeldt, Joachim, Yang, Lixing, Yao, Xiaotong, Yoon, Sung-Soo, Zamora, Jorge, and Zhang, Cheng-Zhong
- Abstract
The impact of somatic structural variants (SVs) on gene expression in cancer is largely unknown. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole-genome sequencing data and RNA sequencing from a common set of 1220 cancer cases, we report hundreds of genes for which the presence within 100 kb of an SV breakpoint associates with altered expression. For the majority of these genes, expression increases rather than decreases with corresponding breakpoint events. Up-regulated cancer-associated genes impacted by this phenomenon include TERT, MDM2, CDK4, ERBB2, CD274, PDCD1LG2, and IGF2. TERT-associated breakpoints involve ~3% of cases, most frequently in liver biliary, melanoma, sarcoma, stomach, and kidney cancers. SVs associated with up-regulation of PD1 and PDL1 genes involve ~1% of non-amplified cases. For many genes, SVs are significantly associated with increased numbers or greater proximity of enhancer regulatory elements near the gene. DNA methylation near the promoter is often increased with nearby SV breakpoint, which may involve inactivation of repressor elements.
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- 2020
33. Additional file 8 of Transcriptome-wide profiles of circular RNA and RNA-binding protein interactions reveal effects on circular RNA biogenesis and cancer pathway expression
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Okholm, Trine Line Hauge, Shashank Sathe, Park, Samuel S., Kamstrup, Andreas Bjerregaard, Rasmussen, Asta Mannstaedt, Shankar, Archana, Chua, Zong Ming, Fristrup, Niels, Nielsen, Morten Muhlig, Vang, Søren, Dyrskjøt, Lars, Aigner, Stefan, Damgaard, Christian Kroun, Yeo, Gene W., and Pedersen, Jakob Skou
- Abstract
Additional file 8: Fig. S1-S6. Pdf file with all supplementary figures (Fig. S1-S6) with corresponding figure legends.
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- 2020
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34. miRNA activity inferred from single cell mRNA expression
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Nielsen, Morten Muhlig, primary and Pedersen, Jakob Skou, additional
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- 2020
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35. Epigenetic and transcriptomic consequences of excess X‐chromosome material in 47,XXX syndrome—A comparison with Turner syndrome and 46,XX females
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Nielsen, Morten Muhlig, primary, Trolle, Christian, additional, Vang, Søren, additional, Hornshøj, Henrik, additional, Skakkebæk, Anne, additional, Hedegaard, Jakob, additional, Nordentoft, Iver, additional, Pedersen, Jakob Skou, additional, and Gravholt, Claus Højbjerg, additional
- Published
- 2020
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- View/download PDF
36. Transcriptome-wide profiles of circular RNA and RNA binding protein interactions reveal effects on circular RNA biogenesis and cancer pathway expression
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Okholm, Trine Line Hauge, primary, Sathe, Shashank, additional, Park, Samuel S., additional, Kamstrup, Andreas Bjerregaard, additional, Rasmussen, Asta Mannstaedt, additional, Shankar, Archana, additional, Fristrup, Niels, additional, Nielsen, Morten Muhlig, additional, Vang, Søren, additional, Dyrskjøt, Lars, additional, Aigner, Stefan, additional, Damgaard, Christian Kroun, additional, Yeo, Gene, additional, and Pedersen, Jakob Skou, additional
- Published
- 2020
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- View/download PDF
37. Passenger Mutations in More Than 2,500 Cancer Genomes: Overall Molecular Functional Impact and Consequences
- Author
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Kumar, Sushant, primary, Warrell, Jonathan, additional, Li, Shantao, additional, McGillivray, Patrick D., additional, Meyerson, William, additional, Salichos, Leonidas, additional, Harmanci, Arif, additional, Martinez-Fundichely, Alexander, additional, Chan, Calvin W.Y., additional, Nielsen, Morten Muhlig, additional, Lochovsky, Lucas, additional, Zhang, Yan, additional, Li, Xiaotong, additional, Lou, Shaoke, additional, Pedersen, Jakob Skou, additional, Herrmann, Carl, additional, Getz, Gad, additional, Khurana, Ekta, additional, and Gerstein, Mark B., additional
- Published
- 2020
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38. Additional file 1 of A site specific model and analysis of the neutral somatic mutation rate in whole-genome cancer data
- Author
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Bertl, Johanna, Qianyun Guo, Juul, Malene, SøRen Besenbacher, Nielsen, Morten Muhlig, HornshøJ, Henrik, Pedersen, Jakob Skou, and Hobolth, Asger
- Abstract
Section S1POLE mutation patterns in colon cancer samples. Section S2 Detailed forward model selection results. Section S3 Mutation patterns in two cancer genes. (PDF 2222 kb)
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- 2018
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39. High-coverage whole-genome analysis of 1220 cancers reveals hundreds of genes deregulated by rearrangement-mediated cis-regulatory alterations
- Author
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Zhang, Yiqun, Chen, Fengju, Fonseca, Nuno A., He, Yao, Fujita, Masashi, Nakagawa, Hidewaki, Zhang, Zemin, Brazma, Alvis, Amin, Samirkumar B., Awadalla, Philip, Bailey, Peter J., Brooks, Angela N., Calabrese, Claudia, Chateigner, Aurélien, Cortés-Ciriano, Isidro, Craft, Brian, Craft, David, Creighton, Chad J., Davidson, Natalie R., Demircioğlu, Deniz, Erkek, Serap, Frenkel-Morgenstern, Milana, Goldman, Mary J., Greger, Liliana, Göke, Jonathan, Hoadley, Katherine A., Hou, Yong, Huska, Matthew R., Kahles, Andre, Khurana, Ekta, Kilpinen, Helena, Korbel, Jan O., Lamaze, Fabien C., Lehmann, Kjong Van, Li, Chang, Li, Siliang, Li, Xiaobo, Li, Xinyue, Liu, Dongbing, Liu, Fenglin, Liu, Xingmin, Nielsen, Morten Muhlig, Pedersen, Jakob Skou, Wu, Kui, Zhu, Shida, Sidiropoulos, Nikos, Weischenfeldt, Joachim, University of St Andrews. School of Medicine, University of St Andrews. Statistics, University of St Andrews. Sir James Mackenzie Institute for Early Diagnosis, University of St Andrews. Cellular Medicine Division, Fonseca, Nuno A [0000-0003-4832-578X], Fujita, Masashi [0000-0002-1457-6233], Brazma, Alvis [0000-0001-5988-7409], Creighton, Chad J [0000-0002-6090-703X], and Apollo - University of Cambridge Repository
- Subjects
0301 basic medicine ,Cancer Research ,Chemistry(all) ,Medizin ,General Physics and Astronomy ,Regulatory Sequences, Nucleic Acid ,Genome ,0302 clinical medicine ,Ecology,Evolution & Ethology ,Neoplasms ,Databases, Genetic ,Cancer genomics ,2.1 Biological and endogenous factors ,Genes, Tumor Suppressor ,Aetiology ,lcsh:Science ,Càncer ,Cancer ,Regulation of gene expression ,Genetics ,Human Biology & Physiology ,Multidisciplinary ,Women's cancers Radboud Institute for Molecular Life Sciences [Radboudumc 17] ,3rd-DAS ,3. Good health ,Women's cancers Radboud Institute for Health Sciences [Radboudumc 17] ,Gene Expression Regulation, Neoplastic ,Enhancer Elements, Genetic ,Regulatory sequence ,030220 oncology & carcinogenesis ,DNA methylation ,PCAWG Structural Variation Working Group ,Genetics & Genomics ,Tumor Suppressor ,Biotechnology ,PCAWG Transcriptome Working Group ,Enhancer Elements ,Science ,Repressor ,QH426 Genetics ,Biology ,Physics and Astronomy(all) ,General Biochemistry, Genetics and Molecular Biology ,Article ,RC0254 ,03 medical and health sciences ,Databases ,Rare Diseases ,Genetic ,SDG 3 - Good Health and Well-being ,Humans ,Enhancer ,Gene ,QH426 ,Computational & Systems Biology ,Neoplastic ,Nucleic Acid ,Whole Genome Sequencing ,RC0254 Neoplasms. Tumors. Oncology (including Cancer) ,Biochemistry, Genetics and Molecular Biology(all) ,Human Genome ,Breakpoint ,PCAWG Consortium ,General Chemistry ,Oncogenes ,Tumour Biology ,DNA Methylation ,Genòmica ,030104 developmental biology ,Gene Expression Regulation ,Genes ,Genomic Structural Variation ,lcsh:Q ,Gene expression ,Digestive Diseases ,Regulatory Sequences ,Genètica - Abstract
The impact of somatic structural variants (SVs) on gene expression in cancer is largely unknown. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole-genome sequencing data and RNA sequencing from a common set of 1220 cancer cases, we report hundreds of genes for which the presence within 100 kb of an SV breakpoint associates with altered expression. For the majority of these genes, expression increases rather than decreases with corresponding breakpoint events. Up-regulated cancer-associated genes impacted by this phenomenon include TERT, MDM2, CDK4, ERBB2, CD274, PDCD1LG2, and IGF2. TERT-associated breakpoints involve ~3% of cases, most frequently in liver biliary, melanoma, sarcoma, stomach, and kidney cancers. SVs associated with up-regulation of PD1 and PDL1 genes involve ~1% of non-amplified cases. For many genes, SVs are significantly associated with increased numbers or greater proximity of enhancer regulatory elements near the gene. DNA methylation near the promoter is often increased with nearby SV breakpoint, which may involve inactivation of repressor elements., In this study the authors consider the structural variants (SVs) present within cancer cases of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium. They report hundreds of genes, including known cancer-associated genes for which the nearby presence of a SV breakpoint is associated with altered expression.
- Published
- 2017
40. A Site Specific Model And Analysis Of The Neutral Somatic Mutation Rate In Whole-Genome Cancer Data
- Author
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Bertl, Johanna, Guo, Qianyun, Rasmussen, Malene Juul, Besenbacher, Søren, Nielsen, Morten Muhlig, Hornshøj, Henrik, Pedersen, Jakob Skou, and Hobolth, Asger
- Abstract
Detailed modelling of the neutral mutational process in cancer cells is crucial for identifying driver mutations and understanding the mutational mechanisms that act during cancer development. The neutral mutational process is very complex: whole-genome analyses have revealed that the mutation rate differs between cancer types, between patients and along the genome depending on the genetic and epigenetic context. Therefore, methods that predict the number of different types of mutations in regions or specific genomic elements must consider local genomic explanatory variables. A major drawback of most methods is the need to average the explanatory variables across the entire region or genomic element. This procedure is particularly problematic if the explanatory variable varies dramatically in the element under consideration.To take into account the fine scale of the explanatory variables, we model the probabilities of different types of mutations for each position in the genome by multinomial logistic regression. We analyse 505 cancer genomes from 14 different cancer types and compare the performance in predicting mutation rate for both regional based models and site-specific models. We show that for 1000 randomly selected genomic positions, the site-specific model predicts the mutation rate much better than regional based models. We use a forward selection procedure to identify the most important explanatory variables. The procedure identifies site-specific conservation (phyloP), replication timing, and expression level as the best predictors for the mutation rate. Finally, our model confirms and quantifies certain well-known mutational signatures.We find that our site-specific multinomial regression model outperforms the regional based models. The possibility of including genomic variables on different scales and patient specific variables makes it a versatile framework for studying different mutational mechanisms. Our model can serve as the neutral null model for the mutational process; regions that deviate from the null model are candidates for elements that drive cancer development.
- Published
- 2017
41. Passenger mutations in 2500 cancer genomes: Overall molecular functional impact and consequences
- Author
-
Kumar, Sushant, primary, Warrell, Jonathan, additional, Li, Shantao, additional, McGillivray, Patrick D., additional, Meyerson, William, additional, Salichos, Leonidas, additional, Harmanci, Arif, additional, Martinez-Fundichely, Alexander, additional, Chan, Calvin W.Y., additional, Nielsen, Morten Muhlig, additional, Lochovsky, Lucas, additional, Zhang, Yan, additional, Li, Xiaotong, additional, Pedersen, Jakob Skou, additional, Herrmann, Carl, additional, Getz, Gad, additional, Khurana, Ekta, additional, and Gerstein, Mark B., additional
- Published
- 2018
- Full Text
- View/download PDF
42. Discovery and characterization of coding and non-coding driver mutations in more than 2,500 whole cancer genomes
- Author
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Rheinbay, Esther, primary, Nielsen, Morten Muhlig, additional, Abascal, Federico, additional, Tiao, Grace, additional, Hornshøj, Henrik, additional, Hess, Julian M., additional, Pedersen, Randi Istrup, additional, Feuerbach, Lars, additional, Sabarinathan, Radhakrishnan, additional, Madsen, Tobias, additional, Kim, Jaegil, additional, Mularoni, Loris, additional, Shuai, Shimin, additional, Lanzós, Andrés, additional, Herrmann, Carl, additional, Maruvka, Yosef E., additional, Shen, Ciyue, additional, Amin, Samirkumar B., additional, Bertl, Johanna, additional, Dhingra, Priyanka, additional, Diamanti, Klev, additional, Gonzalez-Perez, Abel, additional, Guo, Qianyun, additional, Haradhvala, Nicholas J., additional, Isaev, Keren, additional, Juul, Malene, additional, Komorowski, Jan, additional, Kumar, Sushant, additional, Lee, Donghoon, additional, Lochovsky, Lucas, additional, Liu, Eric Minwei, additional, Pich, Oriol, additional, Tamborero, David, additional, Umer, Husen M., additional, Uusküla-Reimand, Liis, additional, Wadelius, Claes, additional, Wadi, Lina, additional, Zhang, Jing, additional, Boroevich, Keith A., additional, Carlevaro-Fita, Joana, additional, Chakravarty, Dimple, additional, Chan, Calvin W.Y., additional, Fonseca, Nuno A., additional, Hamilton, Mark P., additional, Hong, Chen, additional, Kahles, Andre, additional, Kim, Youngwook, additional, Lehmann, Kjong-Van, additional, Johnson, Todd A., additional, Kahraman, Abdullah, additional, Park, Keunchil, additional, Saksena, Gordon, additional, Sieverling, Lina, additional, Sinnott-Armstrong, Nicholas A., additional, Campbell, Peter J., additional, Hobolth, Asger, additional, Kellis, Manolis, additional, Lawrence, Michael S., additional, Raphael, Ben, additional, Rubin, Mark A., additional, Sander, Chris, additional, Stein, Lincoln, additional, Stuart, Josh, additional, Tsunoda, Tatsuhiko, additional, Wheeler, David A., additional, Johnson, Rory, additional, Reimand, Jüri, additional, Gerstein, Mark B., additional, Khurana, Ekta, additional, López-Bigas, Núria, additional, Martincorena, Iñigo, additional, Pedersen, Jakob Skou, additional, and Getz, Gad, additional
- Published
- 2017
- Full Text
- View/download PDF
43. Motif discovery in ranked lists of sequences
- Author
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Nielsen, Morten Muhlig, Tataru, Paula, Madsen, Tobias, Hobolth, Asger, and Pedersen, Jakob Skou
- Abstract
Motif analysis has long been an important method to characterize biological functionality and the current growth of sequencing-based genomics experiments further extends its potential. These diverse experiments often generate sequence lists ranked by some functional property. There is therefore a growing need for motif analysis methods that can exploit this coupled data structure and be tailored for specific biological questions. Here, we present an exploratory motif analysis tool, Regmex (REGular expression Motif EXplorer), which offers several methods to evaluate the correlation of motifs with sequence rank. Regmex uses regular expressions to define motifs or families of motifs and embedded Markov models to calculate exact probabilities for motif observations in sequences. Motif enrichment is optionally calculated using random walk, Brownian bridge, or modified rank based statistics. These features make Regmex well suited for a range of biological sequence analysis problems related to motif discovery, exemplified by microRNA seed enrichment, but also including enrichment problems involving complex motifs and combinations of motifs. We demonstrate a number of usage scenarios that take advantage of the regular expression feature, including enrichments for combinations of different microRNA seed sites. The method is implemented and made publicly available as an R package and supports high parallelization on multi-core machinery.
- Published
- 2016
44. Pan-cancer screen for mutations in non-coding elements with conservation and cancer specificity reveals correlations with expression and survival
- Author
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Hornshøj, Henrik, primary, Nielsen, Morten Muhlig, additional, Sinnott-Armstrong, Nicholas A., additional, Świtnicki, Michał P., additional, Juul, Malene, additional, Madsen, Tobias, additional, Sallari, Richard, additional, Kellis, Manolis, additional, Ørntoft, Torben, additional, Hobolth, Asger, additional, and Pedersen, Jakob Skou, additional
- Published
- 2017
- Full Text
- View/download PDF
45. Non-coding cancer driver candidates identified with a sample- and position-specific model of the somatic mutation rate
- Author
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Juul, Malene, primary, Bertl, Johanna, additional, Guo, Qianyun, additional, Nielsen, Morten Muhlig, additional, Świtnicki, Michał, additional, Hornshøj, Henrik, additional, Madsen, Tobias, additional, Hobolth, Asger, additional, and Pedersen, Jakob Skou, additional
- Published
- 2017
- Full Text
- View/download PDF
46. Profiling of long non-coding RNAs identifies LINC00958 and LINC01296 as candidate oncogenes in bladder cancer
- Author
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Seitz, Anna Katharina, primary, Christensen, Lise Lotte, additional, Christensen, Emil, additional, Faarkrog, Kasper, additional, Ostenfeld, Marie Stampe, additional, Hedegaard, Jakob, additional, Nordentoft, Iver, additional, Nielsen, Morten Muhlig, additional, Palmfeldt, Johan, additional, Thomson, Michelle, additional, Jensen, Michael Theis Solgaard, additional, Nawroth, Roman, additional, Maurer, Tobias, additional, Ørntoft, Torben Falck, additional, Jensen, Jørgen Bjerggaard, additional, Damgaard, Christian Kroun, additional, and Dyrskjøt, Lars, additional
- Published
- 2017
- Full Text
- View/download PDF
47. Author response: Non-coding cancer driver candidates identified with a sample- and position-specific model of the somatic mutation rate
- Author
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Juul, Malene, primary, Bertl, Johanna, additional, Guo, Qianyun, additional, Nielsen, Morten Muhlig, additional, Świtnicki, Michał, additional, Hornshøj, Henrik, additional, Madsen, Tobias, additional, Hobolth, Asger, additional, and Pedersen, Jakob Skou, additional
- Published
- 2017
- Full Text
- View/download PDF
48. SNHG5 promotes colorectal cancer cell survival by counteracting STAU1-mediated mRNA destabilization
- Author
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Damas, Nkerorema Djodji, primary, Marcatti, Michela, additional, Côme, Christophe, additional, Christensen, Lise Lotte, additional, Nielsen, Morten Muhlig, additional, Baumgartner, Roland, additional, Gylling, Helene Maria, additional, Maglieri, Giulia, additional, Rundsten, Carsten Friis, additional, Seemann, Stefan E., additional, Rapin, Nicolas, additional, Thézenas, Simon, additional, Vang, Søren, additional, Ørntoft, Torben, additional, Andersen, Claus Lindbjerg, additional, Pedersen, Jakob Skou, additional, and Lund, Anders H., additional
- Published
- 2016
- Full Text
- View/download PDF
49. Epigenetic and transcriptomic consequences of excess X‐chromosome material in 47,XXXsyndrome—A comparison with Turner syndrome and 46,XXfemales
- Author
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Nielsen, Morten Muhlig, Trolle, Christian, Vang, Søren, Hornshøj, Henrik, Skakkebæk, Anne, Hedegaard, Jakob, Nordentoft, Iver, Pedersen, Jakob Skou, and Gravholt, Claus Højbjerg
- Abstract
47,XXX (triple X) and Turner syndrome (45,X) are sex chromosomal abnormalities with detrimental effects on health with increased mortality and morbidity. In karyotypical normal females, X‐chromosome inactivation balances gene expression between sexes and upregulation of the X chromosome in both sexes maintain stoichiometry with the autosomes. In 47,XXX and Turner syndrome a gene dosage imbalance may ensue from increased or decreased expression from the genes that escape X inactivation, as well as from incomplete X chromosome inactivation in 47,XXX. We aim to study genome‐wide DNA‐methylation and RNA‐expression changes can explain phenotypic traits in 47,XXX syndrome. We compare DNA‐methylation and RNA‐expression data derived from white blood cells of seven women with 47,XXX syndrome, with data from seven female controls, as well as with seven women with Turner syndrome (45,X). To address these questions, we explored genome‐wide DNA‐methylation and transcriptome data in blood from seven females with 47,XXX syndrome, seven females with Turner syndrome, and seven karyotypically normal females (46,XX). Based on promoter methylation, we describe a demethylation of six X‐chromosomal genes (AMOT, HTR2C, IL1RAPL2, STAG2, TCEANC, ZNF673), increased methylation for GEMIN8, and four differentially methylated autosomal regions related to four genes (SPEG, MUC4, SP6, and ZNF492). We illustrate how these changes seem compensated at the transcriptome level although several genes show differential exon usage. In conclusion, our results suggest an impact of the supernumerary X chromosome in 47,XXX syndrome on the methylation status of selected genes despite an overall comparable expression profile.
- Published
- 2020
- Full Text
- View/download PDF
50. Widespread DNA hypomethylation and differential gene expression in Turner syndrome
- Author
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Trolle, Christian, primary, Nielsen, Morten Muhlig, additional, Skakkebæk, Anne, additional, Lamy, Philippe, additional, Vang, Søren, additional, Hedegaard, Jakob, additional, Nordentoft, Iver, additional, Ørntoft, Torben Falck, additional, Pedersen, Jakob Skou, additional, and Gravholt, Claus Højbjerg, additional
- Published
- 2016
- Full Text
- View/download PDF
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