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Artikel ; Online: Implications of polygenic risk-stratified screening for prostate cancer on overdiagnosis.

Pashayan, Nora / Duffy, Stephen W / Neal, David E / Hamdy, Freddie C / Donovan, Jenny L / Martin, Richard M / Harrington, Patricia / Benlloch, Sara / Amin Al Olama, Ali / Shah, Mitul / Kote-Jarai, Zsofia / Easton, Douglas F / Eeles, Rosalind / Pharoah, Paul D

Genetics in medicine : official journal of the American College of Medical Genetics

2015 Band 17, Heft 10, Seite(n) 789–795

Abstract: Purpose: This study aimed to quantify the probability of overdiagnosis of prostate cancer by polygenic risk.: Methods: We calculated the polygenic risk score based on 66 known prostate cancer susceptibility variants for 17,012 men aged 50-69 years (9, ...

Abstract	Purpose: This study aimed to quantify the probability of overdiagnosis of prostate cancer by polygenic risk. Methods: We calculated the polygenic risk score based on 66 known prostate cancer susceptibility variants for 17,012 men aged 50-69 years (9,404 men identified with prostate cancer and 7,608 with no cancer) derived from three UK-based ongoing studies. We derived the probabilities of overdiagnosis by quartiles of polygenic risk considering that the observed prevalence of screen-detected prostate cancer is a combination of underlying incidence, mean sojourn time (MST), test sensitivity, and overdiagnosis. Results: Polygenic risk quartiles 1 to 4 comprised 9, 18, 25, and 48% of the cases, respectively. For a prostate-specific antigen test sensitivity of 80% and MST of 9 years, 43, 30, 25, and 19% of the prevalent screen-detected cancers in quartiles 1 to 4, respectively, were likely to be overdiagnosed cancers. Overdiagnosis decreased with increasing polygenic risk, with 56% decrease between the lowest and the highest polygenic risk quartiles. Conclusion: Targeting screening to men at higher polygenic risk could reduce the problem of overdiagnosis and lead to a better benefit-to-harm balance in screening for prostate cancer.
Mesh-Begriff(e)	Aged ; Algorithms ; Biomarkers, Tumor ; Early Detection of Cancer/methods ; Early Detection of Cancer/standards ; Genetic Loci ; Genetic Testing/methods ; Genetic Testing/standards ; Humans ; Male ; Medical Overuse ; Middle Aged ; Models, Genetic ; Models, Statistical ; Neoplasm Grading ; Neoplasm Staging ; Prostatic Neoplasms/diagnosis ; Prostatic Neoplasms/epidemiology ; Prostatic Neoplasms/genetics ; Risk ; Sensitivity and Specificity ; United Kingdom/epidemiology
Chemische Substanzen	Biomarkers, Tumor
Sprache	Englisch
Erscheinungsdatum	2015-01-08
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1455352-1
ISSN	1530-0366 ; 1098-3600
ISSN (online)	1530-0366
ISSN	1098-3600
DOI	10.1038/gim.2014.192
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Genetic variation in prostate-specific antigen-detected prostate cancer and the effect of control selection on genetic association studies.

Knipe, Duleeka W / Evans, David M / Kemp, John P / Eeles, Rosalind / Easton, Douglas F / Kote-Jarai, Zsofia / Al Olama, Ali Amin / Benlloch, Sara / Donovan, Jenny L / Hamdy, Freddie C / Neal, David E / Smith, George Davey / Lathrop, Mark / Martin, Richard M

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

2014 Band 23, Heft 7, Seite(n) 1356–1365

Abstract: Background: Only a minority of the genetic components of prostate cancer risk have been explained. Some observed associations of SNPs with prostate cancer might arise from associations of these SNPs with circulating prostate-specific antigen (PSA) ... ...

Abstract	Background: Only a minority of the genetic components of prostate cancer risk have been explained. Some observed associations of SNPs with prostate cancer might arise from associations of these SNPs with circulating prostate-specific antigen (PSA) because PSA values are used to select controls. Methods: We undertook a genome-wide association study (GWAS) of screen-detected prostate cancer (ProtecT: 1,146 cases and 1,804 controls); meta-analyzed the results with those from the previously published UK Genetic Prostate Cancer Study (1,854 cases and 1,437 controls); investigated associations of SNPs with prostate cancer using either "low" (PSA < 0.5 ng/mL) or "high" (PSA ≥ 3 ng/mL, biopsy negative) PSA controls; and investigated associations of SNPs with PSA. Results: The ProtecT GWAS confirmed previously reported associations of prostate cancer at three loci: 10q11.23, 17q24.3, and 19q13.33. The meta-analysis confirmed associations of prostate cancer with SNPs near four previously identified loci (8q24.21,10q11.23, 17q24.3, and 19q13.33). When comparing prostate cancer cases with low PSA controls, alleles at genetic markers rs1512268, rs445114, rs10788160, rs11199874, rs17632542, rs266849, and rs2735839 were associated with an increased risk of prostate cancer, but the effect-estimates were attenuated to the null when using high PSA controls (Pheterogeneity in effect-estimates < 0.04). We found a novel inverse association of rs9311171-T with circulating PSA. Conclusions: Differences in effect-estimates for prostate cancer observed when comparing low versus high PSA controls may be explained by associations of these SNPs with PSA. Impact: These findings highlight the need for inferences from genetic studies of prostate cancer risk to carefully consider the influence of control selection criteria.
Mesh-Begriff(e)	Aged ; Genetic Association Studies ; Genetic Predisposition to Disease/genetics ; Genotype ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Prostate-Specific Antigen/blood ; Prostate-Specific Antigen/genetics ; Prostatic Neoplasms/blood ; Prostatic Neoplasms/genetics
Chemische Substanzen	Prostate-Specific Antigen (EC 3.4.21.77)
Sprache	Englisch
Erscheinungsdatum	2014-04-21
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Meta-Analysis ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1153420-5
ISSN	1538-7755 ; 1055-9965
ISSN (online)	1538-7755
ISSN	1055-9965
DOI	10.1158/1055-9965.EPI-13-0889
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Gene and pathway level analyses of germline DNA-repair gene variants and prostate cancer susceptibility using the iCOGS-genotyping array.

Saunders, Edward J / Dadaev, Tokhir / Leongamornlert, Daniel A / Al Olama, Ali Amin / Benlloch, Sara / Giles, Graham G / Wiklund, Fredrik / Grönberg, Henrik / Haiman, Christopher A / Schleutker, Johanna / Nordestgaard, Børge G / Travis, Ruth C / Neal, David / Pasayan, Nora / Khaw, Kay-Tee / Stanford, Janet L / Blot, William J / Thibodeau, Stephen N / Maier, Christiane /

Kibel, Adam S / Cybulski, Cezary / Cannon-Albright, Lisa / Brenner, Hermann / Park, Jong Y / Kaneva, Radka / Batra, Jyotsna / Teixeira, Manuel R / Pandha, Hardev / Govindasami, Koveela / Muir, Ken / Easton, Douglas F / Eeles, Rosalind A / Kote-Jarai, Zsofia

British journal of cancer

2018 Band 118, Heft 6, Seite(n) e9

Abstract: This corrects the article DOI: 10.1038/bjc.2016.50. ...

Abstract	This corrects the article DOI: 10.1038/bjc.2016.50.
Sprache	Englisch
Erscheinungsdatum	2018-02-13
Erscheinungsland	England
Dokumenttyp	Journal Article ; Published Erratum
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/bjc.2017.468
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: AA9int: SNP interaction pattern search using non-hierarchical additive model set

Lin, Hui-Yi / Huang, Po-Yu / Chen, Dung-Tsa / Tung, Heng-Yuan / Sellers, Thomas A. / Pow-Sang, Julio M. / Eeles, Rosalind / Easton, Douglas J. / Kote-Jarai, Zsofia / Amin Al Olama, Ali / Benlloch, Sara / Muir, Kenneth / Giles, Graham G. / Wiklund, Fredrik / Gronberg, Henrik / Haiman, Christopher A. / Schleutker, Johanna / Nordestgaard, Børge G. / Travis, Ruth C. /

Hamdy, Freddie / Neal, David E. / Pashayan, Nora / Khaw, Kay-Tee / Stanford, Janet L. / Blot, William J. / Thibodeau, Stephen N. / Maier, Christiane / Kibel, Adam S. / Cybulski, Cezary / Cannon-Albright, Lisa / Brenner, Hermann / Kaneva, Radka / Batra, Jyotsna / Teixeira, Manuel R. / Pandha, Hardev / Lu, Yong-Jie / Park, Jong Y.

Bioinformatics. 2018 Dec. 15, v. 34, no. 24, p. 4141-4150

2018 , Seite(n) 4141–4150

Abstract: The use of single nucleotide polymorphism (SNP) interactions to predict complex diseases is getting more attention during the past decade, but related statistical methods are still immature. We previously proposed the SNP Interaction Pattern Identifier ( ... ...

Körperschaft	The PRACTICAL Consortium
Abstract	The use of single nucleotide polymorphism (SNP) interactions to predict complex diseases is getting more attention during the past decade, but related statistical methods are still immature. We previously proposed the SNP Interaction Pattern Identifier (SIPI) approach to evaluate 45 SNP interaction patterns/patterns. SIPI is statistically powerful but suffers from a large computation burden. For large-scale studies, it is necessary to use a powerful and computation-efficient method. The objective of this study is to develop an evidence-based mini-version of SIPI as the screening tool or solitary use and to evaluate the impact of inheritance mode and model structure on detecting SNP–SNP interactions. We tested two candidate approaches: the ‘Five-Full’ and ‘AA9int’ method. The Five-Full approach is composed of the five full interaction models considering three inheritance modes (additive, dominant and recessive). The AA9int approach is composed of nine interaction models by considering non-hierarchical model structure and the additive mode. Our simulation results show that AA9int has similar statistical power compared to SIPI and is superior to the Five-Full approach, and the impact of the non-hierarchical model structure is greater than that of the inheritance mode in detecting SNP–SNP interactions. In summary, it is recommended that AA9int is a powerful tool to be used either alone or as the screening stage of a two-stage approach (AA9int+SIPI) for detecting SNP–SNP interactions in large-scale studies. The ‘AA9int’ and ‘parAA9int’ functions (standard and parallel computing version) are added in the SIPI R package, which is freely available at https://linhuiyi.github.io/LinHY_Software/. Supplementary data are available at Bioinformatics online.
Schlagwörter	bioinformatics ; models ; single nucleotide polymorphism
Sprache	Englisch
Erscheinungsverlauf	2018-1215
Umfang	p. 4141-4150
Erscheinungsort	Oxford University Press
Dokumenttyp	Artikel ; Online
Anmerkung	Use and reproduction
ZDB-ID	1468345-3
ISSN	1367-4811 ; 1460-2059
ISSN	1367-4811 ; 1460-2059
DOI	10.1093/bioinformatics/bty461
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel ; Online: SNP interaction pattern identifier (SIPI): an intensive search for SNP–SNP interaction patterns

Lin, Hui-Yi / Chen, Dung-Tsa / Huang, Po-Yu / Liu, Yongxin / Ochoa, Augusto / Zabaleta, Jovanny / Mercante, Donald E. / Fang, Zhide / Sellers, Thomas A. / Pow-Sang, Julio M. / Cheng, Chia-Ho / Eeles, Rosalind / Easton, Douglas J. / Kote-Jarai, Zsofia / Amin Al Olama, Ali / Benlloch, Sara / Muir, Kenneth / Giles, Graham G. / Wiklund, Fredrik /

Bioinformatics. 2017 Mar. 15, v. 33, no. 6 p.822-833

2017

Abstract: Motivation: Testing SNP–SNP interactions is considered as a key for overcoming bottlenecks of genetic association studies. However, related statistical methods for testing SNP–SNP interactions are underdeveloped. Results: We propose the SNP Interaction ... ...

Körperschaft	The Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL) Consortium
Abstract	Motivation: Testing SNP–SNP interactions is considered as a key for overcoming bottlenecks of genetic association studies. However, related statistical methods for testing SNP–SNP interactions are underdeveloped. Results: We propose the SNP Interaction Pattern Identifier (SIPI), which tests 45 biologically meaningful interaction patterns for a binary outcome. SIPI takes non-hierarchical models, inheritance modes and mode coding direction into consideration. The simulation results show that SIPI has higher power than MDR (Multifactor Dimensionality Reduction), AA_Full, Geno_Full (full interaction model with additive or genotypic mode) and SNPassoc in detecting interactions. Applying SIPI to the prostate cancer PRACTICAL consortium data with approximately 21 000 patients, the four SNP pairs in EGFR-EGFR, EGFR-MMP16 and EGFR-CSF1 were found to be associated with prostate cancer aggressiveness with the exact or similar pattern in the discovery and validation sets. A similar match for external validation of SNP–SNP interaction studies is suggested. We demonstrated that SIPI not only searches for more meaningful interaction patterns but can also overcome the unstable nature of interaction patterns. Availability and Implementation: The SIPI software is freely available at http://publichealth.lsuhsc.edu/LinSoftware/. Contact: hlin1@lsuhsc.edu Supplementary information: Supplementary data are available at Bioinformatics online.
Schlagwörter	bioinformatics ; computer software ; models ; patients ; prostatic neoplasms ; single nucleotide polymorphism ; statistical analysis
Sprache	Englisch
Erscheinungsverlauf	2017-0315
Umfang	p. 822-833.
Erscheinungsort	Oxford University Press
Dokumenttyp	Artikel ; Online
Anmerkung	Resource is Open Access
ZDB-ID	1468345-3
ISSN	1460-2059 ; 1367-4811
ISSN	1460-2059 ; 1367-4811
DOI	10.1093/bioinformatics/btw762
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel ; Online: Gene and pathway level analyses of germline DNA-repair gene variants and prostate cancer susceptibility using the iCOGS-genotyping array.

Saunders, Edward J / Dadaev, Tokhir / Leongamornlert, Daniel A / Al Olama, Ali Amin / Benlloch, Sara / Giles, Graham G / Wiklund, Fredrik / Gronberg, Henrik / Haiman, Christopher A / Schleutker, Johanna / Nordestgaard, Borge G / Travis, Ruth C / Neal, David / Pasayan, Nora / Khaw, Kay-Tee / Stanford, Janet L / Blot, William J / Thibodeau, Stephen N / Maier, Christiane /

British journal of cancer

2016 Band 114, Heft 8, Seite(n) 945–952

Abstract: Background: Germline mutations within DNA-repair genes are implicated in susceptibility to multiple forms of cancer. For prostate cancer (PrCa), rare mutations in BRCA2 and BRCA1 give rise to moderately elevated risk, whereas two of B100 common, low- ... ...

Abstract	Background: Germline mutations within DNA-repair genes are implicated in susceptibility to multiple forms of cancer. For prostate cancer (PrCa), rare mutations in BRCA2 and BRCA1 give rise to moderately elevated risk, whereas two of B100 common, low-penetrance PrCa susceptibility variants identified so far by genome-wide association studies implicate RAD51B and RAD23B. Methods: Genotype data from the iCOGS array were imputed to the 1000 genomes phase 3 reference panel for 21 780 PrCa cases and 21 727 controls from the Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL) consortium. We subsequently performed single variant, gene and pathway-level analyses using 81 303 SNPs within 20 Kb of a panel of 179 DNA-repair genes. Results: Single SNP analyses identified only the previously reported association with RAD51B. Gene-level analyses using the SKAT-C test from the SNP-set (Sequence) Kernel Association Test (SKAT) identified a significant association with PrCa for MSH5. Pathway-level analyses suggested a possible role for the translesion synthesis pathway in PrCa risk and Homologous recombination/Fanconi Anaemia pathway for PrCa aggressiveness, even though after adjustment for multiple testing these did not remain significant. Conclusions: MSH5 is a novel candidate gene warranting additional follow-up as a prospective PrCa-risk locus. MSH5 has previously been reported as a pleiotropic susceptibility locus for lung, colorectal and serous ovarian cancers.
Mesh-Begriff(e)	BRCA1 Protein/genetics ; Case-Control Studies ; Cell Cycle Proteins/genetics ; DNA/genetics ; DNA Repair/genetics ; DNA Repair Enzymes/genetics ; DNA-Binding Proteins/genetics ; Genes, BRCA2/physiology ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study/methods ; Genotype ; Germ-Line Mutation/genetics ; Humans ; Male ; Polymorphism, Single Nucleotide/genetics ; Prospective Studies ; Prostatic Neoplasms/genetics ; Risk
Chemische Substanzen	BRCA1 Protein ; Cell Cycle Proteins ; DNA-Binding Proteins ; MSH5 protein, human ; RAD23B protein, human ; RAD51B protein, human ; DNA (9007-49-2) ; DNA Repair Enzymes (EC 6.5.1.-)
Sprache	Englisch
Erscheinungsdatum	2016-03-13
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/bjc.2016.50
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Polyunsaturated fatty acids and prostate cancer risk: a Mendelian randomisation analysis from the PRACTICAL consortium.

Khankari, Nikhil K / Murff, Harvey J / Zeng, Chenjie / Wen, Wanqing / Eeles, Rosalind A / Easton, Douglas F / Kote-Jarai, Zsofia / Al Olama, Ali Amin / Benlloch, Sara / Muir, Kenneth / Giles, Graham G / Wiklund, