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Article ; Online: Impact of germline DNA repair gene variants on prognosis and treatment of men with advanced prostate cancer

Emma B. Hansen / Questa Karlsson / Susan Merson / Sarah Wakerell / Reshma Rageevakumar / Jørgen B. Jensen / Michael Borre / Zsofia Kote-Jarai / Rosalind A. Eeles / Karina D. Sørensen

Scientific Reports, Vol 13, Iss 1, Pp 1-

2023 Volume 11

Abstract: Abstract The clinical importance of germline variants in DNA repair genes (DRGs) is becoming increasingly recognized, but their impact on advanced prostate cancer prognosis remains unclear. A cohort of 221 newly diagnosed metastatic castration-resistant ... ...

Abstract	Abstract The clinical importance of germline variants in DNA repair genes (DRGs) is becoming increasingly recognized, but their impact on advanced prostate cancer prognosis remains unclear. A cohort of 221 newly diagnosed metastatic castration-resistant prostate cancer (mCRPC) patients were screened for pathogenic germline variants in 114 DRGs. The primary endpoint was progression-free survival (PFS) on first-line androgen signaling inhibitor (ARSI) treatment for mCRPC. Secondary endpoints were time to mCRPC progression on initial androgen deprivation therapy (ADT) and overall survival (OS). Twenty-seven patients (12.2%) carried a germline DRG variant. DRG carrier status was independently associated with shorter PFS on first-line ARSI [HR 1.72 (1.06–2.81), P = 0.029]. At initiation of ADT, DRG carrier status was independently associated with shorter progression time to mCRPC [HR 1.56, (1.02–2.39), P = 0.04] and shorter OS [HR 1.99, (1.12–3.52), P = 0.02]. Investigating the contributions of individual germline DRG variants on PFS and OS revealed CHEK2 variants to have little effect. Furthermore, prior taxane treatment was associated with worse PFS on first-line ARSI for DRG carriers excluding CHEK2 (P = 0.0001), but not for noncarriers. In conclusion, germline DRG carrier status holds independent prognostic value for predicting advanced prostate cancer patient outcomes and may potentially inform on optimal treatment sequencing already at the hormone-sensitive stage.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2023-11-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Alcohol Intake and Alcohol–SNP Interactions Associated with Prostate Cancer Aggressiveness

Hui-Yi Lin / Xinnan Wang / Tung-Sung Tseng / Yu-Hsiang Kao / Zhide Fang / Patricia E. Molina / Chia-Ho Cheng / Anders E. Berglund / Rosalind A. Eeles / Kenneth R. Muir / Nora Pashayan / Christopher A. Haiman / Hermann Brenner / Jong Y. Park / The PRACTICAL Consortium

Journal of Clinical Medicine, Vol 10, Iss 3, p

2021 Volume 553

Abstract: Excessive alcohol intake is a well-known modifiable risk factor for many cancers. It is still unclear whether genetic variants or single nucleotide polymorphisms (SNPs) can modify alcohol intake’s impact on prostate cancer (PCa) aggressiveness. The ... ...

Abstract	Excessive alcohol intake is a well-known modifiable risk factor for many cancers. It is still unclear whether genetic variants or single nucleotide polymorphisms (SNPs) can modify alcohol intake’s impact on prostate cancer (PCa) aggressiveness. The objective is to test the alcohol–SNP interactions of the 7501 SNPs in the four pathways (angiogenesis, mitochondria, miRNA, and androgen metabolism-related pathways) associated with PCa aggressiveness. We evaluated the impacts of three excessive alcohol intake behaviors in 3306 PCa patients with European ancestry from the PCa Consortium. We tested the alcohol–SNP interactions using logistic models with the discovery-validation study design. All three excessive alcohol intake behaviors were not significantly associated with PCa aggressiveness. However, the interactions of excessive alcohol intake and three SNPs (rs13107662 [ CAMK2D , p = 6.2 × 10 −6 ], rs9907521 [ PRKCA, p = 7.1 × 10 −5 ], and rs11925452 [ ROBO1, p = 8.2 × 10 −4 ]) were significantly associated with PCa aggressiveness. These alcohol–SNP interactions revealed contrasting effects of excessive alcohol intake on PCa aggressiveness according to the genotypes in the identified SNPs. We identified PCa patients with the rs13107662 ( CAMK2D ) AA genotype, the rs11925452 ( ROBO1 ) AA genotype, and the rs9907521 ( PRKCA) AG genotype were more vulnerable to excessive alcohol intake for developing aggressive PCa. Our findings support that the impact of excessive alcohol intake on PCa aggressiveness was varied by the selected genetic profiles.
Keywords	alcohol intake ; SNP interaction ; prostate cancer ; Medicine ; R
Subject code	616
Language	English
Publishing date	2021-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: An integrative multi-omics analysis to identify candidate DNA methylation biomarkers related to prostate cancer risk

