520 results on '"Knappskog, Stian"'
Search Results
2. Prenatal BRCA1 epimutations contribute significantly to triple-negative breast cancer development
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Nikolaienko, Oleksii, Eikesdal, Hans P., Ognedal, Elisabet, Gilje, Bjørnar, Lundgren, Steinar, Blix, Egil S., Espelid, Helge, Geisler, Jürgen, Geisler, Stephanie, Janssen, Emiel A. M., Yndestad, Synnøve, Minsaas, Laura, Leirvaag, Beryl, Lillestøl, Reidun, Knappskog, Stian, and Lønning, Per E.
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- 2023
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3. Obesity-associated changes in molecular biology of primary breast cancer
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Nguyen, Ha-Linh, Geukens, Tatjana, Maetens, Marion, Aparicio, Samuel, Bassez, Ayse, Borg, Ake, Brock, Jane, Broeks, Annegien, Caldas, Carlos, Cardoso, Fatima, De Schepper, Maxim, Delorenzi, Mauro, Drukker, Caroline A., Glas, Annuska M., Green, Andrew R., Isnaldi, Edoardo, Eyfjörð, Jórunn, Khout, Hazem, Knappskog, Stian, Krishnamurthy, Savitri, Lakhani, Sunil R., Langerod, Anita, Martens, John W. M., McCart Reed, Amy E., Murphy, Leigh, Naulaerts, Stefan, Nik-Zainal, Serena, Nevelsteen, Ines, Neven, Patrick, Piccart, Martine, Poncet, Coralie, Punie, Kevin, Purdie, Colin, Rakha, Emad A., Richardson, Andrea, Rutgers, Emiel, Vincent-Salomon, Anne, Simpson, Peter T., Schmidt, Marjanka K., Sotiriou, Christos, Span, Paul N., Tan, Kiat Tee Benita, Thompson, Alastair, Tommasi, Stefania, Van Baelen, Karen, Van de Vijver, Marc, Van Laere, Steven, van’t Veer, Laura, Viale, Giuseppe, Viari, Alain, Vos, Hanne, Witteveen, Anke T., Wildiers, Hans, Floris, Giuseppe, Garg, Abhishek D., Smeets, Ann, Lambrechts, Diether, Biganzoli, Elia, Richard, François, and Desmedt, Christine
- Published
- 2023
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- View/download PDF
4. A phase I prospective, non-randomized trial of autologous dendritic cell-based cryoimmunotherapy in patients with metastatic castration-resistant prostate cancer
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Thomsen, Liv Cecilie Vestrheim, Honoré, Alfred, Reisæter, Lars Anders Rokne, Almås, Bjarte, Børretzen, Astrid, Helle, Svein Inge, Førde, Kristina, Kristoffersen, Einar Klæboe, Kaada, Silje Helland, Melve, Guro Kristin, Haslerud, Torjan Magne, Biermann, Martin, Bigalke, Iris, Kvalheim, Gunnar, Azeem, Waqas, Olsen, Jan Roger, Gabriel, Benjamin, Knappskog, Stian, Halvorsen, Ole Johan, Akslen, Lars Andreas, Bahn, Duke, Pantel, Klaus, Riethdorf, Sabine, Ragde, Haakon, Gjertsen, Bjørn Tore, Øyan, Anne Margrete, Kalland, Karl-Henning, and Beisland, Christian
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- 2023
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5. Clonal evolution in primary breast cancers under sequential epirubicin and docetaxel monotherapy
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Venizelos, Andreas, Engebrethsen, Christina, Deng, Wei, Geisler, Jürgen, Geisler, Stephanie, Iversen, Gjertrud T., Aas, Turid, Aase, Hildegunn S., Seyedzadeh, Manouchehr, Steinskog, Eli Sihn, Myklebost, Ola, Nakken, Sigve, Vodak, Daniel, Hovig, Eivind, Meza-Zepeda, Leonardo A., Lønning, Per E., Knappskog, Stian, and Eikesdal, Hans P.
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- 2022
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6. DNA methylation changes in response to neoadjuvant chemotherapy are associated with breast cancer survival
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Pedersen, Christine Aaserød, Cao, Maria Dung, Fleischer, Thomas, Rye, Morten B., Knappskog, Stian, Eikesdal, Hans Petter, Lønning, Per Eystein, Tost, Jörg, Kristensen, Vessela N., Tessem, May-Britt, Giskeødegård, Guro F., and Bathen, Tone F.
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- 2022
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7. C/EBPB-dependent adaptation to palmitic acid promotes tumor formation in hormone receptor negative breast cancer
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Liu, Xiao-Zheng, Rulina, Anastasiia, Choi, Man Hung, Pedersen, Line, Lepland, Johanna, Takle, Sina T., Madeleine, Noelly, Peters, Stacey D’mello, Wogsland, Cara Ellen, Grøndal, Sturla Magnus, Lorens, James B., Goodarzi, Hani, Lønning, Per E., Knappskog, Stian, Molven, Anders, and Halberg, Nils
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- 2022
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8. Constitutional BRCA1 Epimutations: A Key for Understanding Basal‐Like Breast and High‐Grade Serous Ovarian Cancer.
