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Andreaggi, K., Bodner, M., Ring, J. D., Ameur, A., Gyllensten, U. B., Parson, W., . . . Allen, M. (2023). Complete Mitochondrial DNA Genome Variation in the Swedish Population. Genes, 14(11), 1989-1989
Open this publication in new window or tab >>Complete Mitochondrial DNA Genome Variation in the Swedish Population
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2023 (English)In: Genes, ISSN 2073-4425, E-ISSN 2073-4425, Vol. 14, no 11, p. 1989-1989Article in journal (Refereed) Published
Abstract [en]

The development of complete mitochondrial genome (mitogenome) reference data for inclusion in publicly available population databases is currently underway, and the generation of more high-quality mitogenomes will only enhance the statistical power of this forensically useful locus. To characterize mitogenome variation in Sweden, the mitochondrial DNA (mtDNA) reads from the SweGen whole genome sequencing (WGS) dataset were analyzed. To overcome the interference from low-frequency nuclear mtDNA segments (NUMTs), a 10% variant frequency threshold was applied for the analysis. In total, 934 forensic-quality mitogenome haplotypes were characterized. Almost 45% of the SweGen haplotypes belonged to haplogroup H. Nearly all mitogenome haplotypes (99.1%) were assigned to European haplogroups, which was expected based on previous mtDNA studies of the Swedish population. There were signature northern Swedish and Finnish haplogroups observed in the dataset (e.g., U5b1, W1a), consistent with the nuclear DNA analyses of the SweGen data. The complete mitogenome analysis resulted in high haplotype diversity (0.9996) with a random match probability of 0.15%. Overall, the SweGen mitogenomes provide a large mtDNA reference dataset for the Swedish population and also contribute to the effort to estimate global mitogenome haplotype frequencies.

Place, publisher, year, edition, pages
MDPI, 2023
National Category
Genetics
Research subject
Molecular Genetics
Identifiers
urn:nbn:se:uu:diva-516819 (URN)10.3390/genes14111989 (DOI)001113996900001 ()38002932 (PubMedID)
Funder
Science for Life Laboratory, SciLifeLab, 2014.0272
Available from: 2023-11-29 Created: 2023-11-29 Last updated: 2023-12-22Bibliographically approved
Llobet, M. O., Johansson, Å., Gyllensten, U. B., Allen, M. & Enroth, S. (2023). Forensic prediction of sex, age, height, body mass index, hip-to-waist ratio, smoking status and lipid lowering drugs using epigenetic markers and plasma proteins. Forensic Science International: Genetics, 65, Article ID 102871.
Open this publication in new window or tab >>Forensic prediction of sex, age, height, body mass index, hip-to-waist ratio, smoking status and lipid lowering drugs using epigenetic markers and plasma proteins
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2023 (English)In: Forensic Science International: Genetics, ISSN 1872-4973, E-ISSN 1878-0326, Vol. 65, article id 102871Article in journal (Refereed) Published
Abstract [en]

The prediction of human characteristics from blood using molecular markers would be very helpful in forensic science. Such information can be particularly important in providing investigative leads in police casework from, for example, blood found at crime scenes in cases without a suspect. Here, we investigated the possibilities and limitations of predicting seven phenotypic traits (sex, age, height, body mass index [BMI], hip-to-waist [WTH] ratio, smoking status and lipid-lowering drug use) using either DNA methylation or plasma proteins separately or in combination. We developed a prediction pipeline starting with the prediction of sex followed by sex-specific, stepwise, individual age, sex-specific anthropometric traits and, finally, lifestyle-related traits. Our data revealed that age, sex and smoking status can be accurately predicted from DNA methylation alone, while the use of plasma proteins was highly accurate for prediction of the WTH ratio, and a combined analysis of the best predictions for BMI and lipid-lowering drug use. In unseen individuals, age was predicted with a standard error of 3.3 years for women and 6.5 years for men, while the accuracy in smoking prediction across both men and women was 0.86. In conclusion, we have developed a stepwise approach for the de-novo prediction of individual characteristics from plasma proteins and DNA methylation markers. These models are accurate and may provide valuable information and investigative leads in future forensic casework.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Epigenetics, Externally visible characteristics (EVC), Phenotyping, Prediction, Proteomics
National Category
Bioinformatics and Systems Biology
Research subject
Biology
Identifiers
urn:nbn:se:uu:diva-500631 (URN)10.1016/j.fsigen.2023.102871 (DOI)001055104500001 ()37054667 (PubMedID)
Funder
Swedish Foundation for Strategic ResearchSwedish Research Council, MA 2022-02056Swedish Research Council, SE 220604FESwedish Cancer SocietySwedish Collegium for Advanced Study (SCAS)
Available from: 2023-04-20 Created: 2023-04-20 Last updated: 2023-09-14Bibliographically approved
van de Vegte, Y., Eppinga, R. P., van der Ende, M. Y., Hagemeijer, Y., Mahendran, Y. V., Salfati, E. Y., . . . van der Harst, P. (2023). Genetic insights into resting heart rate and its role in cardiovascular disease. Nature Communications, 14(1), Article ID 4646.
Open this publication in new window or tab >>Genetic insights into resting heart rate and its role in cardiovascular disease
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2023 (English)In: Nature Communications, E-ISSN 2041-1723, Vol. 14, no 1, article id 4646Article in journal (Refereed) Published
Abstract [en]

The genetics and clinical consequences of resting heart rate (RHR) remain incompletely understood. Here, the authors discover new genetic variants associated with RHR and find that higher genetically predicted RHR decreases risk of atrial fibrillation and ischemic stroke. Resting heart rate is associated with cardiovascular diseases and mortality in observational and Mendelian randomization studies. The aims of this study are to extend the number of resting heart rate associated genetic variants and to obtain further insights in resting heart rate biology and its clinical consequences. A genome-wide meta-analysis of 100 studies in up to 835,465 individuals reveals 493 independent genetic variants in 352 loci, including 68 genetic variants outside previously identified resting heart rate associated loci. We prioritize 670 genes and in silico annotations point to their enrichment in cardiomyocytes and provide insights in their ECG signature. Two-sample Mendelian randomization analyses indicate that higher genetically predicted resting heart rate increases risk of dilated cardiomyopathy, but decreases risk of developing atrial fibrillation, ischemic stroke, and cardio-embolic stroke. We do not find evidence for a linear or non-linear genetic association between resting heart rate and all-cause mortality in contrast to our previous Mendelian randomization study. Systematic alteration of key differences between the current and previous Mendelian randomization study indicates that the most likely cause of the discrepancy between these studies arises from false positive findings in previous one-sample MR analyses caused by weak-instrument bias at lower P-value thresholds. The results extend our understanding of resting heart rate biology and give additional insights in its role in cardiovascular disease development.

Place, publisher, year, edition, pages
Springer Nature, 2023
National Category
Cardiac and Cardiovascular Systems Medical Genetics
Identifiers
urn:nbn:se:uu:diva-511622 (URN)10.1038/s41467-023-39521-2 (DOI)001042222000014 ()37532724 (PubMedID)
Funder
Wellcome trust, 202802/Z/16/Z
Available from: 2023-09-15 Created: 2023-09-15 Last updated: 2023-10-03Bibliographically approved
Zhao, J. H., Stacey, D., Eriksson, N., Macdonald-Dunlop, E., Hedman, Å. K., Kalnapenkis, A., . . . Peters, J. E. (2023). Genetics of circulating inflammatory proteins identifies drivers of immune-mediated disease risk and therapeutic targets. Nature Immunology, 24(9), 1540-1551
Open this publication in new window or tab >>Genetics of circulating inflammatory proteins identifies drivers of immune-mediated disease risk and therapeutic targets
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2023 (English)In: Nature Immunology, ISSN 1529-2908, E-ISSN 1529-2916, Vol. 24, no 9, p. 1540-1551Article in journal (Refereed) Published
Abstract [en]

Circulating proteins have important functions in inflammation and a broad range of diseases. To identify genetic influences on inflammation-related proteins, we conducted a genome-wide protein quantitative trait locus (pQTL) study of 91 plasma proteins measured using the Olink Target platform in 14,824 participants. We identified 180 pQTLs (59 cis, 121 trans). Integration of pQTL data with eQTL and disease genome-wide association studies provided insight into pathogenesis, implicating lymphotoxin-alpha in multiple sclerosis. Using Mendelian randomization (MR) to assess causality in disease etiology, we identified both shared and distinct effects of specific proteins across immune-mediated diseases, including directionally discordant effects of CD40 on risk of rheumatoid arthritis versus multiple sclerosis and inflammatory bowel disease. MR implicated CXCL5 in the etiology of ulcerative colitis (UC) and we show elevated gut CXCL5 transcript expression in patients with UC. These results identify targets of existing drugs and provide a powerful resource to facilitate future drug target prioritization. Here the authors identify genetic effectors of the level of inflammation-related plasma proteins and use Mendelian randomization to identify proteins that contribute to immune-mediated disease risk.

Place, publisher, year, edition, pages
Springer Nature, 2023
National Category
Medical Genetics Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:uu:diva-511130 (URN)10.1038/s41590-023-01588-w (DOI)001046606600005 ()37563310 (PubMedID)
Available from: 2023-09-08 Created: 2023-09-08 Last updated: 2023-09-19Bibliographically approved
Alvez, M. B., Edfors, F., von Feilitzen, K., Zwahlen, M., Mardinoglu, A., peedq227, P.-H. D., . . . Uhlen, M. (2023). Next generation pan-cancer blood proteome profiling using proximity extension assay. Nature Communications, 14, Article ID 08.
Open this publication in new window or tab >>Next generation pan-cancer blood proteome profiling using proximity extension assay
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2023 (English)In: Nature Communications, E-ISSN 2041-1723, Vol. 14, article id 08Article in journal (Refereed) Published
Abstract [en]

Comprehensive and scalable proteomic profiling of plasma samples can improve the screening and diagnosis of cancer patients. Here, the authors use the Olink Proximity Extension Assay technology to characterise the plasma proteomes of 1477 patients across twelve cancer types, and use machine learning to obtain a protein panel for cancer classification. A comprehensive characterization of blood proteome profiles in cancer patients can contribute to a better understanding of the disease etiology, resulting in earlier diagnosis, risk stratification and better monitoring of the different cancer subtypes. Here, we describe the use of next generation protein profiling to explore the proteome signature in blood across patients representing many of the major cancer types. Plasma profiles of 1463 proteins from more than 1400 cancer patients are measured in minute amounts of blood collected at the time of diagnosis and before treatment. An open access Disease Blood Atlas resource allows the exploration of the individual protein profiles in blood collected from the individual cancer patients. We also present studies in which classification models based on machine learning have been used for the identification of a set of proteins associated with each of the analyzed cancers. The implication for cancer precision medicine of next generation plasma profiling is discussed.

Place, publisher, year, edition, pages
Springer Nature, 2023
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-510006 (URN)10.1038/s41467-023-39765-y (DOI)001037322100032 ()37463882 (PubMedID)
Funder
Knut and Alice Wallenberg FoundationSwedish Research Council, 2018-05973Swedish Research Council, 2020-06175
Available from: 2023-08-28 Created: 2023-08-28 Last updated: 2023-08-28
Weishaupt, H., Čančer, M., Rosén, G., Holmberg, K. O., Häggqvist, S., Bunikis, I., . . . Swartling, F. J. (2023). Novel cancer gene discovery using a forward genetic screen in RCAS-PDGFB-driven gliomas. Neuro-Oncology, 25(1), 97-107
Open this publication in new window or tab >>Novel cancer gene discovery using a forward genetic screen in RCAS-PDGFB-driven gliomas
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2023 (English)In: Neuro-Oncology, ISSN 1522-8517, E-ISSN 1523-5866, Vol. 25, no 1, p. 97-107Article in journal (Refereed) Published
Abstract [en]

