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Escala-Garcia, M., Abraham, J., Andrulis, I. L., Anton-Culver, H., Arndt, V., Ashworth, A., . . . Schmidt, M. K. (2020). A network analysis to identify mediators of germline-driven differences in breast cancer prognosis. Nature Communications, 11(1), Article ID 312.
Open this publication in new window or tab >>A network analysis to identify mediators of germline-driven differences in breast cancer prognosis
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2020 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 11, no 1, article id 312Article in journal (Refereed) Published
Abstract [en]

Identifying the underlying genetic drivers of the heritability of breast cancer prognosis remains elusive. We adapt a network-based approach to handle underpowered complex datasets to provide new insights into the potential function of germline variants in breast cancer prognosis. This network-based analysis studies similar to 7.3 million variants in 84,457 breast cancer patients in relation to breast cancer survival and confirms the results on 12,381 independent patients. Aggregating the prognostic effects of genetic variants across multiple genes, we identify four gene modules associated with survival in estrogen receptor (ER)-negative and one in ER-positive disease. The modules show biological enrichment for cancer-related processes such as G-alpha signaling, circadian clock, angiogenesis, and Rho-GTPases in apoptosis.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2020
National Category
Medical Genetics
Identifiers
urn:nbn:se:uu:diva-407461 (URN)10.1038/s41467-019-14100-6 (DOI)000511912200002 ()31949161 (PubMedID)
Funder
EU, Horizon 2020, 634935EU, Horizon 2020, 633784EU, FP7, Seventh Framework Programme, 223175EU, FP7, Seventh Framework Programme, HEALTH-F2-2009-223175EU, FP7, Seventh Framework Programme, 223175 (HEALTH-F2-2009-223175)Swedish Cancer SocietySwedish Research CouncilSwedish Cancer SocietySwedish Research Council, VR 2017-00644EU, European Research Council
Available from: 2020-03-26 Created: 2020-03-26 Last updated: 2020-03-26Bibliographically approved
Kaluza, J., Harris, H. R., Linden, A. & Wolk, A. (2019). Alcohol Consumption and Risk of Chronic Obstructive Pulmonary Disease: A Prospective Cohort Study of Men. American Journal of Epidemiology, 188(5), 907-916
Open this publication in new window or tab >>Alcohol Consumption and Risk of Chronic Obstructive Pulmonary Disease: A Prospective Cohort Study of Men
2019 (English)In: American Journal of Epidemiology, ISSN 0002-9262, E-ISSN 1476-6256, Vol. 188, no 5, p. 907-916Article in journal (Refereed) Published
Abstract [en]

Studies indicate an inverse association between moderate alcohol consumption and chronic inflammatory diseases; however, the association between alcohol consumption and chronic obstructive pulmonary disease (COPD) incidence has not been widely studied. We investigated the associations of total alcohol consumption and intake of specific alcoholic beverages with risk of COPD in a population-based prospective cohort study, the Cohort of Swedish Men (n = 44,254). Alcohol consumption was assessed with a self-administered questionnaire in 1997. During follow-up (1998-2014), 2,177 COPD cases were ascertained. Moderate alcohol consumption was associated with the lowest risk of COPD. A J-shaped association was observed for ethanol consumption (P for nonlinearity = 0.003) and beer consumption (P for nonlinearity < 0.001); for wine consumption, a U-shaped association was observed (P for nonlinearity < 0.001). Defining a "standard drink" as 12 g of ethanol, the multivariable-adjusted hazard ratios were 0.77 (95% confidence interval (CI): 0.66, 0.90) and 0.92 (95% CI: 0.81, 1.05) for beer consumption of 4.1-6.0 and >6.0 standard drinks/week (SDW) versus <1.0 SDW, respectively; 0.80 (95% CI: 0.69, 0.93) and 1.00 (95% CI: 0.83, 1.21) for wine consumption of 2.0-4.0 and >4.0 SDW versus <1.0 SDW, respectively; and 1.10 (95% CI: 0.98, 1.24) and 1.20 (95% CI: 0.99, 1.44) for liquor consumption of 2.0-4.0 and >4.0 SDW versus <1.0 SDW, respectively. In conclusion, our findings suggest that moderate beer and wine consumption, but not liquor consumption, may decrease risk of COPD. Additional studies are needed to confirm these associations.

