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325 results on '"Lønning, P E"'

4. A national precision cancer medicine implementation initiative for Norway

Author

Taskén, Kjetil, Russnes, Hege E. G., Aas, Eline, Bjørge, Line, Blix, Egil S., Enerly, Espen, Fagereng, Gro L., Flobak, Åsmund, Gilje, Bjørnar, Gjertsen, Bjørn T., Guren, Tormod K., Heix, Jutta, Hovig, Eivind, Hovland, Randi, Lønning, Per E., Meza-Zepeda, Leonardo A., Mæhle, Per M., Nilsen, Hilde L., Thoresen, Steinar Ø., Widerberg, Ketil, Smeland, Sigbjørn, and Helland, Åslaug

Published
2022
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8. Epithelial to mesenchymal transition (EMT) is associated with attenuation of succinate dehydrogenase (SDH) in breast cancer through reduced expression of SDHC

Author

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.

Published
2019
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10. Demystifying BRAFMutation Status in Colorectal Liver Metastases

Author

Margonis, Georgios A., Boerner, Thomas, Bachet, Jean-Baptiste, Buettner, Stefan, Moretto, Roberto, Andreatos, Nikolaos, Sartore-Bianchi, Andrea, Wang, Jane, Kamphues, Carsten, Gagniere, Johan, Lonardi, Sara, Løes, Inger M., Wagner, Doris, Spallanzani, Andrea, Sasaki, Kazunari, Burkhart, Richard, Pietrantonio, Filippo, Pikoulis, Emmanouil, Pawlik, Timothy M., Truant, Stéphanie, Orlandi, Armando, Pikouli, Anastasia, Pella, Nicoletta, Beyer, Katharina, Poultsides, George, Seeliger, Hendrik, Aucejo, Federico N., Kornprat, Peter, Kaczirek, Klaus, Lønning, Per E., Kreis, Martin E., Wolfgang, Christopher L., Weiss, Matthew J., Cremolini, Chiara, Benoist, Stéphane, and D’Angelica, Michael

Published
2023
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11. Prognostic and predictive value of ERβ1 and ERβ2 in the Intergroup Exemestane Study (IES)—first results from PathIES†

Author

Speirs, V., Viale, G., Mousa, K., Palmieri, C., Reed, S. N., Nicholas, H., Cheang, M., Jassem, J., Lønning, P. E., Kalaitzaki, E., van de Velde, C. J. H., Rasmussen, B. B., Verhoeven, D. M., Shaaban, A. M., Bartlett, J. M. S., Bliss, J. M., Coombes, R. C., Jassem, J., Brociek, A., Pliszka, A., Andersen, J., Bruun Rasmussen, B., van de Velde, C., Meershoek, E., Paridaens, R., Delorge, A., Coates, A., Camler, R., Coombes, R.C., Mousa, K., Reed, S., Verhoeven, D., Herman, S., Visini, M., and Lonning, P.

Published
2015
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17. Mutation of GATA3 in human breast tumors

Author

Usary, Jerry, Llaca, Victor, Karaca, Gamze, Presswala, Shafaq, Karaca, Mehmet, He, Xiaping, Langerød, Anita, Kåresen, Rolf, Oh, Daniel S, Dressler, Lynn G, Lønning, Per E, Strausberg, Robert L, Chanock, Stephen, Børresen-Dale, Anne-Lise, and Perou, Charles M

Published
2004
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22. Constitutional BRCA1 Methylation and Risk of Incident Triple-Negative Breast Cancer and High-grade Serous Ovarian Cancer

Author

Lønning, Per E., Nikolaienko, Oleksii, Pan, Kathy, Kurian, Allison W., Eikesdal, Hans P., Pettinger, Mary, Anderson, Garnet L., Prentice, Ross L., Chlebowski, Rowan T., and Knappskog, Stian

Abstract

IMPORTANCE: About 25% of all triple-negative breast cancers (TNBCs) and 10% to 20% of high-grade serous ovarian cancers (HGSOCs) harbor BRCA1 promoter methylation. While constitutional BRCA1 promoter methylation has been observed in normal tissues of some individuals, the potential role of normal tissue methylation as a risk factor for incident TNBC or HGSOC is unknown. OBJECTIVE: To assess the potential association between white blood cell BRCA1 promoter methylation and subsequent risk of incident TNBC and HGSOC. DESIGN, SETTING, AND PARTICIPANTS: This case-control study included women who were participating in the Women’s Health Initiative study who had not received a diagnosis of either breast or ovarian cancer before study entrance. A total of 637 women developing incident TNBC and 511 women developing incident HGSOC were matched with cancer-free controls (1841 and 2982, respectively) in a nested case-control design. Cancers were confirmed after central medical record review. Blood samples, which were collected at entry, were analyzed for BRCA1 promoter methylation by massive parallel sequencing. The study was performed in the Mohn Cancer Research Laboratory (Bergen, Norway) between 2019 and 2022. MAIN OUTCOMES AND MEASURES: Associations between BRCA1 methylation and incident TNBC and incident HGSOC were analyzed by Cox proportional hazards regression. RESULTS: Of 2478 cases and controls in the TNBC group and 3493 cases and controls in the HGSOC group, respectively, 7 (0.3%) and 3 (0.1%) were American Indian or Alaska Native, 46 (1.9%) and 30 (0.9%) were Asian, 1 (0.04%) and 1 (0.03%) was Native Hawaiian or Pacific Islander, 326 (13.2%) and 125 (3.6%) were Black or African, 56 (2.3%) and 116 (3.3%) were Hispanic, 2046 (82.6%) and 3257 (93.2%) were White, and 35 (1.4%) and 35 (1.0%) were multiracial. Median (range) age at entry was 62 (50-79) years, with a median interval to diagnosis of 9 (TNBC) and 10 (HGSOC) years. Methylated BRCA1 alleles were present in 194 controls (5.5%). Methylation was associated with risk of incident TNBC (12.4% methylated; HR, 2.35; 95% CI, 1.70-3.23; P < .001) and incident HGSOC (9.4% methylated; HR, 1.93; 95% CI, 1.36-2.73; P < .001). Restricting analyses to individuals with more than 5 years between sampling and cancer diagnosis yielded similar results (TNBC: HR, 2.52; 95% CI, 1.75-3.63; P < .001; HGSOC: HR, 1.82; 95% CI, 1.22-2.72; P = .003). Across individuals, methylation was not haplotype-specific, arguing against an underlying cis-acting factor. Within individuals, BRCA1 methylation was observed on the same allele, indicating clonal expansion from a single methylation event. There was no association found between BRCA1 methylation and germline pathogenic variant status. CONCLUSIONS AND RELEVANCE: The results of this case-control suggest that constitutional normal tissue BRCA1 promoter methylation is significantly associated with risk of incident TNBC and HGSOC, with potential implications for prediction of these cancers. These findings warrant further research to determine if constitutional methylation of tumor suppressor genes are pancancer risk factors.

Published
2022
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24. Molecular portraits of human breast tumours

Author

Perou, Charles M., Sørlie, Therese, Eisen, Michael B., van de Rijn, Matt, Jeffrey, Stefanie S., Rees, Christian A., Pollack, Jonathan R., Ross, Douglas T., Johnsen, Hilde, Akslen, Lars A., Fluge, Øystein, Pergamenschikov, Alexander, Williams, Cheryl, Zhu, Shirley X., Lønning, Per E., Børresen-Dale, Anne-Lise, Brown, Patrick O., and Botstein, David

Published
2000
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42. Prognostic value of metabolic response in breast cancer patients receiving neoadjuvant chemotherapy

Author

Cao Maria D, Giskeødegård Guro F, Bathen Tone F, Sitter Beathe, Bofin Anna, Lønning Per E, Lundgren Steinar, and Gribbestad Ingrid S

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Today's clinical diagnostic tools are insufficient for giving accurate prognosis to breast cancer patients. The aim of our study was to examine the tumor metabolic changes in patients with locally advanced breast cancer caused by neoadjuvant chemotherapy (NAC), relating these changes to clinical treatment response and long-term survival. Methods Patients (n = 89) participating in a randomized open-label multicenter study were allocated to receive either NAC as epirubicin or paclitaxel monotherapy. Biopsies were excised pre- and post-treatment, and analyzed by high resolution magic angle spinning magnetic resonance spectroscopy (HR MAS MRS). The metabolite profiles were examined by paired and unpaired multivariate methods and findings of important metabolites were confirmed by spectral integration of the metabolite peaks. Results All patients had a significant metabolic response to NAC, and pre- and post-treatment spectra could be discriminated with 87.9%/68.9% classification accuracy by paired/unpaired partial least squares discriminant analysis (PLS-DA) (p < 0.001). Similar metabolic responses were observed for the two chemotherapeutic agents. The metabolic responses were related to patient outcome. Non-survivors (< 5 years) had increased tumor levels of lactate (p = 0.004) after treatment, while survivors (≥ 5 years) experienced a decrease in the levels of glycine (p = 0.047) and choline-containing compounds (p ≤ 0.013) and an increase in glucose (p = 0.002) levels. The metabolic responses were not related to clinical treatment response. Conclusions The differences in tumor metabolic response to NAC were associated with breast cancer survival, but not to clinical response. Monitoring metabolic responses to NAC by HR MAS MRS may provide information about tumor biology related to individual prognosis.

Published
2012
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44. Expression of full-length p53 and its isoform Δp53 in breast carcinomas in relation to mutation status and clinical parameters

Author

Deppert Wolfgang, Lønning Per E, Geisler Stephanie B, Bergamaschi Anna, Langerød Anita, Myhre Simen, Baumbusch Lars O, Dornreiter Irene, and Børresen-Dale Anne-Lise

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background The tumor suppressor gene p53 (TP53) controls numerous signaling pathways and is frequently mutated in human cancers. Novel p53 isoforms suggest alternative splicing as a regulatory feature of p53 activity. Results In this study we have analyzed mRNA expression of both wild-type and mutated p53 and its respective Δp53 isoform in 88 tumor samples from breast cancer in relation to clinical parameters and molecular subgroups. Three-dimensional structure differences for the novel internally deleted p53 isoform Δp53 have been predicted. We confirmed the expression of Δp53 mRNA in tumors using quantitative real-time PCR technique. The mRNA expression levels of the two isoforms were strongly correlated in both wild-type and p53-mutated tumors, with the level of the Δp53 isoform being approximately 1/3 of that of the full-length p53 mRNA. Patients expressing mutated full-length p53 and non-mutated (wild-type) Δp53, "mutational hybrids", showed a slightly higher frequency of patients with distant metastasis at time of diagnosis compared to other patients with p53 mutations, but otherwise did not differ significantly in any other clinical parameter. Interestingly, the p53 wild-type tumors showed a wide range of mRNA expression of both p53 isoforms. Tumors with mRNA expression levels in the upper or lower quartile were significantly associated with grade and molecular subtypes. In tumors with missense or in frame mutations the mRNA expression levels of both isoforms were significantly elevated, and in tumors with nonsense, frame shift or splice mutations the mRNA levels were significantly reduced compared to those expressing wild-type p53. Conclusion Expression of p53 is accompanied by the functionally different isoform Δp53 at the mRNA level in cell lines and human breast tumors. Investigations of "mutational hybrid" patients highlighted that wild-type Δp53 does not compensates for mutated p53, but rather may be associated with a worse prognosis. In tumors, both isoforms show strong correlations in different mutation-dependent mRNA expression patterns.

Published
2006
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45. Patterns of genomic evolution in advanced melanoma

Author

Birkeland, E., primary, Zhang, S., additional, Poduval, D., additional, Geisler, J., additional, Nakken, S., additional, Vodak, D., additional, Meza-Zepeda, L. A., additional, Hovig, E., additional, Myklebost, O., additional, Knappskog, S., additional, and Lønning, P. E., additional

Published
2018
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46. Impact of MDM2promoter SNP55 (rs2870820) on risk of endometrial and ovarian cancer

Author

Helwa, Reham, Gansmo, Liv B., Bjørnslett, Merete, Halle, Mari Kyllesø, Werner, Henrica M. J., Romundstad, Pål, Hveem, Kristian, Vatten, Lars, Dørum, Anne, Lønning, Per E., and Knappskog, Stian

Abstract

AbstractBackgroundWhile large GWAS analyses have not found convincing associations between MDM2promoter SNP55 and gynaecological cancers, SNP55 is in linkage disequilibrium with two other functional SNPs in the same promoter, likely to obscure associations between single SNPs and cancer risk. Here, we assessed the impact of SNP55 on risk of endometrial and ovarian cancer, including sub-analyses stratified for other functional SNPs in the region.Material and methodsUsing a custom LightSNiP assay, we genotyped SNP55 in two large hospital-based cohorts of patients with ovarian (n = 1,332) and endometrial (n = 1,363) cancer and compared genotypes to healthy female controls (n = 1,858).ResultsAmong individuals harbouring the SNP309TT genotype, the minor SNP55T-allele was associated with a reduced risk of endometrial (dominant model: OR = 0.63; CI = 0.45–0.88; p = 0.01). Regardless of the genotype in neighbouring SNPs, the SNP55T-allele was also associated with a reduced risk of endometrial cancer before 50 years of age (dominant model: OR = 0.56; CI = 0.34–0.90; p = 0.02). No association between SNP55 status and ovarian cancer risk was observed.ConclusionsMDM2SNP55T-allele may correlate with reduced risk for endometrial cancer in a SNP309T-, but not SNP309G, context.

Published
2021
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47. Assessing Novel Therapies Based on Late-Stage Efficacy: A Dangerous Concept?

Author

Lønning, Per E.

Abstract

Traditionally, the efficacy of novel cancer therapies has been confirmed in patients failing regular treatment before being tested in early disease. Improved understanding of the mechanisms guiding therapeutic efficacy may challenge this dogma, suggesting novel therapies to move into early evaluation based on biological rationales without late-stage efficacy evaluation.

Published
2021
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50. Population distribution and ancestry of the cancer protective MDM2 SNP285 (rs117039649)

Author

Knappskog, S., Gansmo, L. B., Dibirova, K., Metspalu, A., Cybulski, C., Peterlongo, P., Aaltonen, L., Vatten, L., Romundstad, P., Hveem, K., Devilee, P., Evans, G. D., Lin, D., Camp, G. V., Manolopoulos, V. G., Osorio, A., Milani, L., Ozcelik, T., Zalloua, P., Mouzaya, F., Elena Bliznetz, Balanovska, E., Pocheshkova, E., Kucinskas, V., Atramentova, L., Nymadawa, P., Titov, K., Lavryashina, M., Yusupov, Y., Bogdanova, N., Koshel, S., Zamora, J., Wedge, D. C., Charlesworth, D., Dörk, T., Balanovsky, O., and Lønning, P. E.

Subjects
Medical sciences: 700::Clinical medical sciences: 750::Oncology: 762 [VDP], Asia, Polymorphism, Single Nucleotide, Risk Assessment, White People, polymorphism, Gene Frequency, MDM2, Risk Factors, Neoplasms, Databases, Genetic, Data Mining, Humans, Genetic Predisposition to Disease, Polymorphism, Promoter Regions, Genetic, Biology, Medisinske fag: 700::Klinisk medisinske fag: 750::Onkologi: 762 [VDP], promoter, Manchester Cancer Research Centre, ResearchInstitutes_Networks_Beacons/mcrc, Proto-Oncogene Proteins c-mdm2, SNP285, Protective Factors, Europe, Haplotypes, Midical sciences: 700::Clinical medical sciences: 750::Oncology: 762 [VDP], SNP309, Human medicine, Research Paper
Abstract

The MDM2 promoter SNP285C is located on the SNP309G allele. While SNP309G enhances Sp1 transcription factor binding and MDM2 transcription, SNP285C antagonizes Sp1 binding and reduces the risk of breast-, ovary- and endometrial cancer. Assessing SNP285 and 309 genotypes across 25 different ethnic populations (>10.000 individuals), the incidence of SNP285C was 6-8% across European populations except for Finns (1.2%) and Saami (0.3%). The incidence decreased towards the Middle-East and Eastern Russia, and SNP285C was absent among Han Chinese, Mongolians and African Americans. Interhaplotype variation analyses estimated SNP285C to have originated about 14,700 years ago (95% CI: 8,300 – 33,300). Both this estimate and the geographical distribution suggest SNP285C to have arisen after the separation between Caucasians and modern day East Asians (17,000 - 40,000 years ago). We observed a strong inverse correlation (r = -0.805; p < 0.001) between the percentage of SNP309G alleles harboring SNP285C and the MAF for SNP309G itself across different populations suggesting selection and environmental adaptation with respect to MDM2 expression in recent human evolution. In conclusion, we found SNP285C to be a pan-Caucasian variant. Ethnic variation regarding distribution of SNP285C needs to be taken into account when assessing the impact of MDM2 SNPs on cancer risk. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Published
2014
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