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15. CYP19A1 fine-mapping and Mendelian randomization: estradiol is causal for endometrial cancer

Author

Thompson, Deborah J, O'Mara, Tracy A, Glubb, Dylan M, Painter, Jodie N, Cheng, Timothy, Folkerd, Elizabeth, Doody, Deborah, Dennis, Joe, Webb, Penelope M, Gorman, Maggie, Martin, Lynn, Hodgson, Shirley, Michailidou, Kyriaki, Tyrer, Jonathan P, Maranian, Mel J, Hall, Per, Czene, Kamila, Darabi, Hatef, Li, Jingmei, Fasching, Peter A, Hein, Alexander, Beckmann, Matthias W, Ekici, Arif B, Dörk, Thilo, Hillemanns, Peter, Dürst, Matthias, Runnebaum, Ingo, Zhao, Hui, Depreeuw, Jeroen, Schrauwen, Stefanie, Amant, Frederic, Goode, Ellen L, Fridley, Brooke L, Dowdy, Sean C, Winham, Stacey J, Salvesen, Helga B, Trovik, Jone, Njolstad, Tormund S, Werner, Henrica MJ, Ashton, Katie, Proietto, Tony, Otton, Geoffrey, Carvajal-Carmona, Luis, Tham, Emma, Liu, Tao, Mints, Miriam, Scott, Rodney J, McEvoy, Mark, Attia, John, Holliday, Elizabeth G, Montgomery, Grant W, Martin, Nicholas G, Nyholt, Dale R, Henders, Anjali K, Hopper, John L, Traficante, Nadia, Ruebner, Matthias, Swerdlow, Anthony J, Burwinkel, Barbara, Brenner, Hermann, Meindl, Alfons, Brauch, Hiltrud, Lindblom, Annika, Lambrechts, Diether, Chang-Claude, Jenny, Couch, Fergus J, Giles, Graham G, Kristensen, Vessela N, Cox, Angela, Bolla, Manjeet K, Wang, Qin, Bojesen, Stig E, Shah, Mitul, Luben, Robert, Khaw, Kay-Tee, Pharoah, Paul DP, Dunning, Alison M, Tomlinson, Ian, Dowsett, Mitch, Easton, Douglas F, and Spurdle, Amanda B

Subjects
Uterine Cancer, Genetics, Cancer, Prevention, Aging, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Age Factors, Alleles, Aromatase, Body Mass Index, Case-Control Studies, Endometrial Neoplasms, Estradiol, Female, Gene-Environment Interaction, Genetic Association Studies, Genetic Predisposition to Disease, Genotype, Humans, Phenotype, Polymorphism, Single Nucleotide, endometrial cancer, CYP19A1, estradiol, Australian National Endometrial Cancer Study Group, National Study of Endometrial Cancer Genetics Group, for RENDOCAS, AOCS Group, Biological Sciences, Medical and Health Sciences, Oncology & Carcinogenesis
Abstract

Candidate gene studies have reported CYP19A1 variants to be associated with endometrial cancer and with estradiol (E2) concentrations. We analyzed 2937 single nucleotide polymorphisms (SNPs) in 6608 endometrial cancer cases and 37 925 controls and report the first genome wide-significant association between endometrial cancer and a CYP19A1 SNP (rs727479 in intron 2, P=4.8×10(-11)). SNP rs727479 was also among those most strongly associated with circulating E2 concentrations in 2767 post-menopausal controls (P=7.4×10(-8)). The observed endometrial cancer odds ratio per rs727479 A-allele (1.15, CI=1.11-1.21) is compatible with that predicted by the observed effect on E2 concentrations (1.09, CI=1.03-1.21), consistent with the hypothesis that endometrial cancer risk is driven by E2. From 28 candidate-causal SNPs, 12 co-located with three putative gene-regulatory elements and their risk alleles associated with higher CYP19A1 expression in bioinformatical analyses. For both phenotypes, the associations with rs727479 were stronger among women with a higher BMI (Pinteraction=0.034 and 0.066 respectively), suggesting a biologically plausible gene-environment interaction.

Published
2016

17. Meta-analysis of genome-wide association studies identifies common susceptibility polymorphisms for colorectal and endometrial cancer near SH2B3 and TSHZ1.