Place, publisher, year, edition, pages
OXFORD UNIV PRESS INC, 2019
Keywords
alcohol consumption, chronic obstructive pulmonary disease, ethanol, prospective cohort studies
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:uu:diva-397298 (URN)10.1093/aje/kwz020 (DOI)000492993400016 ()30877760 (PubMedID)
Funder
Swedish Research Council
Available from: 2019-12-06 Created: 2019-12-06 Last updated: 2019-12-06Bibliographically approved
Kaluza, J., Stackelberg, O., Harris, H. R., Björck, M. & Wolk, A. (2019). Anti-inflammatory diet and risk of abdominal aortic aneurysm in two Swedish cohorts. Heart, 105(24), 1876-1883
Open this publication in new window or tab >>Anti-inflammatory diet and risk of abdominal aortic aneurysm in two Swedish cohorts
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2019 (English)In: Heart, ISSN 1355-6037, E-ISSN 1468-201X, Vol. 105, no 24, p. 1876-1883Article in journal (Refereed) Published
Abstract [en]

Objective The relationship between dietary patterns and development of abdominal aortic aneurysm (AAA) is not well understood. Thus, we prospectively evaluated the association between the anti-inflammatory potential of diet and risk of AAA. Methods The study population included the Cohort of Swedish Men (45 072 men) and the Swedish Mammography Cohort (36 633 women), aged 45-83 years at baseline. The anti-inflammatory potential of diet was estimated using Anti-inflammatory Diet Index (AIDI) based on 11 foods with anti-inflammatory potential and 5 with proinflammatory potential (maximum 16 points) that was validated againsthigh sensitivity C reactive protein (hsCRP). Cox proportional hazard regression models were used to estimate HRs and 95% CIs. During the 14.9 years of follow-up (1 217 263 person-years), 1528 AAA cases (277 (18%) ruptured, 1251 non-ruptured) were ascertained via the Swedish Inpatient Register, the National Cause of Death Register and the Register for Vascular Surgery (Swedvasc). Results We observed an inverse association between the AIDI and AAA risk in women and men; HRs between extreme quartiles of the AIDI (>= 8 vs <= 5 points) were 0.55 (95% CI 0.36 to 0.83) in women and 0.81 (95% CI 0.68 to 0.98) in men. The AIDI was inversely associated with both ruptured and non-ruptured AAA incidence; the HR of participants in the highest quartile of AIDI compared with those in the lowest quartile was 0.61 (95% CI 0.41 to 0.90) for ruptured AAA and 0.79 (95% CI 0.65 to 0.95) for non-ruptured AAA. Conclusion Adherence to diet with a high anti-inflammatory potential was associated with a reduced AAA risk, an association that was even more pronounced for AAA rupture.

Place, publisher, year, edition, pages
BMJ Publishing Group Ltd, 2019
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-402390 (URN)10.1136/heartjnl-2019-315031 (DOI)000503800100008 ()31296589 (PubMedID)
Funder
Swedish Research Council, VR 2015-02302Forte, Swedish Research Council for Health, Working Life and Welfare, FORTE 2015-00778Swedish Research Council Formas, 2016-00308Swedish Research Council, 2017-00644
Available from: 2020-01-24 Created: 2020-01-24 Last updated: 2020-01-24Bibliographically approved
Law, P. J., Timofeeva, M., Fernandez-Rozadilla, C., Timofeeva, A., Broderick, P., Studd, J., . . . Thibodeau, S. N. (2019). Association analyses identify 31 new risk loci for colorectal cancer susceptibility. Nature Communications, 10, Article ID 2154.
Open this publication in new window or tab >>Association analyses identify 31 new risk loci for colorectal cancer susceptibility
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2019 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 10, article id 2154Article in journal (Refereed) Published
Abstract [en]

Colorectal cancer (CRC) is a leading cause of cancer-related death worldwide, and has a strong heritable basis. We report a genome-wide association analysis of 34,627 CRC cases and 71,379 controls of European ancestry that identifies SNPs at 31 new CRC risk loci. We also identify eight independent risk SNPs at the new and previously reported European CRC loci, and a further nine CRC SNPs at loci previously only identified in Asian populations. We use in situ promoter capture Hi-C (CHi-C), gene expression, and in silico annotation methods to identify likely target genes of CRC SNPs. Whilst these new SNP associations implicate target genes that are enriched for known CRC pathways such as Wnt and BMP, they also highlight novel pathways with no prior links to colorectal tumourigenesis. These findings provide further insight into CRC susceptibility and enhance the prospects of applying genetic risk scores to personalised screening and prevention.

National Category
Medical Genetics Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-387286 (URN)10.1038/s41467-019-09775-w (DOI)000467836900008 ()31089142 (PubMedID)
Funder
EU, FP7, Seventh Framework Programme, 258236EU, FP7, Seventh Framework ProgrammeEU, European Research Council, 268648EU, FP7, Seventh Framework Programme, 201413EU, FP7, Seventh Framework Programme, 223175 (HEALTH-F2-2009-223175)
Available from: 2019-06-24 Created: 2019-06-24 Last updated: 2019-06-24Bibliographically approved
Warensjö Lemming, E., Byberg, L., Stattin, K., Ahmad, S., Lind, L., Elmsfahl, S., . . . Michaëlsson, K. (2019). Dietary Pattern Specific Protein Biomarkers for Cardiovascular Disease: A Cross-Sectional Study in 2 Independent Cohorts. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 8(11), Article ID e011860.
Open this publication in new window or tab >>Dietary Pattern Specific Protein Biomarkers for Cardiovascular Disease: A Cross-Sectional Study in 2 Independent Cohorts
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2019 (English)In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, ISSN 2047-9980, E-ISSN 2047-9980, Vol. 8, no 11, article id e011860Article in journal (Refereed) Published
Abstract [en]

Background: Mechanisms related to the influence of diet on the development of cardiovascular disease are not entirely understood, and protein biomarkers may help to understand these pathways. Studies of biomarkers identified with multiplex proteomic methods and dietary patterns are largely lacking.

Methods and Results: Dietary patterns were generated through principal component analysis in 2 population‐based Swedish cohorts, the EpiHealth (EpiHealth study; n=20 817 men and women) and the SMCC (Swedish Mammography Cohort Clinical [n=4650 women]). A set of 184 protein cardiovascular disease biomarkers were measured with 2 high‐throughput, multiplex immunoassays. Discovery and replication multivariable linear regression analyses were used to investigate the associations between the principal component analysis–generated dietary patterns and the cardiovascular disease–associated protein biomarkers, first in the EpiHealth (n=2240) and then in the Swedish Mammography Cohort Clinical. Four main dietary patterns were identified in the EpiHealth, and 3 patterns were identified in the Swedish Mammography Cohort Clinical. The healthy and the Western/traditional patterns were found in both cohorts. In the EpiHealth, 57 protein biomarkers were associated with 3 of the dietary patterns, and 41 of these associations were replicated in the Swedish Mammography Cohort Clinical, with effect estimates ranging from 0.057 to 0.083 (P‐value range, 5.0×10−2–1.4×10−9) for each SD increase in the relative protein concentration. Independent associations were established between dietary patterns and the 21 protein biomarkers. Two proteins, myeloperoxidase and resistin, were associated with both the healthy and the light meal pattern but in opposite directions.

Conclusions: We have discovered and replicated independent associations between dietary patterns and 21 biomarkers linked to cardiovascular disease, which have a role in the pathways related to inflammation, endothelial and immune function, cell adhesion, and metabolism

Keywords
cardiovascular disease, dietary patterns, EpiHealth study, inflammation, proteomics, Swedish Mammography Cohort Clinical
National Category
Nutrition and Dietetics
Identifiers
urn:nbn:se:uu:diva-394981 (URN)10.1161/JAHA.118.011860 (DOI)000484576200019 ()31433701 (PubMedID)
Funder
Swedish Research Council, 2017-06100Swedish Research Council, 2015-05997Swedish Research Council, 2015-03257Forte, Swedish Research Council for Health, Working Life and Welfare, 2017-00721Swedish Research Council, 2017/49 (180)
Available from: 2019-10-11 Created: 2019-10-11 Last updated: 2019-10-11Bibliographically approved
Larsson, S. C., Wolk, A. & Bäck, M. (2019). Dietary patterns, food groups, and incidence of aortic valve stenosis: A prospective cohort study.. International Journal of Cardiology, 283, 184-188
Open this publication in new window or tab >>Dietary patterns, food groups, and incidence of aortic valve stenosis: A prospective cohort study.
2019 (English)In: International Journal of Cardiology, ISSN 0167-5273, E-ISSN 1874-1754, Vol. 283, p. 184-188Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: The role of diet in the development of aortic valve stenosis (AVS) is unknown. We therefore examined the associations of two dietary patterns, including a modified Dietary Approaches to Stop Hypertension (mDASH) diet and a modified Mediterranean (mMED) diet, and the food items included in these dietary patterns with incidence of aortic valve stenosis (AVS) in a population-based cohort study.

METHODS: The study cohort comprised 74,401 Swedish adults (54% men) who were free of cardiovascular disease at the time of completion of a baseline questionnaire about habitual diet and other risk factors for chronic diseases. Participants were followed-up through linkage with nationwide registers on hospitalization and causes of death.

RESULTS: During 1,132,617 person-years (mean 15.2 years) of follow-up, 1338 incident AVS cases (801 in men and 537 in women) were ascertained. We found no significant associations of the mDASH and mMED dietary patterns or the food groups and beverages included in these diets (i.e., fruit, vegetables, legumes and nuts, whole grains, fish, low-fat dairy foods, full-fat dairy foods, red and processed meat, and sweetened beverages) with risk of AVS. The hazard ratios (95% confidence interval) of AVS per one standard deviation increase in the mDASH and mMED diet scores were respectively 1.02 (0.96-1.07) and 1.00 (0.95-1.06).

CONCLUSION: This study found no evidence that diet plays a role in the development of AVS.

Keywords
Aortic valve stenosis, Diet, Dietary patterns, Foods, Prospective studies
National Category
Nutrition and Dietetics Cardiac and Cardiovascular Systems Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-368144 (URN)10.1016/j.ijcard.2018.11.007 (DOI)000461330100039 ()30416029 (PubMedID)
Funder
Swedish Research Council, 2016-01042
Available from: 2018-12-04 Created: 2018-12-04 Last updated: 2019-11-19Bibliographically approved
Huyghe, J. R., Bien, S. A., Harrison, T. A., Kang, H. M., Chen, S., Schmit, S. L., . . . Peters, U. (2019). Discovery of common and rare genetic risk variants for colorectal cancer. Nature Genetics, 51(1), 76-87
Open this publication in new window or tab >>Discovery of common and rare genetic risk variants for colorectal cancer
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2019 (English)In: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 51, no 1, p. 76-87Article in journal (Refereed) Published
Abstract [en]

To further dissect the genetic architecture of colorectal cancer (CRC), we performed whole-genome sequencing of 1,439 cases and 720 controls, imputed discovered sequence variants and Haplotype Reference Consortium panel variants into genome-wide association study data, and tested for association in 34,869 cases and 29,051 controls. Findings were followed up in an additional 23,262 cases and 38,296 controls. We discovered a strongly protective 0.3% frequency variant signal at CHD1. In a combined meta-analysis of 125,478 individuals, we identified 40 new independent signals at P < 5 x 10(-8), bringing the number of known independent signals for CRC to similar to 100. New signals implicate lower-frequency variants, Kruppel-like factors, Hedgehog signaling, Hippo-YAP signaling, long noncoding RNAs and somatic drivers, and support a role for immune function. Heritability analyses suggest that CRC risk is highly polygenic, and larger, more comprehensive studies enabling rare variant analysis will improve understanding of biology underlying this risk and influence personalized screening strategies and drug development.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2019
National Category
Medical Genetics Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-373313 (URN)10.1038/s41588-018-0286-6 (DOI)000454108800015 ()30510241 (PubMedID)
Available from: 2019-01-16 Created: 2019-01-16 Last updated: 2019-11-19Bibliographically approved
Yang, Y., Wu, L., Shu, X., Lu, Y., Shu, X.-O., Cai, Q., . . . Long, J. (2019). Genetic Data from Nearly 63,000 Women of European Descent Predicts DNA Methylation Biomarkers and Epithelial Ovarian Cancer Risk. Cancer Research, 79(3), 505-517
Open this publication in new window or tab >>Genetic Data from Nearly 63,000 Women of European Descent Predicts DNA Methylation Biomarkers and Epithelial Ovarian Cancer Risk
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2019 (English)In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 79, no 3, p. 505-517Article in journal (Refereed) Published
Abstract [en]

DNA methylation is instrumental for gene regulation. Global changes in the epigenetic landscape have been recognized as a hallmark of cancer. However, the role of DNA methylation in epithelial ovarian cancer (EOC) remains unclear. In this study, high-density genetic and DNA methylation data in white blood cells from the Framingham Heart Study (N = 1,595) were used to build genetic models to predict DNA methylation levels. These prediction models were then applied to the summary statistics of a genome-wide association study (GWAS) of ovarian cancer including 22,406 EOC cases and 40,941 controls to investigate genetically predicted DNA methylation levels in association with EOC risk. Among 62,938 CpG sites investigated, genetically predicted methylation levels at 89 CpG were significantly associated with EOC risk at a Bonferroni-corrected threshold of P < 7.94 x 10(-7). Of them, 87 were located at GWAS-identified EOC susceptibility regions and two resided in a genomic region not previously reported to be associated with EOC risk. Integrative analyses of genetic, methylation, and gene expression data identified consistent directions of associations across 12 CpG, five genes, and EOC risk, suggesting that methylation at these 12 CpG may influence EOC risk by regulating expression of these five genes, namely MAPT, HOXB3, ABHD8, ARHGAP27, and SKAP1. We identified novel DNA methylation markers associated with EOC risk and propose that methylation at multiple CpG may affect EOC risk via regulation of gene expression. Significance: Identification of novel DNA methylation markers associated with EOC risk suggests that methylation at multiple CpG may affect EOC risk through regulation of gene expression.

Place, publisher, year, edition, pages
AMER ASSOC CANCER RESEARCH, 2019
National Category
Medical Genetics
Identifiers
urn:nbn:se:uu:diva-377214 (URN)10.1158/0008-5472.CAN-18-2726 (DOI)000457394600011 ()30559148 (PubMedID)
Funder
Swedish Research CouncilEU, European Research Council
Available from: 2019-02-25 Created: 2019-02-25 Last updated: 2019-02-25Bibliographically approved
Bien, S. A., Su, Y.-R., Conti, D. V., Harrison, T. A., Qu, C., Guo, X., . . . Peters, U. (2019). Genetic variant predictors of gene expression provide new insight into risk of colorectal cancer. Human Genetics, 138(4), 307-326
Open this publication in new window or tab >>Genetic variant predictors of gene expression provide new insight into risk of colorectal cancer
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2019 (English)In: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 138, no 4, p. 307-326Article in journal (Refereed) Published
Abstract [en]

Genome-wide association studies have reported 56 independently associated colorectal cancer (CRC) risk variants, most of which are non-coding and believed to exert their effects by modulating gene expression. The computational method PrediXcan uses cis-regulatory variant predictors to impute expression and perform gene-level association tests in GWAS without directly measured transcriptomes. In this study, we used reference datasets from colon (n=169) and whole blood (n=922) transcriptomes to test CRC association with genetically determined expression levels in a genome-wide analysis of 12,186 cases and 14,718 controls. Three novel associations were discovered from colon transverse models at FDR0.2 and further evaluated in an independent replication including 32,825 cases and 39,933 controls. After adjusting for multiple comparisons, we found statistically significant associations using colon transcriptome models with TRIM4 (discovery P=2.2x10(-4), replication P=0.01), and PYGL (discovery P=2.3x10(-4), replication P=6.7x10(-4)). Interestingly, both genes encode proteins that influence redox homeostasis and are related to cellular metabolic reprogramming in tumors, implicating a novel CRC pathway linked to cell growth and proliferation. Defining CRC risk regions as one megabase up- and downstream of one of the 56 independent risk variants, we defined 44 non-overlapping CRC-risk regions. Among these risk regions, we identified genes associated with CRC (P<0.05) in 34/44 CRC-risk regions. Importantly, CRC association was found for two genes in the previously reported 2q25 locus, CXCR1 and CXCR2, which are potential cancer therapeutic targets. These findings provide strong candidate genes to prioritize for subsequent laboratory follow-up of GWAS loci. This study is the first to implement PrediXcan in a large colorectal cancer study and findings highlight the utility of integrating transcriptome data in GWAS for discovery of, and biological insight into, risk loci.

National Category
Medical Genetics Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-383482 (URN)10.1007/s00439-019-01989-8 (DOI)000465974800002 ()30820706 (PubMedID)
Funder
Swedish Research CouncilEU, FP7, Seventh Framework Programme, 312057Swedish Research Council, K2015-55X-22674-01-4Swedish Research Council, K2008-55X-20157-03-3Swedish Research Council, K2006-72X-20157-01-2EU, European Research Council
Note

Correction in: HUMAN GENETICS, Volume: 138, Issue: 7, Pages: 789-791, DOI: 10.1007/s00439-019-02030-8

Available from: 2019-05-16 Created: 2019-05-16 Last updated: 2019-08-16Bibliographically approved
Wu, L., Wang, J., Cai, Q., Cavazos, T. B., Emami, N. C., Long, J., . . . Riboli, E. (2019). Identification of Novel Susceptibility Loci and Genes for Prostate Cancer Risk: A Transcriptome-Wide Association Study in over 140,000 European Descendants. Cancer Research, 79(13), 3192-3204
Open this publication in new window or tab >>Identification of Novel Susceptibility Loci and Genes for Prostate Cancer Risk: A Transcriptome-Wide Association Study in over 140,000 European Descendants
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2019 (English)In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 79, no 13, p. 3192-3204Article in journal (Refereed) Published
Abstract [en]

Genome-wide association study-identified prostate cancer risk variants explain only a relatively small fraction of its familial relative risk, and the genes responsible for many of these identified associations remain unknown. To discover novel prostate cancer genetic loci and possible causal genes at previously identified risk loci, we performed a transcriptome-wide association study in 79,194 cases and 61,112 controls of European ancestry. Using data from the Genotype-Tissue Expression Project, we established genetic models to predict gene expression across the transcriptome for both prostate models and cross-tissue models and evaluated model performance using two independent datasets. We identified significant associations for 137 genes at P < 2.61 x 10(-6), a Bonferroni-corrected threshold, including nine genes that remained significant at P < 2.61 x 10(-6) after adjusting for all known prostate cancer risk variants in nearby regions. Of the 128 remaining associated genes, 94 have not yet been reported as potential target genes at known loci. We silenced 14 genes and many showed a consistent effect on viability and colony-forming efficiency in three cell lines. Our study provides substantial new information to advance our understanding of prostate cancer genetics and biology. Significance: This study identifies novel prostate cancer genetic loci and possible causal genes, advancing our understanding of the molecular mechanisms that drive prostate cancer.

Place, publisher, year, edition, pages
AMER ASSOC CANCER RESEARCH, 2019
National Category
Cancer and Oncology Medical Genetics
Identifiers
urn:nbn:se:uu:diva-390910 (URN)10.1158/0008-5472.CAN-18-3536 (DOI)000473533400008 ()31101764 (PubMedID)
Available from: 2019-08-16 Created: 2019-08-16 Last updated: 2019-08-16Bibliographically approved
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ORCID iD: ORCID iD iconorcid.org/0000-0001-7387-6845

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