Lang Wu / Yaohua Yang / Xingyi Guo / Xiao-Ou Shu / Qiuyin Cai / Xiang Shu / Bingshan Li / Ran Tao / Chong Wu / Jason B. Nikas / Yanfa Sun / Jingjing Zhu / Monique J. Roobol / Graham G. Giles / Hermann Brenner / Esther M. John / Judith Clements / Eli Marie Grindedal / Jong Y. Park /

Janet L. Stanford / Zsofia Kote-Jarai / Christopher A. Haiman / Rosalind A. Eeles / Wei Zheng / Jirong Long / The PRACTICAL consortium / CRUK Consortium / BPC3 Consortium / CAPS Consortium / PEGASUS Consortium

Nature Communications, Vol 11, Iss 1, Pp 1-

2020 Volume 11

Abstract: Genome wide association studies have identified multiple loci associated with risk of developing prostate cancer but the functional significance of many of these are unknown. Here, after generating models to predict methylation, the authors identify CpG ... ...

Abstract	Genome wide association studies have identified multiple loci associated with risk of developing prostate cancer but the functional significance of many of these are unknown. Here, after generating models to predict methylation, the authors identify CpG methylation sites associated with prostate cancer.
Keywords	Science ; Q
Language	English
Publishing date	2020-08-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: An integrative multi-omics analysis to identify candidate DNA methylation biomarkers related to prostate cancer risk

Nature Communications, Vol 11, Iss 1, Pp 1-

2020 Volume 11

Abstract	Genome wide association studies have identified multiple loci associated with risk of developing prostate cancer but the functional significance of many of these are unknown. Here, after generating models to predict methylation, the authors identify CpG methylation sites associated with prostate cancer.
Keywords	Science ; Q
Language	English
Publishing date	2020-08-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Telomere length shows no association with BRCA1 and BRCA2 mutation status.

Emma Killick / Malgorzata Tymrakiewicz / Clara Cieza-Borrella / Paula Smith / Deborah J Thompson / Karen A Pooley / Doug F Easton / Elizabeth Bancroft / Elizabeth Page / Daniel Leongamornlert / IMPACT collaborators / Zsofia Kote-Jarai / Rosalind A Eeles

PLoS ONE, Vol 9, Iss 1, p e

2014 Volume 86659

Abstract: This study aimed to determine whether telomere length (TL) is a marker of cancer risk or genetic status amongst two cohorts of BRCA1 and BRCA2 mutation carriers and controls. The first group was a prospective set of 665 male BRCA1/2 mutation carriers and ...

Abstract	This study aimed to determine whether telomere length (TL) is a marker of cancer risk or genetic status amongst two cohorts of BRCA1 and BRCA2 mutation carriers and controls. The first group was a prospective set of 665 male BRCA1/2 mutation carriers and controls (mean age 53 years), all healthy at time of enrollment and blood donation, 21 of whom have developed prostate cancer whilst on study. The second group consisted of 283 female BRCA1/2 mutation carriers and controls (mean age 48 years), half of whom had been diagnosed with breast cancer prior to enrollment. TL was quantified by qPCR from DNA extracted from peripheral blood lymphocytes. Weighted and unweighted Cox regressions and linear regression analyses were used to assess whether TL was associated with BRCA1/2 mutation status or cancer risk. We found no evidence for association between developing cancer or being a BRCA1 or BRCA2 mutation carrier and telomere length. It is the first study investigating TL in a cohort of genetically predisposed males and although TL and BRCA status was previously studied in females our results don't support the previous finding of association between hereditary breast cancer and shorter TL.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2014-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Author Correction