Author

Cheng, Timothy HT, Thompson, Deborah, Painter, Jodie, O'Mara, Tracy, Gorman, Maggie, Martin, Lynn, Palles, Claire, Jones, Angela, Buchanan, Daniel D, Win, Aung Ko, Hopper, John, Jenkins, Mark, Lindor, Noralane M, Newcomb, Polly A, Gallinger, Steve, Conti, David, Schumacher, Fred, Casey, Graham, Giles, Graham G, Pharoah, Paul, Peto, Julian, Cox, Angela, Swerdlow, Anthony, Couch, Fergus, Cunningham, Julie M, Goode, Ellen L, Winham, Stacey J, Lambrechts, Diether, Fasching, Peter, Burwinkel, Barbara, Brenner, Hermann, Brauch, Hiltrud, Chang-Claude, Jenny, Salvesen, Helga B, Kristensen, Vessela, Darabi, Hatef, Li, Jingmei, Liu, Tao, Lindblom, Annika, Hall, Per, de Polanco, Magdalena Echeverry, Sans, Monica, Carracedo, Angel, Castellvi-Bel, Sergi, Rojas-Martinez, Augusto, Aguiar Jnr, Samuel, Teixeira, Manuel R, Dunning, Alison M, Dennis, Joe, Otton, Geoffrey, Proietto, Tony, Holliday, Elizabeth, Attia, John, Ashton, Katie, Scott, Rodney J, McEvoy, Mark, Dowdy, Sean C, Fridley, Brooke L, Werner, Henrica MJ, Trovik, Jone, Njolstad, Tormund S, Tham, Emma, Mints, Miriam, Runnebaum, Ingo, Hillemanns, Peter, Dörk, Thilo, Amant, Frederic, Schrauwen, Stefanie, Hein, Alexander, Beckmann, Matthias W, Ekici, Arif, Czene, Kamila, Meindl, Alfons, Bolla, Manjeet K, Michailidou, Kyriaki, Tyrer, Jonathan P, Wang, Qin, Ahmed, Shahana, Healey, Catherine S, Shah, Mitul, Annibali, Daniela, Depreeuw, Jeroen, Al-Tassan, Nada A, Harris, Rebecca, Meyer, Brian F, Whiffin, Nicola, Hosking, Fay J, Kinnersley, Ben, Farrington, Susan M, Timofeeva, Maria, Tenesa, Albert, Campbell, Harry, Haile, Robert W, Hodgson, Shirley, Carvajal-Carmona, Luis, Cheadle, Jeremy P, Easton, Douglas, Dunlop, Malcolm, Houlston, Richard, and Spurdle, Amanda

Subjects
Humans, Colorectal Neoplasms, Endometrial Neoplasms, Genetic Predisposition to Disease, Intracellular Signaling Peptides and Proteins, Proteins, Homeodomain Proteins, Neoplasm Proteins, Polymorphism, Genetic, Alleles, Female, Male, Genome-Wide Association Study, Polymorphism, Genetic
Abstract

High-risk mutations in several genes predispose to both colorectal cancer (CRC) and endometrial cancer (EC). We therefore hypothesised that some lower-risk genetic variants might also predispose to both CRC and EC. Using CRC and EC genome-wide association series, totalling 13,265 cancer cases and 40,245 controls, we found that the protective allele [G] at one previously-identified CRC polymorphism, rs2736100 near TERT, was associated with EC risk (odds ratio (OR) = 1.08, P = 0.000167); this polymorphism influences the risk of several other cancers. A further CRC polymorphism near TERC also showed evidence of association with EC (OR = 0.92; P = 0.03). Overall, however, there was no good evidence that the set of CRC polymorphisms was associated with EC risk, and neither of two previously-reported EC polymorphisms was associated with CRC risk. A combined analysis revealed one genome-wide significant polymorphism, rs3184504, on chromosome 12q24 (OR = 1.10, P = 7.23 × 10(-9)) with shared effects on CRC and EC risk. This polymorphism, a missense variant in the gene SH2B3, is also associated with haematological and autoimmune disorders, suggesting that it influences cancer risk through the immune response. Another polymorphism, rs12970291 near gene TSHZ1, was associated with both CRC and EC (OR = 1.26, P = 4.82 × 10(-8)), with the alleles showing opposite effects on the risks of the two cancers.

Published
2015

22. ATAD2 overexpression links to enrichment of B-MYB-translational signatures and development of aggressive endometrial carcinoma

Author

Krakstad, Camilla, Tangen, Ingvild L, Hoivik, Erling A, Halle, Mari K, Berg, Anna, Werner, Henrica M, Ræder, Maria B, Kusonmano, Kanthida, Zou, June X, Øyan, Anne M, Stefansson, Ingunn, Trovik, Jone, Kalland, Karl-Henning, Chen, Hong-Wu, and Salvesen, Helga B

Subjects
Biotechnology, Uterine Cancer, Cancer, Genetics, ATPases Associated with Diverse Cellular Activities, Adenosine Triphosphatases, Biomarkers, Tumor, Cell Cycle Proteins, DNA-Binding Proteins, Endometrial Neoplasms, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Gene Ontology, Humans, Immunohistochemistry, Kaplan-Meier Estimate, Middle Aged, Oligonucleotide Array Sequence Analysis, Outcome Assessment, Health Care, Prognosis, Proportional Hazards Models, Prospective Studies, Trans-Activators, endometrial cancer, ATAD2, biomarker, molecular profiling, Oncology and Carcinogenesis
Abstract