Background Malignant gliomas, the most common malignant brain tumors in adults, represent a heterogeneous group of diseases with poor prognosis. Retroviruses can cause permanent genetic alterations that modify genes close to the viral integration site. Methods Here we describe the use of a high-throughput pipeline coupled to the commonly used tissue-specific retroviral RCAS-TVA mouse tumor model system. Utilizing next-generation sequencing, we show that retroviral integration sites can be reproducibly detected in malignant stem cell lines generated from RCAS-PDGFB-driven glioma biopsies. Results A large fraction of common integration sites contained genes that have been dysregulated or misexpressed in glioma. Others overlapped with loci identified in previous glioma-related forward genetic screens, but several novel putative cancer-causing genes were also found. Integrating retroviral tagging and clinical data, Ppfibp1 was highlighted as a frequently tagged novel glioma-causing gene. Retroviral integrations into the locus resulted in Ppfibp1 upregulation, and Ppfibp1-tagged cells generated tumors with shorter latency on orthotopic transplantation. In human gliomas, increased PPFIBP1 expression was significantly linked to poor prognosis and PDGF treatment resistance. Conclusions Altogether, the current study has demonstrated a novel approach to tagging glioma genes via forward genetics, validating previous results, and identifying PPFIBP1 as a putative oncogene in gliomagenesis.

Place, publisher, year, edition, pages
Oxford University Press, 2023
Keywords
forward genetics screen, glioblastoma, liprin-beta-1, PDGFB, RCAS
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-496938 (URN)10.1093/neuonc/noac158 (DOI)000834326400001 ()35738865 (PubMedID)
Funder
EU, Horizon 2020, 640275Swedish Cancer SocietySwedish Research CouncilRagnar Söderbergs stiftelseSwedish Childhood Cancer Foundation
Available from: 2023-02-22 Created: 2023-02-22 Last updated: 2023-02-22Bibliographically approved
Wen, J., Trost, B., Engchuan, W., Halvorsen, M., Pallotto, L. M., Mitina, A., . . . Szatkiewicz, J. P. (2023). Rare tandem repeat expansions associate with genes involved in synaptic and neuronal signaling functions in schizophrenia. Molecular Psychiatry, 28(1), 475-482
Open this publication in new window or tab >>Rare tandem repeat expansions associate with genes involved in synaptic and neuronal signaling functions in schizophrenia
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2023 (English)In: Molecular Psychiatry, ISSN 1359-4184, E-ISSN 1476-5578, Vol. 28, no 1, p. 475-482Article in journal (Refereed) Published
Abstract [en]

Tandem repeat expansions (TREs) are associated with over 60 monogenic disorders and have recently been implicated in complex disorders such as cancer and autism spectrum disorder. The role of TREs in schizophrenia is now emerging. In this study, we have performed a genome-wide investigation of TREs in schizophrenia. Using genome sequence data from 1154 Swedish schizophrenia cases and 934 ancestry-matched population controls, we have detected genome-wide rare (<0.1% population frequency) TREs that have motifs with a length of 2-20 base pairs. We find that the proportion of individuals carrying rare TREs is significantly higher in the schizophrenia group. There is a significantly higher burden of rare TREs in schizophrenia cases than in controls in genic regions, particularly in postsynaptic genes, in genes overlapping brain expression quantitative trait loci, and in brain-expressed genes that are differentially expressed between schizophrenia cases and controls. We demonstrate that TRE-associated genes are more constrained and primarily impact synaptic and neuronal signaling functions. These results have been replicated in an independent Canadian sample that consisted of 252 schizophrenia cases of European ancestry and 222 ancestry-matched controls. Our results support the involvement of rare TREs in schizophrenia etiology.

Place, publisher, year, edition, pages
Springer Nature, 2023
National Category
Psychiatry
Identifiers
urn:nbn:se:uu:diva-502306 (URN)10.1038/s41380-022-01857-4 (DOI)000884206400002 ()36380236 (PubMedID)
Funder
Swedish Research Council, D0886501Swedish Research CouncilKnut and Alice Wallenberg FoundationKnut and Alice Wallenberg Foundation, 2014.0272Swedish Research Council, 2017-00641Swedish Research Council, 2018-05973
Available from: 2023-05-24 Created: 2023-05-24 Last updated: 2023-05-29Bibliographically approved
Kierczak, M., Rafati, N., Höglund, J., Gourlé, H., Lo Faro, V., Schmitz, D., . . . Johansson, Å. (2022). Contribution of rare whole-genome sequencing variants to plasma protein levels and the missing heritability. Nature Communications, 13, Article ID 2532.
Open this publication in new window or tab >>Contribution of rare whole-genome sequencing variants to plasma protein levels and the missing heritability
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2022 (English)In: Nature Communications, E-ISSN 2041-1723, Vol. 13, article id 2532Article in journal (Refereed) Published
Abstract [en]

Despite the success of genome-wide association studies, much of the genetic contribution to complex traits remains unexplained. Here, we analysed high coverage whole genome sequencing data, to evaluate the contribution of rare genetic variants to 414 plasma proteins. The frequency distribution of genetic variants was skewed towards the rare spectrum, and damaging variants were more often rare. We estimated that less than 4.3% of the narrow-sense heritability is expected to be explained by rare variants in our cohort. Using a gene-based approach, we identified Cis-associations for 237 of the proteins, which is slightly more compared to a GWAS (N=213), and we identified 34 loci in Trans. Several associations were driven by rare variants, and rare variants had on average larger phenotypic effects. We conclude therefore that rare variants could be of  importance for precision medicine applications, but have a more limited contribution to the missing heritability of complex diseases.

Place, publisher, year, edition, pages
Springer Nature, 2022
Keywords
Rare variants, SKAT, Protein Biomarkers, Hidden heritability, Missing heritability, GWAS
National Category
Medical Genetics
Identifiers
urn:nbn:se:uu:diva-470178 (URN)10.1038/s41467-022-30208-8 (DOI)000792848500027 ()35534486 (PubMedID)
Funder
Swedish Research Council, 2019-01497Swedish Heart Lung Foundation, 20200687Knut and Alice Wallenberg FoundationScience for Life Laboratory, SciLifeLabSwedish National Infrastructure for Computing (SNIC), SNIC 2018/8-372Swedish Research Council, 2018-05973
Note

Titel in Thesis: The contribution of rare whole genome sequencing variants to plasma protein levels and to the missing heritability

De fem första författarna delar förstaförfattarskapet

Available from: 2022-03-21 Created: 2022-03-21 Last updated: 2023-03-28Bibliographically approved
Höijer, I., Emmanouilidou, A., Östlund, R., van Schendel, R., Bozorgpana, S., Tijsterman, M., . . . Ameur, A. (2022). CRISPR-Cas9 induces large structural variants at on-target and off-target sites in vivo that segregate across generations. Nature Communications, 13, Article ID 627.
Open this publication in new window or tab >>CRISPR-Cas9 induces large structural variants at on-target and off-target sites in vivo that segregate across generations
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2022 (English)In: Nature Communications, E-ISSN 2041-1723, Vol. 13, article id 627Article in journal (Refereed) Published
Abstract [en]

CRISPR-Cas9 genome editing has potential to cure diseases without current treatments, but therapies must be safe. Here we show that CRISPR-Cas9 editing can introduce unintended mutations in vivo, which are passed on to the next generation. By editing fertilized zebrafish eggs using four guide RNAs selected for off-target activity in vitro, followed by long-read sequencing of DNA from >1100 larvae, juvenile and adult fish across two generations, we find that structural variants (SVs), i.e., insertions and deletions >= 50 bp, represent 6% of editing outcomes in founder larvae. These SVs occur both at on-target and off-target sites. Our results also illustrate that adult founder zebrafish are mosaic in their germ cells, and that 26% of their offspring carries an off-target mutation and 9% an SV. Hence, pre-testing for off-target activity and SVs using patient material is advisable in clinical applications, to reduce the risk of unanticipated effects with potentially large implications.

Place, publisher, year, edition, pages
Springer NatureSpringer Nature, 2022
National Category
Medical Genetics
Identifiers
urn:nbn:se:uu:diva-468369 (URN)10.1038/s41467-022-28244-5 (DOI)000752241200003 ()35110541 (PubMedID)
Available from: 2022-03-01 Created: 2022-03-01 Last updated: 2024-01-15Bibliographically approved
Enroth, S., Ivansson, E., Hedlund Lindberg, J., Lycke, M., Bergman, J., Reneland, A., . . . Gyllensten, U. (2022). Data-driven analysis of a validated risk score for ovarian cancer identifies clinically distinct patterns during follow-up and treatment. Communications Medicine, 2(1), Article ID 124.
Open this publication in new window or tab >>Data-driven analysis of a validated risk score for ovarian cancer identifies clinically distinct patterns during follow-up and treatment
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2022 (English)In: Communications Medicine, E-ISSN 2730-664X, Vol. 2, no 1, article id 124Article in journal (Refereed) Published
Abstract [en]

Background

Ovarian cancer is the eighth most common cancer among women and due to late detection prognosis is poor with an overall 5-year survival of 30–50%. Novel biomarkers are needed to reduce diagnostic surgery and enable detection of early-stage cancer by population screening. We have previously developed a risk score based on an 11-biomarker plasma protein assay to distinguish benign tumors (cysts) from malignant ovarian cancer in women with adnexal ovarian mass.

Methods

Protein concentrations of 11 proteins were characterized in plasma from 1120 clinical samples with a custom version of the proximity extension assay. The performance of the assay was evaluated in terms of prediction accuracy based on receiver operating characteristics (ROC) and multiple hypothesis adjusted Fisher’s Exact tests on achieved sensitivity and specificity.

Results

The assay’s performance is validated in two independent clinical cohorts with a sensitivity of 0.83/0.91 and specificity of 0.88/0.92. We also show that the risk score follows the clinical development and is reduced upon treatment, and increased with relapse and cancer progression. Data-driven modeling of the risk score patterns during a 2-year follow-up after diagnosis identifies four separate risk score trajectories linked to clinical development and survival. A Cox proportional hazard regression analysis of 5-year survival shows that at time of diagnosis the risk score is the second-strongest predictive variable for survival after tumor stage, whereas MUCIN-16 (CA-125) alone is not significantly predictive.

Conclusion

The robust performance of the biomarker assay across clinical cohorts and the correlation with clinical development indicates its usefulness both in the diagnostic work-up of women with adnexal ovarian mass and for predicting their clinical course.

Place, publisher, year, edition, pages
Springer Nature, 2022
National Category
Cancer and Oncology
Research subject
Molecular Life Sciences
Identifiers
urn:nbn:se:uu:diva-486157 (URN)10.1038/s43856-022-00193-6 (DOI)001088269800001 ()36196264 (PubMedID)
Funder
Uppsala UniversitySwedish Cancer SocietySwedish Foundation for Strategic ResearchSwedish Research CouncilSjöberg FoundationVinnova
Note

These authors contributed equally: Karin Stålberg, Karin Sundfeldt, Ulf Gyllensten

Available from: 2022-10-04 Created: 2022-10-04 Last updated: 2024-01-19Bibliographically approved
Projects
Human Genomics - Assessing human diversity by genome and transcriptome analysis using techniques for massively parallel sequencing (MPS) [2008-03135_VR]; Uppsala UniversityIdentification of genetic and environmental determinants of the human lipidome, the glycome and chronic inflammatory and allergic reactions, using population- and cohort-based genomic scanning [2009-03573_VR]; Uppsala UniversityApplication for 3rd generation DNA sequencing technology to the Swedish National Infrastructure for Large-Scale DNA sequencing (SNISS) [2010-05866_VR]; Uppsala UniversityEvaluation of the use of repeat HPV testing and self-sampling in primary screening for cervical cancer: a randomised study [2011-00554_VR]; Uppsala UniversityGenome-Scale Metabolic Modelling - A Systems Biology Approach to Human Physiology [2011-05252_VR]; Uppsala UniversityGenetic architecture of human quantitative clinical traits: Contribution of rare and common genetic variants to the missing heritability [2012-02884_VR]; Uppsala UniversityEvaluation of the use of self-sampling and repeated HPV testing in primary screening for cervical cancer: a randomised study [2013-03482_VR]; Uppsala UniversitySystems-level analysis of genetic and environmental effects on the microRNA profile and functional consequences for gene expression and risk of cardiovascular, inflammatory and autoimmune disease [2015-02711_VR]; Uppsala UniversityBiomarker test for cervical, ovarian or endometrial cancer [2016-00294_ VINNOVA]; Uppsala UniversityA study of the feasibility of the introduction of a Swedish HPV test for the management and prevention of cervical disease in the Eastern Cape, South Africa [2016-07318_Forte]; Uppsala UniversityDevelopment of a protein biomarker test for preoperative diagnosis of ovarian cancer. [2017-03586_ VINNOVA]; Uppsala UniversityIntegrated multi-omics analyses of DNA, RNA and protein using next-generation DNA sequencing [2020-06175_VR]; Uppsala University
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-6316-3355

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