Molly Went / Amit Sud / Asta Försti / Britt-Marie Halvarsson / Niels Weinhold / Scott Kimber / Mark van Duin / Gudmar Thorleifsson / Amy Holroyd / David C. Johnson / Ni Li / Giulia Orlando / Philip J. Law / Mina Ali / Bowang Chen / Jonathan S. Mitchell / Daniel F. Gudbjartsson / Rowan Kuiper / Owen W. Stephens /

Uta Bertsch / Peter Broderick / Chiara Campo / Obul R Bandapalli / Hermann Einsele / Walter A. Gregory / Urban Gullberg / Jens Hillengass / Per Hoffmann / Graham H. Jackson / Karl-Heinz Jöckel / Ellinor Johnsson / Sigurður Y. Kristinsson / Ulf-Henrik Mellqvist / Hareth Nahi / Douglas Easton / Paul Pharoah / Alison Dunning / Julian Peto / Federico Canzian / Anthony Swerdlow / Rosalind A. Eeles / Zsofia Kote-Jarai / Kenneth Muir / Nora Pashayan / The PRACTICAL consortium / Jolanta Nickel / Markus M. Nöthen / Thorunn Rafnar / Fiona M. Ross / Miguel Inacio da Silva Filho

Nature Communications, Vol 10, Iss 1, Pp 1-

Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma

2019 Volume 3

Abstract: The original version of this Article contained an error in the spelling of a member of the PRACTICAL Consortium, Manuela Gago-Dominguez, which was incorrectly given as Manuela Gago Dominguez. This has now been corrected in both the PDF and HTML versions ... ...

Abstract	The original version of this Article contained an error in the spelling of a member of the PRACTICAL Consortium, Manuela Gago-Dominguez, which was incorrectly given as Manuela Gago Dominguez. This has now been corrected in both the PDF and HTML versions of the Article. Furthermore, in the original HTML version of this Article, the order of authors within the author list was incorrect. The PRACTICAL consortium was incorrectly listed after Richard S. Houlston and should have been listed after Nora Pashayan. This error has been corrected in the HTML version of the Article; the PDF version was correct at the time of publication.
Keywords	Science ; Q
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Author Correction

Jayaram Vijayakrishnan / James Studd / Peter Broderick / Ben Kinnersley / Amy Holroyd / Philip J. Law / Rajiv Kumar / James M. Allan / Christine J. Harrison / Anthony V. Moorman / Ajay Vora / Eve Roman / Sivaramakrishna Rachakonda / Sally E. Kinsey / Eamonn Sheridan / Pamela D. Thompson / Julie A. Irving / Rolf Koehler / Per Hoffmann /

Nature Communications, Vol 10, Iss 1, Pp 1-

Genome-wide association study identifies susceptibility loci for B-cell childhood acute lymphoblastic leukemia

2019 Volume 3

Abstract	The original version of this Article contained an error in the spelling of a member of the PRACTICAL Consortium, Manuela Gago-Dominguez, which was incorrectly given as Manuela Gago Dominguez. This has now been corrected in both the PDF and HTML versions of the Article. Furthermore, in the original HTML version of this Article, the order of authors within the author list was incorrect. The PRACTICAL consortium was incorrectly listed after Richard S. Houlston and should have been listed after Nora Pashayan. This error has been corrected in the HTML version of the Article; the PDF version was correct at the time of publication.
Keywords	Science ; Q
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Association between Adult Height and Risk of Colorectal, Lung, and Prostate Cancer

Nikhil K Khankari / Xiao-Ou Shu / Wanqing Wen / Peter Kraft / Sara Lindström / Ulrike Peters / Joellen Schildkraut / Fredrick Schumacher / Paolo Bofetta / Angela Risch / Heike Bickeböller / Christopher I Amos / Douglas Easton / Rosalind A Eeles / Stephen B Gruber / Christopher A Haiman / David J Hunter / Stephen J Chanock / Brandon L Pierce /

Wei Zheng / Colorectal Transdisciplinary Study (CORECT) / Discovery, Biology, and Risk of Inherited Variants in Breast Cancer (DRIVE) / Elucidating Loci Involved in Prostate Cancer Susceptibility (ELLIPSE) / Transdisciplinary Research in Cancer of the Lung (TRICL)

PLoS Medicine, Vol 13, Iss 9, p e

Results from Meta-analyses of Prospective Studies and Mendelian Randomization Analyses.

