5 results on '"Anita Sveen"'
Search Results
2. Gene expression profiles of CMS2-epithelial/canonical colorectal cancers are largely driven by DNA copy number gains
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Maren Høland, Anita Sveen, Sharmini Alagaratnam, Arild Nesbakken, Kaja Christine Graue Berg, Ragnhild A. Lothe, Stine A. Danielsen, Marianne Berg, and Kjetil Søreide
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Male ,0301 basic medicine ,Cancer Research ,DNA Copy Number Variations ,DNA Mutational Analysis ,Gene Dosage ,Biology ,medicine.disease_cause ,Article ,03 medical and health sciences ,0302 clinical medicine ,Chromosome instability ,Gene expression ,Cancer genomics ,Tumor Microenvironment ,Genetics ,medicine ,Humans ,Molecular Biology ,Gene ,Regulation of gene expression ,Gene Expression Profiling ,Gene Amplification ,Microsatellite instability ,medicine.disease ,Colorectal cancer ,Survival Analysis ,Gene Expression Regulation, Neoplastic ,Gene expression profiling ,030104 developmental biology ,Molecular Diagnostic Techniques ,TOX3 ,030220 oncology & carcinogenesis ,Cancer research ,Female ,Microsatellite Instability ,Colorectal Neoplasms ,Transcriptome ,Carcinogenesis ,Microsatellite Repeats - Abstract
About 80% of colorectal cancers (CRCs) have chromosomal instability, which is an integral part of aggressive malignancy development, but the importance of specific copy number aberrations (CNAs) in modulating gene expression, particularly within the framework of clinically relevant molecular subtypes, remains mostly elusive. We performed DNA copy number profiling of 257 stage I-IV primary CRCs and integrative gene expression analysis in 151 microsatellite stable (MSS) tumors, focusing on high-level amplifications and the effect of CNAs on the characteristics of the gene expression-based consensus molecular subtypes (CMS). The results were validated in 323 MSS tumors from TCGA. Novel recurrent high-level amplifications (≥15 additional copies) with a major impact on gene expression were found for TOX3 (16q) at 1.5% frequency, as well as for CCND2 (12p) and ANXA11 (10q) at 1% frequency, in addition to the well-known targets ERBB2 (17q) and MYC (8q). Focal amplifications with ≥15 or ≥5 additional copies of at least one of these regions were associated with a poor overall survival among patients with stage I-III MSS CRCs (multivariable hazard ratio ≥3.2, p ≤ 0.01). All high-level amplifications were focal and had a more consistent relationship with gene expression than lower amplitude and/or broad-range amplifications, suggesting specific targeting during carcinogenesis. Genome-wide, copy number driven gene expression was enriched for pathways characteristic of the CMS2-epithelial/canonical subtype, including DNA repair and cell cycle progression. Furthermore, 50% of upregulated genes in CMS2-epithelial/canonical MSS CRCs were driven by CNAs, an enrichment compared with the other CMS groups, and associated with the stronger correspondence between CNAs and gene expression in malignant epithelial cells than in the cells of the tumor microenvironment (fibroblasts, endothelial cells, leukocytes). In conclusion, we identify novel recurrent amplifications with impact on gene expression in CRC and provide the first evidence that CMS2 may have a stronger copy-number related genetic basis than subtypes more heavily influenced by gene expression signals from the tumor microenvironment. publishedVersion
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- 2019
3. Transcriptional and functional consequences of TP53 splice mutations in colorectal cancer
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Marianne Grønlie Guren, Ragnhild A. Lothe, Arild Nesbakken, Ina A. Eilertsen, Stine A. Danielsen, Anita Sveen, Merete Hektoen, Jørgen Smeby, Rolf Inge Skotheim, Bjarne Johannessen, Peter W. Eide, and Andreas M. Hoff
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Genetics ,Gene isoform ,Cancer Research ,endocrine system diseases ,Colorectal cancer ,Druggability ,RNA ,Disease ,Biology ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,medicine.disease ,lcsh:RC254-282 ,Article ,Exon ,medicine ,Coding region ,splice ,Cancer genetics ,neoplasms ,Molecular Biology - Abstract
TP53 mutations are common in colorectal cancer (CRC). Most TP53 sequencing studies have been restricted to coding regions, but recent studies have revealed that splice mutations can generate transcript variants with distinct tumorigenic and prognostic properties. Here, we performed unrestricted sequencing of all coding sequences and splice regions of TP53 in a single-hospital series of 401 primary CRCs. TP53 splice mutations were detected in 4% of the cases (N = 16), considerably more frequent than reported in major databases, and they were mutually exclusive to exon mutations. RNA sequencing revealed high-level expression of aberrant transcript variants in the majority of splice mutated tumors (75%). Most variants were predicted to produce truncated TP53 proteins, including one sample expressing the potentially oncogenic and druggable p53ψ isoform. Despite heterogeneous transcript structures, downstream transcriptional profiling revealed that TP53 splice mutations had similar effects on TP53 target gene expression and pathway activity as exonic mutations. Intriguingly, TP53 splice mutations were associated with worse 5-year relapse-free survival in stage II disease, compared to both TP53 wild-type and exon mutations (P = 0.007). These data highlight the importance of including splice regions when examining the biological and clinical consequences of TP53 mutations in CRC.