We have explored the potential for clinical implementation of ATAD2 as a biomarker for aggressive endometrial cancer by investigating to what extent immunohistochemical (IHC) staining for ATAD2 is feasible, reflects clinical phenotype and molecular subgroups of endometrial carcinomas. Increased expression of the ATAD2 gene has been implicated in cancer development and progression in a number of tissues, but few studies have investigated ATAD2 expression using IHC. Here we show that high ATAD2 protein expression is significantly associated with established clinical-pathological variables for aggressive endometrial cancer, also in the subset of estrogen receptor α (ERα) positive tumors. Protein and mRNA expression of ATAD2 were highly correlated (P < 0.001), suggesting that IHC staining may represent a more clinically applicable measure of ATAD2 level in routinely collected formalin fixed paraffin embedded specimens. Gene expression alterations in samples with high ATAD2 expression revealed upregulation of several cancer-related genes (B-MYB, CDCs, E2Fs) and gene sets that previously have been linked to aggressive disease and potential for new targeting therapies. Our results support that IHC staining for ATAD2 may be a clinically applicable biomarker reflecting clinical phenotype and targetable alterations in endometrial carcinomas to be further explored in controlled clinical trials.

Published
2015

23. Fine-mapping of the HNF1B multicancer locus identifies candidate variants that mediate endometrial cancer risk

Author

Painter, Jodie N, O'Mara, Tracy A, Batra, Jyotsna, Cheng, Timothy, Lose, Felicity A, Dennis, Joe, Michailidou, Kyriaki, Tyrer, Jonathan P, Ahmed, Shahana, Ferguson, Kaltin, Healey, Catherine S, Kaufmann, Susanne, Hillman, Kristine M, Walpole, Carina, Moya, Leire, Pollock, Pamela, Jones, Angela, Howarth, Kimberley, Martin, Lynn, Gorman, Maggie, Hodgson, Shirley, De Polanco, Ma Magdalena Echeverry, Sans, Monica, Carracedo, Angel, Castellvi-Bel, Sergi, Rojas-Martinez, Augusto, Santos, Erika, Teixeira, Manuel R, Carvajal-Carmona, Luis, Shu, Xiao-Ou, Long, Jirong, Zheng, Wei, Xiang, Yong-Bing, Montgomery, Grant W, Webb, Penelope M, Scott, Rodney J, McEvoy, Mark, Attia, John, Holliday, Elizabeth, Martin, Nicholas G, Nyholt, Dale R, Henders, Anjali K, Fasching, Peter A, Hein, Alexander, Beckmann, Matthias W, Renner, Stefan P, Dörk, Thilo, Hillemanns, Peter, Dürst, Matthias, Runnebaum, Ingo, Lambrechts, Diether, Coenegrachts, Lieve, Schrauwen, Stefanie, Amant, Frederic, Winterhoff, Boris, Dowdy, Sean C, Goode, Ellen L, Teoman, Attila, Salvesen, Helga B, Trovik, Jone, Njolstad, Tormund S, Werner, Henrica MJ, Ashton, Katie, Proietto, Tony, Otton, Geoffrey, Tzortzatos, Gerasimos, Mints, Miriam, Tham, Emma, Hall, Per, Czene, Kamila, Liu, Jianjun, Li, Jingmei, Hopper, John L, Southey, Melissa C, Ekici, Arif B, Ruebner, Matthias, Johnson, Nicola, Peto, Julian, Burwinkel, Barbara, Marme, Frederik, Brenner, Hermann, Dieffenbach, Aida K, Meindl, Alfons, Brauch, Hiltrud, Lindblom, Annika, Depreeuw, Jeroen, Moisse, Matthieu, Chang-Claude, Jenny, Rudolph, Anja, Couch, Fergus J, Olson, Janet E, Giles, Graham G, Bruinsma, Fiona, Cunningham, Julie M, Fridley, Brooke L, Børresen-Dale, Anne-Lise, Kristensen, Vessela N, Cox, Angela, Swerdlow, Anthony J, and Orr, Nicholas

Subjects
Cancer, Biotechnology, Human Genome, Prevention, Genetics, 2.1 Biological and endogenous factors, Aetiology, Alleles, Case-Control Studies, Cell Line, Tumor, Chromosome Mapping, Computational Biology, Databases, Genetic, Endometrial Neoplasms, Epigenesis, Genetic, Female, Genetic Loci, Genetic Variation, Genome-Wide Association Study, Genotype, Haplotypes, Hepatocyte Nuclear Factor 1-beta, Humans, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Promoter Regions, Genetic, RNA, Messenger, Risk Factors, White People, National Study of Endometrial Cancer Genetics Group, CHIBCHA Consortium, Australian National Endometrial Cancer Study Group, RENDOCAS, Australian Ovarian Cancer Study, GENICA Network, Biological Sciences, Medical and Health Sciences, Genetics & Heredity
Abstract