- Author
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Lønning, Per E., Nikolaienko, Oleksii, Knappskog, Stian, and Hitchins, Megan
- Abstract
Germline pathogenic genetic variants in the BRCA1 and BRCA2 genes are the most frequent causes of familial breast and ovarian cancer. Contrasting BRCA2, epimutations in the BRCA1 gene are frequently detected in tissue from triple‐negative breast (TNBC) and high‐grade serous ovarian cancers (HGSOC). While studies over the last decade have reported BRCA1 epimutations in white blood cells (WBC) from breast and ovarian cancer patients, the potential hazard ratio for incident TNBC and HGSOC was not formally assessed until recently. Conducting a prospective nested case‐control study on women participating in the American Women's Health Initiative Study, we provided firm evidence that mosaic WBC BRCA1 epimutations, even at allele frequencies < 0.1%, are associated with a significantly increased risk of both incident HGSOC and TNBC > 5 years after WBC collection. In a second study assessing BRCA1 epimutations in WBC and matched tumor samples from TNBC, our results indicated such epimutations to be the underlying cause of around 20% of TNBC, far exceeding the percentage of cases carrying BRCA1 germline pathogenic genetic variants. We detected primary constitutional BRCA1 epimutations in tissues derived from all three germ layers. They occur independently of BRCA1 promoter haplotypes but are present on the same allele in all WBC within affected individuals. Moreover, epimutations are consistently found on the same allele in normal and tumor breast tissue as well as in WBC. This finding, together with BRCA1 epimutations detected in WBC from newborns, strongly indicates an early embryonic event with clonal expansion affecting all germ layers. Future work in the field must lead to an understanding of exactly when and how the BRCA1 epimutations occur and, most importantly, whether primary constitutional epimutations in genes other than BRCA1 may cause an elevated risk of other cancer types. [ABSTRACT FROM AUTHOR]
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- 2024
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9. Somatic mutations reveal asymmetric cellular dynamics in the early human embryo.
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Ju, Young Seok, Martincorena, Inigo, Gerstung, Moritz, Petljak, Mia, Alexandrov, Ludmil B, Rahbari, Raheleh, Wedge, David C, Davies, Helen R, Ramakrishna, Manasa, Fullam, Anthony, Martin, Sancha, Alder, Christopher, Patel, Nikita, Gamble, Steve, O'Meara, Sarah, Giri, Dilip D, Sauer, Torril, Pinder, Sarah E, Purdie, Colin A, Borg, Åke, Stunnenberg, Henk, van de Vijver, Marc, Tan, Benita KT, Caldas, Carlos, Tutt, Andrew, Ueno, Naoto T, van 't Veer, Laura J, Martens, John WM, Sotiriou, Christos, Knappskog, Stian, Span, Paul N, Lakhani, Sunil R, Eyfjörd, Jórunn Erla, Børresen-Dale, Anne-Lise, Richardson, Andrea, Thompson, Alastair M, Viari, Alain, Hurles, Matthew E, Nik-Zainal, Serena, Campbell, Peter J, and Stratton, Michael R
- Subjects
Blood Cells ,Humans ,Mutagenesis ,Cell Lineage ,Embryonic Development ,Mutation ,Mosaicism ,Germ-Line Mutation ,Genome ,Human ,Adult ,Embryo ,Mammalian ,Mutation Rate ,Embryo ,Mammalian ,Genome ,Human ,General Science & Technology - Abstract
Somatic cells acquire mutations throughout the course of an individual's life. Mutations occurring early in embryogenesis are often present in a substantial proportion of, but not all, cells in postnatal humans and thus have particular characteristics and effects. Depending on their location in the genome and the proportion of cells they are present in, these mosaic mutations can cause a wide range of genetic disease syndromes and predispose carriers to cancer. They have a high chance of being transmitted to offspring as de novo germline mutations and, in principle, can provide insights into early human embryonic cell lineages and their contributions to adult tissues. Although it is known that gross chromosomal abnormalities are remarkably common in early human embryos, our understanding of early embryonic somatic mutations is very limited. Here we use whole-genome sequences of normal blood from 241 adults to identify 163 early embryonic mutations. We estimate that approximately three base substitution mutations occur per cell per cell-doubling event in early human embryogenesis and these are mainly attributable to two known mutational signatures. We used the mutations to reconstruct developmental lineages of adult cells and demonstrate that the two daughter cells of many early embryonic cell-doubling events contribute asymmetrically to adult blood at an approximately 2:1 ratio. This study therefore provides insights into the mutation rates, mutational processes and developmental outcomes of cell dynamics that operate during early human embryogenesis.
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- 2017
10. Impact of the APOBEC3A/B deletion polymorphism on risk of ovarian cancer
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Gansmo, Liv B., Sofiyeva, Nigar, Bjørnslett, Merete, Romundstad, Pål, Hveem, Kristian, Vatten, Lars, Dørum, Anne, Lønning, Per E., and Knappskog, Stian
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- 2021
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11. Frequent somatic transfer of mitochondrial DNA into the nuclear genome of human cancer cells
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Ju, Young Seok, Tubio, Jose MC, Mifsud, William, Fu, Beiyuan, Davies, Helen R, Ramakrishna, Manasa, Li, Yilong, Yates, Lucy, Gundem, Gunes, Tarpey, Patrick S, Behjati, Sam, Papaemmanuil, Elli, Martin, Sancha, Fullam, Anthony, Gerstung, Moritz, Group, ICGC Prostate Cancer Working, Group, ICGC Bone Cancer Working, Group, ICGC Breast Cancer Working, Nangalia, Jyoti, Green, Anthony R, Caldas, Carlos, Borg, Åke, Tutt, Andrew, Lee, Ming Ta Michael, Veer, Laura J van't, Tan, Benita KT, Aparicio, Samuel, Span, Paul N, Martens, John WM, Knappskog, Stian, Vincent-Salomon, Anne, Børresen-Dale, Anne-Lise, Eyfjörd, Jórunn Erla, Flanagan, Adrienne M, Foster, Christopher, Neal, David E, Cooper, Colin, Eeles, Rosalind, Lakhani, Sunil R, Desmedt, Christine, Thomas, Gilles, Richardson, Andrea L, Purdie, Colin A, Thompson, Alastair M, McDermott, Ultan, Yang, Fengtang, Nik-Zainal, Serena, Campbell, Peter J, and Stratton, Michael R
- Subjects
Biochemistry and Cell Biology ,Genetics ,Biological Sciences ,Stem Cell Research - Nonembryonic - Human ,Human Genome ,Stem Cell Research ,Cancer ,1.1 Normal biological development and functioning ,Underpinning research ,Aetiology ,2.1 Biological and endogenous factors ,Generic health relevance ,Amino Acid Sequence ,Cell Line ,Tumor ,Cell Nucleus ,Chromosomes ,DNA Copy Number Variations ,DNA End-Joining Repair ,DNA Replication ,DNA ,Mitochondrial ,Genome ,Human ,Genome ,Mitochondrial ,HeLa Cells ,Humans ,In Situ Hybridization ,Fluorescence ,Mitochondria ,Molecular Sequence Data ,Neoplasms ,Reproducibility of Results ,Sequence Analysis ,DNA ,ICGC Prostate Cancer Working Group ,ICGC Bone Cancer Working Group ,ICGC Breast Cancer Working Group ,Hela Cells ,Medical and Health Sciences ,Bioinformatics - Abstract
Mitochondrial genomes are separated from the nuclear genome for most of the cell cycle by the nuclear double membrane, intervening cytoplasm, and the mitochondrial double membrane. Despite these physical barriers, we show that somatically acquired mitochondrial-nuclear genome fusion sequences are present in cancer cells. Most occur in conjunction with intranuclear genomic rearrangements, and the features of the fusion fragments indicate that nonhomologous end joining and/or replication-dependent DNA double-strand break repair are the dominant mechanisms involved. Remarkably, mitochondrial-nuclear genome fusions occur at a similar rate per base pair of DNA as interchromosomal nuclear rearrangements, indicating the presence of a high frequency of contact between mitochondrial and nuclear DNA in some somatic cells. Transmission of mitochondrial DNA to the nuclear genome occurs in neoplastically transformed cells, but we do not exclude the possibility that some mitochondrial-nuclear DNA fusions observed in cancer occurred years earlier in normal somatic cells.
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- 2015
12. Hans Petter Eikesdal
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Straume, Oddbjørn, primary, Knappskog, Stian, primary, Dahl, Olav, primary, Mella, Olav, primary, and Lønning, Per Eystein, primary
- Published
- 2023
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13. Germline pathogenic variants in patients with high-grade gastroenteropancreatic neuroendocrine neoplasms
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Venizelos, Andreas, primary, Sorbye, Halfdan, additional, Elvebakken, Hege, additional, Perren, Aurel, additional, Lothe, Inger Marie B, additional, Couvelard, Anne, additional, Hjortland, Geir Olav, additional, Sundlöv, Anna, additional, Svensson, Johanna, additional, Garresori, Harrish, additional, Kersten, Christian, additional, Hofsli, Eva, additional, Detlefsen, Sönke, additional, Vestermark, Lene W, additional, Ladekarl, Morten, additional, Tabaksblat, Elizaveta Mitkina, additional, and Knappskog, Stian, additional
- Published
- 2023
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14. PrenatalBRCA1epimutations contribute significantly to triple-negative breast cancer development
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Nikolaienko, Oleksii, primary, Eikesdal, Hans Petter, additional, Gilje, Bjørnar, additional, Lundgren, Steinar, additional, Blix, Egil Støre, additional, Espelid, Helge, additional, Geisler, Jürgen, additional, Geisler, Stephanie, additional, Janssen, Emiel A. M., additional, Yndestad, Synnøve, additional, Minsaas, Laura, additional, Leirvaag, Beryl, additional, Lillestøl, Reidun, additional, Knappskog, Stian, additional, and Lønning, Per Eystein, additional
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- 2023
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15. Molecular and phenotypic characteristics influencing the degree of cytoreduction in high‐grade serous ovarian carcinomas
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Torkildsen, Cecilie Fredvik, primary, Thomsen, Liv Cecilie Vestrheim, additional, Sande, Ragnar Kvie, additional, Krakstad, Camilla, additional, Stefansson, Ingunn, additional, Lamark, Eva Karin, additional, Knappskog, Stian, additional, and Bjørge, Line, additional
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- 2023
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16. Assessment of tumor suppressor promoter methylation in healthy individuals
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Poduval, Deepak B., Ognedal, Elisabet, Sichmanova, Zuzana, Valen, Eivind, Iversen, Gjertrud T., Minsaas, Laura, Lønning, Per E., and Knappskog, Stian
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- 2020
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17. ctDNA detected by ddPCR reveals changes in tumour load in metastatic malignant melanoma treated with bevacizumab
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Forthun, Rakel Brendsdal, Hovland, Randi, Schuster, Cornelia, Puntervoll, Hanne, Brodal, Hans Petter, Namløs, Heidi Maria, Aasheim, Lars Birger, Meza-Zepeda, Leonardo A., Gjertsen, Bjørn Tore, Knappskog, Stian, and Straume, Oddbjørn
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- 2019
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18. Supplementary Figure from Mutational Signature 3 Detected from Clinical Panel Sequencing is Associated with Responses to Olaparib in Breast and Ovarian Cancers
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Batalini, Felipe, primary, Gulhan, Doga C., primary, Mao, Victor, primary, Tran, Antuan, primary, Polak, Madeline, primary, Xiong, Niya, primary, Tayob, Nabihah, primary, Tung, Nadine M., primary, Winer, Eric P., primary, Mayer, Erica L., primary, Knappskog, Stian, primary, Lønning, Per E., primary, Matulonis, Ursula A., primary, Konstantinopoulos, Panagiotis A., primary, Solit, David B., primary, Won, Helen, primary, Eikesdal, Hans P., primary, Park, Peter J., primary, and Wulf, Gerburg M., primary
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- 2023
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19. Supplementary Table from Mutational Signature 3 Detected from Clinical Panel Sequencing is Associated with Responses to Olaparib in Breast and Ovarian Cancers
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Batalini, Felipe, primary, Gulhan, Doga C., primary, Mao, Victor, primary, Tran, Antuan, primary, Polak, Madeline, primary, Xiong, Niya, primary, Tayob, Nabihah, primary, Tung, Nadine M., primary, Winer, Eric P., primary, Mayer, Erica L., primary, Knappskog, Stian, primary, Lønning, Per E., primary, Matulonis, Ursula A., primary, Konstantinopoulos, Panagiotis A., primary, Solit, David B., primary, Won, Helen, primary, Eikesdal, Hans P., primary, Park, Peter J., primary, and Wulf, Gerburg M., primary
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- 2023
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20. Supplementary Figures from Golgi-Localized PAQR4 Mediates Antiapoptotic Ceramidase Activity in Breast Cancer
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Pedersen, Line, primary, Panahandeh, Pouda, primary, Siraji, Muntequa I., primary, Knappskog, Stian, primary, Lønning, Per Eystein, primary, Gordillo, Ruth, primary, Scherer, Philipp E., primary, Molven, Anders, primary, Teigen, Knut, primary, and Halberg, Nils, primary
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- 2023
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21. Supplementary Table S1 from Golgi-Localized PAQR4 Mediates Antiapoptotic Ceramidase Activity in Breast Cancer
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Pedersen, Line, primary, Panahandeh, Pouda, primary, Siraji, Muntequa I., primary, Knappskog, Stian, primary, Lønning, Per Eystein, primary, Gordillo, Ruth, primary, Scherer, Philipp E., primary, Molven, Anders, primary, Teigen, Knut, primary, and Halberg, Nils, primary
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- 2023
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22. Supplementary Data from Gene Expression Profiling–Based Identification of Molecular Subtypes in Stage IV Melanomas with Different Clinical Outcome
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Jönsson, Göran, primary, Busch, Christian, primary, Knappskog, Stian, primary, Geisler, Jürgen, primary, Miletic, Hrvoje, primary, Ringnér, Markus, primary, Lillehaug, Johan R., primary, Borg, Åke, primary, and Lønning, Per Eystein, primary
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- 2023
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23. Data from Exploring Breast Cancer Estrogen Disposition: The Basis for Endocrine Manipulation
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Lønning, Per E., primary, Haynes, Ben P., primary, Straume, Anne H., primary, Dunbier, Anita, primary, Helle, Hildegunn, primary, Knappskog, Stian, primary, and Dowsett, Mitch, primary
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- 2023
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24. Data from Gene Expression Profiling–Based Identification of Molecular Subtypes in Stage IV Melanomas with Different Clinical Outcome
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Jönsson, Göran, primary, Busch, Christian, primary, Knappskog, Stian, primary, Geisler, Jürgen, primary, Miletic, Hrvoje, primary, Ringnér, Markus, primary, Lillehaug, Johan R., primary, Borg, Åke, primary, and Lønning, Per Eystein, primary
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- 2023
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25. Supplementary Methods, Figure 1 from Exploring Breast Cancer Estrogen Disposition: The Basis for Endocrine Manipulation
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Lønning, Per E., primary, Haynes, Ben P., primary, Straume, Anne H., primary, Dunbier, Anita, primary, Helle, Hildegunn, primary, Knappskog, Stian, primary, and Dowsett, Mitch, primary
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- 2023
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26. Abstract P6-10-04: Homologous recombination deficiency across subtypes of primary breast cancer
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Engebrethsen, Christina, primary, Yndestad, Synnøve, additional, Herencia-Ropero, Andrea, additional, Nikolaienko, Oleksii, additional, Vintermyr, Olav Karsten, additional, Lillestøl, Reidun K., additional, Minsaas, Laura, additional, Leirvaag, Beryl, additional, Iversen, Gjertrud, additional, Gilje, Bjørnar, additional, Blix, Egil, additional, Espelid, Helge, additional, Lundgren, Steinar, additional, Geisler, Jürgen, additional, Vassbotn, Liv Jorunn, additional, Aase, Hildegunn S., additional, Aas, Turid, additional, Llop-Guevara, Alba, additional, Serra, Violeta, additional, Lønning, Per Eystein, additional, Knappskog, Stian, additional, and Eikesdal, Hans Petter, additional
- Published
- 2023
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27. Obesity-associated changes in molecular biology of primary breast cancer
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Desmedt, Christine, primary, Nguyen, Ha-Linh, additional, Geukens, Tatjana, additional, Maetens, Marion, additional, Aparicio, Samuel, additional, Bassez, Ayse, additional, Borg, Åke, additional, Brock, Jane, additional, Broeks, Annegien, additional, Caldas, Carlos, additional, Cardoso, Fatima, additional, De Schepper, Maxim, additional, Delorenzi, Mauro, additional, Drukker, Caroline, additional, Glas, Annuska, additional, Green, Andrew, additional, Isnaldi, Edoardo, additional, Eyfjörd, Jórunn, additional, Khout, Hazem, additional, Knappskog, Stian, additional, Krishnamurthy, Savitri, additional, Lakhani, Sunil, additional, Langerod, Anita, additional, Martens, John, additional, Reed, Amy McCart, additional, Murphy, Leigh, additional, Naulaerts, Stefan, additional, Nik-Zainal, Serena, additional, Nevelsteen, Ines, additional, Neven, Patrick, additional, Piccart, Martine, additional, Poncet, Coralie, additional, Punie, Kevin, additional, Purdie, Colin, additional, Rakha, Emad, additional, Richardson, Andrea, additional, Rutgers, Emiel, additional, Vincent-Salomon, Anne, additional, Simpson, Peter, additional, Schmidt, Marjanka, additional, Sotiriou, Christos, additional, Span, Paul, additional, Tan, Kiat Tee Benita, additional, Thompson, Alastair, additional, Tommasi, Stefania, additional, Baelen, Karen Van, additional, de Vijver, Marc van, additional, Laere, Steven Van, additional, Veer, Laura Van 'T, additional, Viale, Giuseppe, additional, Viari, Alain, additional, Vos, Hanne, additional, Witteveen, Anke, additional, Wildiers, Hans, additional, Floris, Giuseppe, additional, Garg, Abhishek, additional, Smeets, Ann, additional, Lambrechts, Diether, additional, Biganzoli, Elia, additional, and Richard, François, additional
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- 2023
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28. Mutation Spectrum in Liquid Versus Solid Biopsies From Patients With Advanced Gastroenteropancreatic Neuroendocrine Carcinoma
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Knappskog, Stian, primary, Grob, Tobias, additional, Venizelos, Andreas, additional, Amstutz, Ursula, additional, Hjortland, Geir O., additional, Lothe, Inger M., additional, Kersten, Christian, additional, Hofsli, Eva, additional, Sundlöv, Anna, additional, Elvebakken, Hege, additional, Garresori, Herish, additional, Couvelard, Anne, additional, Svensson, Johanna, additional, Sorbye, Halfdan, additional, and Perren, Aurel, additional
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- 2023
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29. Obesity-associated changes in molecular biology of primary breast cancer.
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Nguyen, Ha Linh, Geukens, Tatjana, Maetens, Marion, Aparicio, Samuel, Bassez, Ayse, Borg, Åke A., Brock, Jane, Broeks, Annegien, Caldas, Carlos, Cardoso, Fatima, De Schepper, Maxim, Delorenzi, Mauro, Drukker, Caroline A, Glas, Annuska M, Green, Andrew R, Isnaldi, Edoardo, Eyfjörð, Jórunn, Khout, Hazem, Knappskog, Stian, Krishnamurthy, Savitri, Lakhani, Sunil R, Langerod, Anita, Martens, John W M, McCart Reed, Amy AE, Murphy, Leigh, Naulaerts, Stefan, Nik-Zainal, Serena, Nevelsteen, Ines, Neven, Patrick, Piccart, Martine, Poncet, Coralie, Punie, Kevin, Purdie, Colin, Rakha, Emad A, Richardson, Andrea, Rutgers, Emiel, Vincent-Salomon, Anne, Simpson, Peter T, Schmidt, Marjanka K, Sotiriou, Christos, Span, Paul N, Tan, Benita Kiat Tee BK, Thompson, Alastair, Tommasi, Stefania, Van Baelen, Karen, Van de Vijver, Marc, Van Laere, Steven, Van't Veer, Laura, Viale, Giuseppe, Viari, Alain, Vos, Hanne, Witteveen, Anke T, Wildiers, Hans, Floris, Giuseppe, Garg, Abhishek D, Smeets, Ann, Lambrechts, Diether, Biganzoli, Elia, Richard, François, Desmedt, Christine, Nguyen, Ha Linh, Geukens, Tatjana, Maetens, Marion, Aparicio, Samuel, Bassez, Ayse, Borg, Åke A., Brock, Jane, Broeks, Annegien, Caldas, Carlos, Cardoso, Fatima, De Schepper, Maxim, Delorenzi, Mauro, Drukker, Caroline A, Glas, Annuska M, Green, Andrew R, Isnaldi, Edoardo, Eyfjörð, Jórunn, Khout, Hazem, Knappskog, Stian, Krishnamurthy, Savitri, Lakhani, Sunil R, Langerod, Anita, Martens, John W M, McCart Reed, Amy AE, Murphy, Leigh, Naulaerts, Stefan, Nik-Zainal, Serena, Nevelsteen, Ines, Neven, Patrick, Piccart, Martine, Poncet, Coralie, Punie, Kevin, Purdie, Colin, Rakha, Emad A, Richardson, Andrea, Rutgers, Emiel, Vincent-Salomon, Anne, Simpson, Peter T, Schmidt, Marjanka K, Sotiriou, Christos, Span, Paul N, Tan, Benita Kiat Tee BK, Thompson, Alastair, Tommasi, Stefania, Van Baelen, Karen, Van de Vijver, Marc, Van Laere, Steven, Van't Veer, Laura, Viale, Giuseppe, Viari, Alain, Vos, Hanne, Witteveen, Anke T, Wildiers, Hans, Floris, Giuseppe, Garg, Abhishek D, Smeets, Ann, Lambrechts, Diether, Biganzoli, Elia, Richard, François, and Desmedt, Christine
- Abstract
Obesity is associated with an increased risk of developing breast cancer (BC) and worse prognosis in BC patients, yet its impact on BC biology remains understudied in humans. This study investigates how the biology of untreated primary BC differs according to patients' body mass index (BMI) using data from >2,000 patients. We identify several genomic alterations that are differentially prevalent in overweight or obese patients compared to lean patients. We report evidence supporting an ageing accelerating effect of obesity at the genetic level. We show that BMI-associated differences in bulk transcriptomic profile are subtle, while single cell profiling allows detection of more pronounced changes in different cell compartments. These analyses further reveal an elevated and unresolved inflammation of the BC tumor microenvironment associated with obesity, with distinct characteristics contingent on the estrogen receptor status. Collectively, our analyses imply that obesity is associated with an inflammaging-like phenotype. We conclude that patient adiposity may play a significant role in the heterogeneity of BC and should be considered for BC treatment tailoring., SCOPUS: ar.j, info:eu-repo/semantics/published
- Published
- 2023
30. Epithelial to mesenchymal transition (EMT) is associated with attenuation of succinate dehydrogenase (SDH) in breast cancer through reduced expression of SDHC
- Author
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Røsland, Gro V., Dyrstad, Sissel E., Tusubira, Deusdedit, Helwa, Reham, Tan, Tuan Zea, Lotsberg, Maria L., Pettersen, Ina K. N., Berg, Anna, Kindt, Charlotte, Hoel, Fredrik, Jacobsen, Kirstine, Arason, Ari J., Engelsen, Agnete S. T., Ditzel, Henrik J., Lønning, Per E., Krakstad, Camilla, Thiery, Jean P., Lorens, James B., Knappskog, Stian, and Tronstad, Karl J.
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- 2019
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31. Influence of p53 Isoform Expression on Survival in High-Grade Serous Ovarian Cancers
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Bischof, Katharina, Knappskog, Stian, Hjelle, Sigrun M., Stefansson, Ingunn, Woie, Kathrine, Salvesen, Helga B., Gjertsen, Bjorn T., and Bjorge, Line
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- 2019
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32. epialleleR: an R/Bioconductor package for sensitive allele-specific methylation analysis in NGS data
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Nikolaienko, Oleksii, primary, Lønning, Per Eystein, additional, and Knappskog, Stian, additional
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- 2022
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33. Bortezomib abrogates temozolomide-induced autophagic flux through an ATG5 dependent pathway
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Rahman, Mohummad Aminur, primary, Engelsen, Agnete S. T., additional, Sarowar, Shahin, additional, Bindesbøll, Christian, additional, Birkeland, Even, additional, Goplen, Dorota, additional, Lotsberg, Maria L., additional, Knappskog, Stian, additional, Simonsen, Anne, additional, and Chekenya, Martha, additional
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- 2022
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34. APOBEC3A /Bdeletion polymorphism and endometrial cancer risk
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Sofiyeva, Nigar, primary, Krakstad, Camilla, additional, Halle, Mari K., additional, O'Mara, Tracy A., additional, Romundstad, Pål, additional, Hveem, Kristian, additional, Vatten, Lars, additional, Lønning, Per E., additional, Gansmo, Liv B., additional, and Knappskog, Stian, additional
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- 2022
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35. Constitutional BRCA1 Methylation and Risk of Incident Triple-Negative Breast Cancer and High-grade Serous Ovarian Cancer
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Lønning, Per E., primary, Nikolaienko, Oleksii, additional, Pan, Kathy, additional, Kurian, Allison W., additional, Eikesdal, Hans P., additional, Pettinger, Mary, additional, Anderson, Garnet L., additional, Prentice, Ross L., additional, Chlebowski, Rowan T., additional, and Knappskog, Stian, additional
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- 2022
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36. 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, 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Tirabosco, Roberto, Tojo, Marta, Tommasi, Stefania, Toon, Christopher W, Toprak, Umut H, Torrents, David, Tortora, Giampaolo, Tost, Jörg, Totoki, Yasushi, Townend, David, Traficante, Nadia, Treilleux, Isabelle, Trotta, Jean-Rémi, Trümper, Lorenz HP, Tsao, Ming, Tsunoda, Tatsuhiko, MC Tubio, Jose, 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, Villasante, Izar, Vincent-Salomon, Anne, Visakorpi, Tapio, Voet, Douglas, Vyas, 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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, Lixing, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yao, Xiaotong, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yoon, Sung-Soo, Yousif, Fouad, Yu, Jun, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zamora, Jorge, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Cheng-Zhong, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Jing, 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
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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37. Combined burden and functional impact tests for cancer driver discovery using DriverPower
- Author
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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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38. Integrative pathway enrichment analysis of multivariate omics data
- Author
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Yulia, Ng, Alvin Wei Tian, Ng, Anthony, Nicholson, Jonathan, Nicol, David, Nie, Yongzhan, Nielsen, G Petur, Nik-Zainal, Serena, Noble, Michael S, Nones, Katia, Northcott, Paul A, Notta, Faiyaz, O’Connor, Brian D, O’Donnell, Peter, O’Donovan, Maria, O’Meara, Sarah, O’Neill, Brian Patrick, O’Neill, J Robert, Ocana, David, Ochoa, Angelica, Oesper, Layla, Ogden, Christopher, Ohdan, Hideki, Ohi, Kazuhiro, Ohno-Machado, Lucila, Oien, Karin A, Ojesina, Akinyemi I, Ojima, Hidenori, Okusaka, Takuji, Omberg, Larsson, Ong, Choon Kiat, Ossowski, Stephan, Ott, German, Ouellette, BF Francis, P’ng, Christine, Paiella, Salvatore, Pairojkul, Chawalit, Pajic, Marina, Pan-Hammarström, Qiang, Papaemmanuil, Elli, Papatheodorou, Irene, Paramasivam, Nagarajan, Park, Ji Wan, Park, Joong-Won, Park, Peter J, Parker, Joel S, Parsons, Simon L, Pass, Harvey, Pasternack, Danielle, Pastore, Alessandro, Patch, Ann-Marie, Pauporté, Iris, Pea, Antonio, Pearson, John V, Pedamallu, Chandra Sekhar, Pederzoli, Paolo, 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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
- Full Text
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39. Germline pathogenic variants in patients with high-grade gastroenteropancreatic neuroendocrine neoplasms
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Venizelos, Andreas, Sorbye, Halfdan, Elvebakken, Hege, Perren, Aurel, Lothe, Inger Marie B, Couvelard, Anne, Hjortland, Geir Olav, Sundlöv, Anna, Svensson, Johanna, Garresori, Harrish, Kersten, Christian, Hofsli, Eva, Detlefsen, Sönke, Vestermark, Lene W, Ladekarl, Morten, Tabaksblat, Elizaveta Mitkina, and Knappskog, Stian
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570 Life sciences ,biology ,610 Medicine & health - Abstract
High-grade gastroenteropancreatic (HG-GEP) NEN are highly aggressive cancers. The molecular etiology of these tumors remains unclear and the prevalence of pathogenic germline variants in patients with HG-GEP-NEN is unknown. We assessed sequencing data of 360 cancer genes in normal tissue, from 240 patients with HG GEP-NEN; 198 patients with NEC and 42 with NET G3. Applying strict criteria, we identified pathogenic germline variants and compared the frequency with previously reported data from 33 different cancer types. We found a recurrent MYOC variant in 3 patients and a recurrent MUTYH variant in 2 patients, indicating that these genes may be important underlying risk factors for HG-GEP-NEN, when mutated. Further, germline variants were found in canonical tumor suppressor genes, such as TP53, RB1, BRIP1 and BAP1. Overall, we found that 4.5% of patients with NEC and 9.5% of patients with NET G3 carry germline pathogenic or highly likely pathogenic variants. Applying identical criteria for variant classification in-silico to mined data from 33 other cancer types, the median percentage of patients carrying pathogenic or highly likely pathogenic variants was 3.4% (range: 0-17%). The patients with NEC and pathogenic germline variants had a median overall survival of 9 months, similar to what is generally expected for metastatic GEP-NEC. A patient with NET G3 and pathogenic MUTYH variant had much shorter overall survival than expected. The fraction of HG GEP-NEN with germline pathogenic variants is relatively high, but still
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- 2023
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40. Pathway and network analysis of more than 2500 whole cancer genomes
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Reyna, Matthew A, Haan, David, Paczkowska, Marta, Verbeke, Lieven PC, Vazquez, Miguel, Kahraman, Abdullah, Pulido-Tamayo, Sergio, Barenboim, Jonathan, Wadi, Lina, Dhingra, Priyanka, Shrestha, Raunak, Getz, Gad, Lawrence, Michael S, Pedersen, Jakob Skou, Rubin, Mark A, Wheeler, David A, Brunak, Søren, Izarzugaza, Jose MG, Khurana, Ekta, Marchal, Kathleen, von Mering, Christian, Sahinalp, S Cenk, Valencia, Alfonso, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Bandopadhayay, Pratiti, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Busanovich, John, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Guo, Qianyun, Gut, Ivo G, 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, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kellis, Manolis, Kim, Jaegil, Kim, Jong K, Kim, Youngwook, Komorowski, Jan, Korbel, Jan O, Kumar, Sushant, Lanzós, Andrés, Larsson, Erik, Lee, Donghoon, Lehmann, Kjong-Van, Li, Shantao, Li, Xiaotong, Lin, Ziao, Liu, Eric Minwei, Lochovsky, Lucas, Lou, Shaoke, Madsen, Tobias, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Maruvka, Yosef E, McGillivray, Patrick D, Meyerson, William, Muiños, Ferran, Mularoni, Loris, Nakagawa, Hidewaki, Nielsen, Morten Muhlig, Park, Keunchil, Park, Kiejung, Pons, Tirso, Reyes-Salazar, Iker, Rheinbay, Esther, Rubio-Perez, Carlota, Saksena, Gordon, Salichos, Leonidas, Sander, Chris, Schumacher, Steven E, Shackleton, Mark, Shapira, Ofer, Shen, Ciyue, Shuai, Shimin, Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stein, Lincoln D, Tamborero, David, Tiao, Grace, Tsunoda, Tatsuhiko, Umer, Husen M, Uusküla-Reimand, Liis, Wadelius, Claes, Wang, Jiayin, Warrell, Jonathan, Waszak, Sebastian M, Weischenfeldt, Joachim, Wu, Guanming, Yu, Jun, Zhang, Jing, Zhang, Xuanping, Zhang, Yan, Zhao, Zhongming, Zou, Lihua, Reimand, Jüri, Stuart, Joshua M, Raphael, Benjamin J, Aaltonen, Lauri A, 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, 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, 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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, Lixing, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yao, Xiaotong, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yoon, Sung-Soo, Yousif, Fouad, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Ke, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zamora, Jorge, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Cheng-Zhong, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Junjun, Zhang, Xiuqing, Zhang, Zemin, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, and Veer, L van’t