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- 2019
4. Abstracts from the 3rd Conference on Aneuploidy and Cancer: Clinical and Experimental Aspects
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J. Xu, N. Page, Ruediger Hehlmann, Marthe Løvf, Victor Guryev, Sarah Grasedieck, J. Stein, Paola Cavaliere, Diana C.J. Spierings, S. Bhattacharya, Caroline Jansson, Allan Bradley, Andrew L. Trinh, Zuzana Storchova, Mat Bloomfield, G. Stein, Tristan V. de Jong, Nicolaas C. Baudoin, Jonas M. SveeStrømme, H. Ding, J. Vecerova, Xue Gong, Christina Raftopoulou, Nancy Halsema, Nataliya Huleyuk, Rolf Inge Skotheim, Jordi Camps, Mathew Bloomfield, Christof Börgermann, Anita Sveen, Steven Horne, Bjarne Johannessen, Julian Swoboda, Vladimir P. Baklaushev, A. Fritz, Anders Valind, N. Donnelly, Henry H.Q. Heng, Aracelli Acevedo-Colina, Peter H. Duesberg, A. A. Stepanenko, Rainer Engers, C. Kruse, Mark D. Vincent, Yi-Hong Zhou, Lars Bullinger, Sunyoung Hwang, Fani-Marlen Roumelioti, Vladimir P. Chekhonin, R. Berezney, Martha R. Stampfer, Batoul Y. Abdallah, Guo Liu, C. Tye, David Porubsky, Jenny Karlsson, James C. Garbe, Verena Passerini, Oksana A. Kovaleva, Xinhe Huang, Andrej Schevchenko, N. Sehgal, Frank G. Rücker, Milena Dürrbaum, Karina Hoekstra-Wakker, Daniela Cimini, David Gisselsson, Ellen K. Silbergeld, Stanislav Avdieiev, Bianca Habermann, S V Andreieva, Anke van den Berg, Hans Tobias Gustafsson, Daniele Mandrioli, Jonathan R. Pollack, A. Voskanyan, Floris Foijer, Josef Dietz, Thomas Liehr, Stefan Biesterfeld, Athel Cornish-Bowden, Melissa J. Perry, Fiorella Belpoggi, Christine J. Ye, B. Stojkovicz, Lukas Vrba, Peter M. Lansdorp, Maria Colomé Tatché, Ciara O’Sullivan, Ragnhild A. Lothe, Mirjam E. Belderbos, Hinke G. Kazemier, Eveline S. J. M. de Bont, Kateryna Korets, Alfred Böcking, David Rasnick, Joshua M. Nicholson, Michelle A. Digman, Isabel Quintanilla, Sen Zhao, Yegor S. Vassetzky, Jennifer A. Marshall Graves, Bernard W. Futscher, Mark A. LaBarge, Aaron Taudt, Leonid Berynskyy, Maria Chiourea, Robert C. Dickson, Dmytro Mykytenko, Andreas M. Hoff, Noah Dephoure, C. Marcelo Aldaz, Bjorn Bakker, Christian Klose, Sarantis Gagos, Alice Fabarius, Eduardo M. Torres, and Kimberly Soto
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Genetics ,Philosophy ,Biochemistry (medical) ,Molecular Medicine ,Theology ,Molecular Biology ,Biochemistry ,Genetics (clinical) ,3. Good health - Abstract