Common variants in the hepatocyte nuclear factor 1 homeobox B (HNF1B) gene are associated with the risk of Type II diabetes and multiple cancers. Evidence to date indicates that cancer risk may be mediated via genetic or epigenetic effects on HNF1B gene expression. We previously found single-nucleotide polymorphisms (SNPs) at the HNF1B locus to be associated with endometrial cancer, and now report extensive fine-mapping and in silico and laboratory analyses of this locus. Analysis of 1184 genotyped and imputed SNPs in 6608 Caucasian cases and 37 925 controls, and 895 Asian cases and 1968 controls, revealed the best signal of association for SNP rs11263763 (P = 8.4 × 10(-14), odds ratio = 0.86, 95% confidence interval = 0.82-0.89), located within HNF1B intron 1. Haplotype analysis and conditional analyses provide no evidence of further independent endometrial cancer risk variants at this locus. SNP rs11263763 genotype was associated with HNF1B mRNA expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas. Genetic analyses prioritized rs11263763 and four other SNPs in high-to-moderate linkage disequilibrium as the most likely causal SNPs. Three of these SNPs map to the extended HNF1B promoter based on chromatin marks extending from the minimal promoter region. Reporter assays demonstrated that this extended region reduces activity in combination with the minimal HNF1B promoter, and that the minor alleles of rs11263763 or rs8064454 are associated with decreased HNF1B promoter activity. Our findings provide evidence for a single signal associated with endometrial cancer risk at the HNF1B locus, and that risk is likely mediated via altered HNF1B gene expression.

Published
2015

24. Candidate locus analysis of the TERT–CLPTM1L cancer risk region on chromosome 5p15 identifies multiple independent variants associated with endometrial cancer risk

Author

Carvajal-Carmona, Luis G, O’Mara, Tracy A, Painter, Jodie N, Lose, Felicity A, Dennis, Joe, Michailidou, Kyriaki, Tyrer, Jonathan P, Ahmed, Shahana, Ferguson, Kaltin, Healey, Catherine S, Pooley, Karen, Beesley, Jonathan, Cheng, Timothy, Jones, Angela, Howarth, Kimberley, Martin, Lynn, Gorman, Maggie, Hodgson, Shirley, National Study of Endometrial Cancer Genetics Group (NSECG), The Australian National Endometrial Cancer Study Group (ANECS), Wentzensen, Nicholas, Fasching, Peter A, Hein, Alexander, Beckmann, Matthias W, Renner, Stefan P, Dörk, Thilo, Hillemanns, Peter, Dürst, Matthias, Runnebaum, Ingo, Lambrechts, Diether, Coenegrachts, Lieve, Schrauwen, Stefanie, Amant, Frederic, Winterhoff, Boris, Dowdy, Sean C, Goode, Ellen L, Teoman, Attila, Salvesen, Helga B, Trovik, Jone, Njolstad, Tormund S, Werner, Henrica MJ, Scott, Rodney J, Ashton, Katie, Proietto, Tony, Otton, Geoffrey, Wersäll, Ofra, Mints, Miriam, Tham, Emma, RENDOCAS, Hall, Per, Czene, Kamila, Liu, Jianjun, Li, Jingmei, Hopper, John L, Southey, Melissa C, Australian Ovarian Cancer Study (AOCS), Ekici, Arif B, Ruebner, Matthias, Johnson, Nichola, Peto, Julian, Burwinkel, Barbara, Marme, Frederik, Brenner, Hermann, Dieffenbach, Aida K, Meindl, Alfons, Brauch, Hiltrud, The GENICA Network, Lindblom, Annika, Depreeuw, Jeroen, Moisse, Matthieu, Chang-Claude, Jenny, Rudolph, Anja, Couch, Fergus J, Olson, Janet E, Giles, Graham G, Bruinsma, Fiona, Cunningham, Julie M, Fridley, Brooke L, Børresen-Dale, Anne-Lise, Kristensen, Vessela N, Cox, Angela, Swerdlow, Anthony J, Orr, Nicholas, Bolla, Manjeet K, Wang, Qin, Weber, Rachel Palmieri, Chen, Zhihua, Shah, Mitul, Pharoah, Paul DP, Dunning, Alison M, Tomlinson, Ian, Easton, Douglas F, Spurdle, Amanda B, and Thompson, Deborah J

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Oncology and Carcinogenesis, Genetic Testing, Human Genome, Prevention, Cancer, Uterine Cancer, 2.1 Biological and endogenous factors, Aetiology, Chromosomes, Human, Pair 5, Databases, Nucleic Acid, Female, Gene Expression Regulation, Neoplastic, Genetic Loci, Haplotypes, Humans, Membrane Proteins, Models, Genetic, Neoplasm Proteins, Polymorphism, Single Nucleotide, Promoter Regions, Genetic, Risk Factors, Telomerase, National Study of Endometrial Cancer Genetics Group, Australian National Endometrial Cancer Study Group, RENDOCAS, Australian Ovarian Cancer Study, GENICA Network, Complementary and Alternative Medicine, Paediatrics and Reproductive Medicine, Genetics & Heredity, Reproductive medicine
Abstract

Several studies have reported associations between multiple cancer types and single-nucleotide polymorphisms (SNPs) on chromosome 5p15, which harbours TERT and CLPTM1L, but no such association has been reported with endometrial cancer. To evaluate the role of genetic variants at the TERT-CLPTM1L region in endometrial cancer risk, we carried out comprehensive fine-mapping analyses of genotyped and imputed SNPs using a custom Illumina iSelect array which includes dense SNP coverage of this region. We examined 396 SNPs (113 genotyped, 283 imputed) in 4,401 endometrial cancer cases and 28,758 controls. Single-SNP and forward/backward logistic regression models suggested evidence for three variants independently associated with endometrial cancer risk (P = 4.9 × 10(-6) to P = 7.7 × 10(-5)). Only one falls into a haplotype previously associated with other cancer types (rs7705526, in TERT intron 1), and this SNP has been shown to alter TERT promoter activity. One of the novel associations (rs13174814) maps to a second region in the TERT promoter and the other (rs62329728) is in the promoter region of CLPTM1L; neither are correlated with previously reported cancer-associated SNPs. Using TCGA RNASeq data, we found significantly increased expression of both TERT and CLPTM1L in endometrial cancer tissue compared with normal tissue (TERT P = 1.5 × 10(-18), CLPTM1L P = 1.5 × 10(-19)). Our study thus reports a novel endometrial cancer risk locus and expands the spectrum of cancer types associated with genetic variation at 5p15, further highlighting the importance of this region for cancer susceptibility.

Published
2015

26. #925 Validation of single-cell profiling data from recurrent low stage endometrial cancer; low vimentin is a robust marker for poor prognosis in endometrial cancer, including in low-stage tumors

Author

Lien, Hilde Eide, primary, Hjelmeland, Marta Espevold, additional, Berg, Hege Fredriksen, additional, Halle, Mari Kyllesø, additional, Haldorsen, Ingfrid Salvesen, additional, Trovik, Jone, additional, Akslen, Lars Andreas, additional, and Krakstad, Camilla, additional

Published
2023
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29. Integrated Genomic Analysis of the 8q24 Amplification in Endometrial Cancers Identifies ATAD2 as Essential to MYC-Dependent Cancers

Author

Raeder, Maria B, Birkeland, Even, Trovik, Jone, Krakstad, Camilla, Shehata, Shyemaa, Schumacher, Steven, Zack, Travis I, Krohn, Antje, Werner, Henrica MJ, Moody, Susan E, Wik, Elisabeth, Stefansson, Ingunn M, Holst, Frederik, Oyan, Anne M, Tamayo, Pablo, Mesirov, Jill P, Kalland, Karl H, Akslen, Lars A, Simon, Ronald, Beroukhim, Rameen, and Salvesen, Helga B

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biotechnology, Genetics, Uterine Cancer, Rare Diseases, Cancer, Breast Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, ATPases Associated with Diverse Cellular Activities, Adenosine Triphosphatases, Cell Line, Tumor, DNA-Binding Proteins, Endometrial Neoplasms, Female, Genes, myc, Genomics, Humans, Immunoblotting, In Situ Hybridization, Fluorescence, General Science & Technology
Abstract

Chromosome 8q24 is the most commonly amplified region across multiple cancer types, and the typical length of the amplification suggests that it may target additional genes to MYC. To explore the roles of the genes most frequently included in 8q24 amplifications, we analyzed the relation between copy number alterations and gene expression in three sets of endometrial cancers (N = 252); and in glioblastoma, ovarian, and breast cancers profiled by TCGA. Among the genes neighbouring MYC, expression of the bromodomain-containing gene ATAD2 was the most associated with amplification. Bromodomain-containing genes have been implicated as mediators of MYC transcriptional function, and indeed ATAD2 expression was more closely associated with expression of genes known to be upregulated by MYC than was MYC itself. Amplifications of 8q24, expression of genes downstream from MYC, and overexpression of ATAD2 predicted poor outcome and increased from primary to metastatic lesions. Knockdown of ATAD2 and MYC in seven endometrial and 21 breast cancer cell lines demonstrated that cell lines that were dependent on MYC also depended upon ATAD2. These same cell lines were also the most sensitive to the histone deacetylase (HDAC) inhibitor Trichostatin-A, consistent with prior studies identifying bromodomain-containing proteins as targets of inhibition by HDAC inhibitors. Our data indicate high ATAD2 expression is a marker of aggressive endometrial cancers, and suggest specific inhibitors of ATAD2 may have therapeutic utility in these and other MYC-dependent cancers.