- Subjects
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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41. 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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42. Genomic footprints of activated telomere maintenance mechanisms in cancer
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Okusaka, Takuji, Omberg, Larsson, Ong, Choon Kiat, Ott, German, Ouellette, BF Francis, P’ng, Christine, Paczkowska, Marta, Paiella, Salvatore, Pairojkul, Chawalit, Pajic, Marina, Pan-Hammarström, Qiang, Papaemmanuil, Elli, Papatheodorou, Irene, Paramasivam, Nagarajan, Park, Ji Wan, Park, Joong-Won, Park, Keunchil, Park, Kiejung, Parker, Joel S, Parsons, Simon L, Pass, Harvey, Pasternack, Danielle, Pastore, Alessandro, Patch, Ann-Marie, Pauporté, Iris, Pea, Antonio, Pedamallu, Chandra Sekhar, Pedersen, Jakob Skou, Pederzoli, Paolo, Peifer, Martin, Pennell, Nathan A, Perou, Charles M, Perry, Marc D, Petersen, Gloria M, Peto, Myron, Petrelli, Nicholas, Petryszak, Robert, Pfister, Stefan M, Phillips, Mark, Pich, Oriol, Pickett, Hilda A, Pihl, Todd D, Pillay, Nischalan, Pinder, Sarah, Pinese, Mark, Pinho, Andreia V, Pitkänen, Esa, Pivot, Xavier, Piñeiro-Yáñez, Elena, Planko, Laura, Plass, Christoph, Polak, Paz, Pons, Tirso, Popescu, Irinel, Potapova, Olga, Prasad, Aparna, Preston, Shaun R, 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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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43. Tumor cells interact with red blood cells via galectin-4 - a short report
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Helwa, Reham, Heller, Anette, Knappskog, Stian, and Bauer, Andrea S.
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- 2017
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44. High PTEN gene expression is a negative prognostic marker in human primary breast cancers with preserved p53 function
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Yndestad, Synnøve, Austreid, Eilin, Knappskog, Stian, Chrisanthar, Ranjan, Lilleng, Peer Kåre, Lønning, Per Eystein, and Eikesdal, Hans Petter
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- 2017
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45. Mutational Signature 3 Detected from Clinical Panel Sequencing is Associated with Responses to Olaparib in Breast and Ovarian Cancers
- Author
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Batalini, Felipe, primary, Gulhan, Doga C., additional, Mao, Victor, additional, Tran, Antuan, additional, Polak, Madeline, additional, Xiong, Niya, additional, Tayob, Nabihah, additional, Tung, Nadine M., additional, Winer, Eric P., additional, Mayer, Erica L., additional, Knappskog, Stian, additional, Lønning, Per E., additional, Matulonis, Ursula A., additional, Konstantinopoulos, Panagiotis A., additional, Solit, David B., additional, Won, Helen, additional, Eikesdal, Hans P., additional, Park, Peter J., additional, and Wulf, Gerburg M., additional
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- 2022
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46. Is APOBEC3A/B deletion polymorphism associated with the risk of ovarian cancer in Norwegian population? A case-control study (237)
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Gansmo, Liv, primary, Sofiyeva, Nigar, additional, Bjørnslett, Merete, additional, Lønning, Per, additional, and Knappskog, Stian, additional
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- 2022
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47. Association of APOBEC3A/B deletion variant with endometrial cancer risk in Norwegian population: A case-control study (242)
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Sofiyeva, Nigar, primary, Krakstad, Camilla, additional, Gansmo, Liv, additional, Lønning, Per, additional, and Knappskog, Stian, additional
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- 2022
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48. White Blood Cell BRCA1 Promoter Methylation Status and Ovarian Cancer Risk
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Lønning, Per E., Berge, Elisabet O., Bjørnslett, Merete, Minsaas, Laura, Chrisanthar, Ranjan, Høberg-Vetti, Hildegunn, Dulary, Cécile, Busato, Florence, Bjørneklett, Silje, Eriksen, Christine, Kopperud, Reidun, Axcrona, Ulrika, Davidson, Ben, Bjørge, Line, Evans, D. Gareth, Howell, Anthony, Salvesen, Helga B., Janszky, Imre, Hveem, Kristian, Romundstad, Pål R., Vatten, Lars J., Tost, Jörg, Dørum, Anne, and Knappskog, Stian
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- 2018
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49. APOBEC3A/B deletion polymorphism and cancer risk
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Gansmo, Liv B, Romundstad, Paal, Hveem, Kristian, Vatten, Lars, Nik-Zainal, Serena, Lønning, Per Eystein, and Knappskog, Stian
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- 2018
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50. UTRtech™: Exploiting mRNA Targeting To Increase Protein Secretion From Mammalian Cells
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Stern, Beate, Gjerdrum, Christine, Knappskog, Stian, Minsaas, Laura, Nylund, Stian, Olsen, Lene C., Olsen, Litta, Oveland, Eystein, Ravneberg, Hanne, Trösse, Christiane, Tveit, Anja, Vollsund, Endre, Hesketh, John E., Tauler, Albert, Pryme, Ian F., and Smith, Rodney, editor
- Published
- 2007
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Catalog
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