Author(s): Cornish-Bowden, Athel; Cornish-Bowden, Athel; Rasnick, David; Heng, Henry H; Horne, Steven; Abdallah, Batoul; Liu, Guo; Ye, Christine J; Bloomfield, Mathew; Vincent, Mark D; Aldaz, C Marcelo; Karlsson, Jenny; Valind, Anders; Jansson, Caroline; Gisselsson, David; Graves, Jennifer A Marshall; Stepanenko, Aleksei A; Andreieva, Svitlana V; Korets, Kateryna V; Mykytenko, Dmytro O; Huleyuk, Nataliya L; Baklaushev, Vladimir P; Kovaleva, Oksana A; Chekhonin, Vladimir P; Vassetzky, Yegor S; Avdieiev, Stanislav S; Bakker, Bjorn; Taudt, Aaron S; Belderbos, Mirjam E; Porubsky, David; Spierings, Diana CJ; de Jong, Tristan V; Halsema, Nancy; Kazemier, Hinke G; Hoekstra-Wakker, Karina; Bradley, Allan; de Bont, Eveline SJM; van den Berg, Anke; Guryev, Victor; Lansdorp, Peter M; Tatche, Maria Colome; Foijer, Floris; Liehr, Thomas; Baudoin, Nicolaas C; Nicholson, Joshua M; Soto, Kimberly; Quintanilla, Isabel; Camps, Jordi; Cimini, Daniela; Durrbaum, M; Donnelly, N; Passerini, V; Kruse, C; Habermann, B; Storchova, Z; Mandrioli, Daniele; Belpoggi, Fiorella; Silbergeld, Ellen K; Perry, Melissa J; Skotheim, Rolf I; Lovf, Marthe; Johannessen, Bjarne; Hoff, Andreas M; Zhao, Sen; SveeStromme, Jonas M; Sveen, Anita; Lothe, Ragnhild A; Hehlmann, R; Voskanyan, A; Fabarius, A; Bocking, Alfred; Biesterfeld, Stefan; Berynskyy, Leonid; Borgermann, Christof; Engers, Rainer; Dietz, Josef; Fritz, A; Sehgal, N; Vecerova, J; Stojkovicz, B; Ding, H; Page, N; Tye, C; Bhattacharya, S; Xu, J
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- 2017
5. Correction: Tumour-infiltrating CD8+ lymphocytes and colorectal cancer recurrence by tumour and nodal stage
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George Nicholson, Rachel Kerr, Anita Sveen, Ian Tomlinson, Arild Nesbakken, David N. Church, Jarle Bruun, Kay Lawson, Marco Novelli, Mark A. Glaire, Wanja Kildal, David J. Kerr, Ragnhild A. Lothe, Dahmane Oukrif, Enric Domingo, and Håvard E. Danielsen
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Male ,Oncology ,Cancer Research ,medicine.medical_specialty ,Colorectal cancer ,CD8-Positive T-Lymphocytes ,Tumour biomarkers ,Cohort Studies ,Lactones ,03 medical and health sciences ,Lymphocytes, Tumor-Infiltrating ,0302 clinical medicine ,Internal medicine ,Antineoplastic Combined Chemotherapy Protocols ,medicine ,Humans ,Sulfones ,Stage (cooking) ,Capecitabine ,Aged ,Neoplasm Staging ,business.industry ,Correction ,medicine.disease ,3. Good health ,Bevacizumab ,Survival Rate ,030220 oncology & carcinogenesis ,Tumour immunology ,Female ,Neoplasm Recurrence, Local ,Colorectal Neoplasms ,business ,NODAL ,CD8/Lymphocytes ,Follow-Up Studies - Abstract
Intratumoural T-cell infiltrate intensity cortes wrelaith clinical outcome in stage II/III colorectal cancer (CRC). We aimed to determine whether this association varies across this heterogeneous group.We performed a pooled analysis of 1804 CRCs from the QUASAR2 and VICTOR trials. Intratumoural CD8In QUASAR2, intratumoural CD8The prognostic value of intratumoural CD8
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- 2019
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