Published
2013

34. Supplementary Video Clips VCS1+2 and Optical Datsets ODS1+2 from PIK3CA Amplification Associates with Aggressive Phenotype but Not Markers of AKT-MTOR Signaling in Endometrial Carcinoma

Author

Holst, Frederik, primary, Werner, Henrica M.J., primary, Mjøs, Siv, primary, Hoivik, Erling A., primary, Kusonmano, Kanthida, primary, Wik, Elisabeth, primary, Berg, Anna, primary, Birkeland, Even, primary, Gibson, William J., primary, Halle, Mari K., primary, Trovik, Jone, primary, Cherniack, Andrew D., primary, Kalland, Karl-Henning, primary, Mills, Gordon B., primary, Singer, Christian F., primary, Krakstad, Camilla, primary, Beroukhim, Rameen, primary, and Salvesen, Helga B., primary

Published
2023
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36. Supplementary Figure 2 from Lack of Estrogen Receptor-α Is Associated with Epithelial–Mesenchymal Transition and PI3K Alterations in Endometrial Carcinoma

Author

Wik, Elisabeth, primary, Ræder, Maria B., primary, Krakstad, Camilla, primary, Trovik, Jone, primary, Birkeland, Even, primary, Hoivik, Erling A., primary, Mjos, Siv, primary, Werner, Henrica M.J., primary, Mannelqvist, Monica, primary, Stefansson, Ingunn M., primary, Oyan, Anne M., primary, Kalland, Karl H., primary, Akslen, Lars A., primary, and Salvesen, Helga B., primary

Published
2023
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37. Supplementary Table 3 from Lack of Estrogen Receptor-α Is Associated with Epithelial–Mesenchymal Transition and PI3K Alterations in Endometrial Carcinoma

Author

Wik, Elisabeth, primary, Ræder, Maria B., primary, Krakstad, Camilla, primary, Trovik, Jone, primary, Birkeland, Even, primary, Hoivik, Erling A., primary, Mjos, Siv, primary, Werner, Henrica M.J., primary, Mannelqvist, Monica, primary, Stefansson, Ingunn M., primary, Oyan, Anne M., primary, Kalland, Karl H., primary, Akslen, Lars A., primary, and Salvesen, Helga B., primary

Published
2023
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38. Supplementary Table 1 from Lack of Estrogen Receptor-α Is Associated with Epithelial–Mesenchymal Transition and PI3K Alterations in Endometrial Carcinoma

Author

Wik, Elisabeth, primary, Ræder, Maria B., primary, Krakstad, Camilla, primary, Trovik, Jone, primary, Birkeland, Even, primary, Hoivik, Erling A., primary, Mjos, Siv, primary, Werner, Henrica M.J., primary, Mannelqvist, Monica, primary, Stefansson, Ingunn M., primary, Oyan, Anne M., primary, Kalland, Karl H., primary, Akslen, Lars A., primary, and Salvesen, Helga B., primary

Published
2023
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39. Supplementary figure 1 from Potential Targets' Analysis Reveals Dual PI3K/mTOR Pathway Inhibition as a Promising Therapeutic Strategy for Uterine Leiomyosarcomas—an ENITEC Group Initiative

Author

Cuppens, Tine, primary, Annibali, Daniela, primary, Coosemans, An, primary, Trovik, Jone, primary, ter Haar, Natalja, primary, Colas, Eva, primary, Garcia-Jimenez, Angel, primary, Van de Vijver, Koen, primary, Kruitwagen, Roy P.M., primary, Brinkhuis, Mariël, primary, Zikan, Michal, primary, Dundr, Pavel, primary, Huvila, Jutta, primary, Carpén, Olli, primary, Haybaeck, Johannes, primary, Moinfar, Farid, primary, Salvesen, Helga B., primary, Stukan, Maciej, primary, Mestdagh, Carole, primary, Zweemer, Ronald P., primary, Massuger, Leonardus F., primary, Mallmann, Michael R., primary, Wardelmann, Eva, primary, Mints, Miriam, primary, Verbist, Godelieve, primary, Thomas, Debby, primary, Gommé, Ellen, primary, Hermans, Els, primary, Moerman, Philippe, primary, Bosse, Tjalling, primary, and Amant, Frédéric, primary