2016 Volume 1002118

Abstract: Background Observational studies examining associations between adult height and risk of colorectal, prostate, and lung cancers have generated mixed results. We conducted meta-analyses using data from prospective cohort studies and further carried out ... ...

Abstract	Background Observational studies examining associations between adult height and risk of colorectal, prostate, and lung cancers have generated mixed results. We conducted meta-analyses using data from prospective cohort studies and further carried out Mendelian randomization analyses, using height-associated genetic variants identified in a genome-wide association study (GWAS), to evaluate the association of adult height with these cancers. Methods and findings A systematic review of prospective studies was conducted using the PubMed, Embase, and Web of Science databases. Using meta-analyses, results obtained from 62 studies were summarized for the association of a 10-cm increase in height with cancer risk. Mendelian randomization analyses were conducted using summary statistics obtained for 423 genetic variants identified from a recent GWAS of adult height and from a cancer genetics consortium study of multiple cancers that included 47,800 cases and 81,353 controls. For a 10-cm increase in height, the summary relative risks derived from the meta-analyses of prospective studies were 1.12 (95% CI 1.10, 1.15), 1.07 (95% CI 1.05, 1.10), and 1.06 (95% CI 1.02, 1.11) for colorectal, prostate, and lung cancers, respectively. Mendelian randomization analyses showed increased risks of colorectal (odds ratio [OR] = 1.58, 95% CI 1.14, 2.18) and lung cancer (OR = 1.10, 95% CI 1.00, 1.22) associated with each 10-cm increase in genetically predicted height. No association was observed for prostate cancer (OR = 1.03, 95% CI 0.92, 1.15). Our meta-analysis was limited to published studies. The sample size for the Mendelian randomization analysis of colorectal cancer was relatively small, thus affecting the precision of the point estimate. Conclusions Our study provides evidence for a potential causal association of adult height with the risk of colorectal and lung cancers and suggests that certain genetic factors and biological pathways affecting adult height may also affect the risk of these cancers.
Keywords	Medicine ; R
Subject code	610
Language	English
Publishing date	2016-09-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Genome-wide association study identifies susceptibility loci for B-cell childhood acute lymphoblastic leukemia

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 9

Abstract: While GWAS have uncovered susceptibility loci for B-cell precursor acute lymphoblastic leukemia (BCP-ALL), much of the heritable risk remains undiscovered. Here, the authors perform a meta-analysis of two existing BCP-ALL GWAS together with an ... ...

Abstract	While GWAS have uncovered susceptibility loci for B-cell precursor acute lymphoblastic leukemia (BCP-ALL), much of the heritable risk remains undiscovered. Here, the authors perform a meta-analysis of two existing BCP-ALL GWAS together with an unpublished GWAS to identify risk loci at 8q24.21 and 2q22.3.
Keywords	Science ; Q
Language	English
Publishing date	2018-04-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma

Uta Bertsch / Peter Broderick / Chiara Campo / Obul R Bandapalli / Hermann Einsele / Walter A. Gregory / Urban Gullberg / Jens Hillengass / Per Hoffmann / Graham H. Jackson / Karl-Heinz Jöckel / Ellinor Johnsson / Sigurður Y. Kristinsson / Ulf-Henrik Mellqvist / Hareth Nahi / Douglas Easton / Paul Pharoah / Alison Dunning / Julian Peto / Federico Canzian / Anthony Swerdlow / Rosalind A. Eeles / ZSofia Kote-Jarai / Kenneth Muir / Nora Pashayan / Jolanta Nickel / Markus M. Nöthen / Thorunn Rafnar / Fiona M. Ross / Miguel Inacio da Silva Filho / Hauke Thomsen

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 10

Abstract: Multiple myeloma is a cancer of the plasma cells, and the complete aetiology of the disease is still unclear. Here the authors perform an additional GWAS analysis followed by a meta-analysis with existing GWAS and replication genotyping and identify 6 ... ...

Abstract	Multiple myeloma is a cancer of the plasma cells, and the complete aetiology of the disease is still unclear. Here the authors perform an additional GWAS analysis followed by a meta-analysis with existing GWAS and replication genotyping and identify 6 novel risk loci and utilise gene expression, epigenetic profiling and in situ Hi-C data to further our understanding of MM susceptibility.
Keywords	Science ; Q
Language	English
Publishing date	2018-09-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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