Published
2023
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40. Supplementary Figure S1 from PIK3CA Amplification Associates with Aggressive Phenotype but Not Markers of AKT-MTOR Signaling in Endometrial Carcinoma

Author

Holst, Frederik, primary, Werner, Henrica M.J., primary, Mjøs, Siv, primary, Hoivik, Erling A., primary, Kusonmano, Kanthida, primary, Wik, Elisabeth, primary, Berg, Anna, primary, Birkeland, Even, primary, Gibson, William J., primary, Halle, Mari K., primary, Trovik, Jone, primary, Cherniack, Andrew D., primary, Kalland, Karl-Henning, primary, Mills, Gordon B., primary, Singer, Christian F., primary, Krakstad, Camilla, primary, Beroukhim, Rameen, primary, and Salvesen, Helga B., primary

Published
2023
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41. Supplementary Figure 1 from High Phospho-Stathmin(Serine38) Expression Identifies Aggressive Endometrial Cancer and Suggests an Association with PI3K Inhibition

Author

Wik, Elisabeth, primary, Birkeland, Even, primary, Trovik, Jone, primary, Werner, Henrica M.J., primary, Hoivik, Erling A., primary, Mjos, Siv, primary, Krakstad, Camilla, primary, Kusonmano, Kanthida, primary, Mauland, Karen, primary, Stefansson, Ingunn M., primary, Holst, Frederik, primary, Petersen, Kjell, primary, Oyan, Anne M., primary, Simon, Ronald, primary, Kalland, Karl H., primary, Ricketts, William, primary, Akslen, Lars A., primary, and Salvesen, Helga B., primary

Published
2023
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42. Supplementary Figure 1 from Lack of Estrogen Receptor-α Is Associated with Epithelial–Mesenchymal Transition and PI3K Alterations in Endometrial Carcinoma

Author

Wik, Elisabeth, primary, Ræder, Maria B., primary, Krakstad, Camilla, primary, Trovik, Jone, primary, Birkeland, Even, primary, Hoivik, Erling A., primary, Mjos, Siv, primary, Werner, Henrica M.J., primary, Mannelqvist, Monica, primary, Stefansson, Ingunn M., primary, Oyan, Anne M., primary, Kalland, Karl H., primary, Akslen, Lars A., primary, and Salvesen, Helga B., primary

Published
2023
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43. Supplementary Table 2 from Lack of Estrogen Receptor-α Is Associated with Epithelial–Mesenchymal Transition and PI3K Alterations in Endometrial Carcinoma

Author

Wik, Elisabeth, primary, Ræder, Maria B., primary, Krakstad, Camilla, primary, Trovik, Jone, primary, Birkeland, Even, primary, Hoivik, Erling A., primary, Mjos, Siv, primary, Werner, Henrica M.J., primary, Mannelqvist, Monica, primary, Stefansson, Ingunn M., primary, Oyan, Anne M., primary, Kalland, Karl H., primary, Akslen, Lars A., primary, and Salvesen, Helga B., primary

Published
2023
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45. Supplementary Table 4 from Lack of Estrogen Receptor-α Is Associated with Epithelial–Mesenchymal Transition and PI3K Alterations in Endometrial Carcinoma

Author

Wik, Elisabeth, primary, Ræder, Maria B., primary, Krakstad, Camilla, primary, Trovik, Jone, primary, Birkeland, Even, primary, Hoivik, Erling A., primary, Mjos, Siv, primary, Werner, Henrica M.J., primary, Mannelqvist, Monica, primary, Stefansson, Ingunn M., primary, Oyan, Anne M., primary, Kalland, Karl H., primary, Akslen, Lars A., primary, and Salvesen, Helga B., primary

Published
2023
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46. Supplementary Methods from PIK3CA Amplification Associates with Aggressive Phenotype but Not Markers of AKT-MTOR Signaling in Endometrial Carcinoma

Author

Holst, Frederik, primary, Werner, Henrica M.J., primary, Mjøs, Siv, primary, Hoivik, Erling A., primary, Kusonmano, Kanthida, primary, Wik, Elisabeth, primary, Berg, Anna, primary, Birkeland, Even, primary, Gibson, William J., primary, Halle, Mari K., primary, Trovik, Jone, primary, Cherniack, Andrew D., primary, Kalland, Karl-Henning, primary, Mills, Gordon B., primary, Singer, Christian F., primary, Krakstad, Camilla, primary, Beroukhim, Rameen, primary, and Salvesen, Helga B., primary

Published
2023
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47. Supplementary Figure 2 from High Phospho-Stathmin(Serine38) Expression Identifies Aggressive Endometrial Cancer and Suggests an Association with PI3K Inhibition

Author

Wik, Elisabeth, primary, Birkeland, Even, primary, Trovik, Jone, primary, Werner, Henrica M.J., primary, Hoivik, Erling A., primary, Mjos, Siv, primary, Krakstad, Camilla, primary, Kusonmano, Kanthida, primary, Mauland, Karen, primary, Stefansson, Ingunn M., primary, Holst, Frederik, primary, Petersen, Kjell, primary, Oyan, Anne M., primary, Simon, Ronald, primary, Kalland, Karl H., primary, Ricketts, William, primary, Akslen, Lars A., primary, and Salvesen, Helga B., primary

Published
2023
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49. Supplementary Figure 1 from Genome-Wide Association Study Identifies a Possible Susceptibility Locus for Endometrial Cancer

Author

Long, Jirong, primary, Zheng, Wei, primary, Xiang, Yong-Bing, primary, Lose, Felicity, primary, Thompson, Deborah, primary, Tomlinson, Ian, primary, Yu, Herbert, primary, Wentzensen, Nicolas, primary, Lambrechts, Diether, primary, Dörk, Thilo, primary, Dubrowinskaja, Natalia, primary, Goodman, Marc T., primary, Salvesen, Helga B., primary, Fasching, Peter A., primary, Scott, Rodney J., primary, Delahanty, Ryan, primary, Zheng, Ying, primary, O'Mara, Tracy, primary, Healey, Catherine S., primary, Hodgson, Shirley, primary, Risch, Harvey, primary, Yang, Hannah P., primary, Amant, Frederic, primary, Turmanov, Nurzhan, primary, Schwake, Anita, primary, Lurie, Galina, primary, Trovik, Jone, primary, Beckmann, Matthias W., primary, Ashton, Katie, primary, Ji, Bu-Tian, primary, Bao, Ping-Ping, primary, Howarth, Kimberly, primary, Lu, Lingeng, primary, Lissowska, Jolanta, primary, Coenegrachts, Lieve, primary, Kaidarova, Dilyara, primary, Dürst, Matthias, primary, Thompson, Pamela J., primary, Krakstad, Camilla, primary, Ekici, Arif B., primary, Otton, Geoffrey, primary, Shi, Jiajun, primary, Zhang, Ben, primary, Gorman, Maggie, primary, Brinton, Louise, primary, Coosemans, An, primary, Matsuno, Rayna K., primary, Halle, Mari K., primary, Hein, Alexander, primary, Proietto, Anthony, primary, Cai, Hui, primary, Lu, Wei, primary, Dunning, Alison, primary, Easton, Douglas, primary, Gao, Yu-Tang, primary, Cai, Qiuyin, primary, Spurdle, Amanda B., primary, and Shu, Xiao-Ou, primary

Published
2023
Full Text
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50. Supplementary Figure 2 from Genome-Wide Association Study Identifies a Possible Susceptibility Locus for Endometrial Cancer

Author

Long, Jirong, primary, Zheng, Wei, primary, Xiang, Yong-Bing, primary, Lose, Felicity, primary, Thompson, Deborah, primary, Tomlinson, Ian, primary, Yu, Herbert, primary, Wentzensen, Nicolas, primary, Lambrechts, Diether, primary, Dörk, Thilo, primary, Dubrowinskaja, Natalia, primary, Goodman, Marc T., primary, Salvesen, Helga B., primary, Fasching, Peter A., primary, Scott, Rodney J., primary, Delahanty, Ryan, primary, Zheng, Ying, primary, O'Mara, Tracy, primary, Healey, Catherine S., primary, Hodgson, Shirley, primary, Risch, Harvey, primary, Yang, Hannah P., primary, Amant, Frederic, primary, Turmanov, Nurzhan, primary, Schwake, Anita, primary, Lurie, Galina, primary, Trovik, Jone, primary, Beckmann, Matthias W., primary, Ashton, Katie, primary, Ji, Bu-Tian, primary, Bao, Ping-Ping, primary, Howarth, Kimberly, primary, Lu, Lingeng, primary, Lissowska, Jolanta, primary, Coenegrachts, Lieve, primary, Kaidarova, Dilyara, primary, Dürst, Matthias, primary, Thompson, Pamela J., primary, Krakstad, Camilla, primary, Ekici, Arif B., primary, Otton, Geoffrey, primary, Shi, Jiajun, primary, Zhang, Ben, primary, Gorman, Maggie, primary, Brinton, Louise, primary, Coosemans, An, primary, Matsuno, Rayna K., primary, Halle, Mari K., primary, Hein, Alexander, primary, Proietto, Anthony, primary, Cai, Hui, primary, Lu, Wei, primary, Dunning, Alison, primary, Easton, Douglas, primary, Gao, Yu-Tang, primary, Cai, Qiuyin, primary, Spurdle, Amanda B., primary, and Shu, Xiao-Ou, primary

Published
2023
Full Text
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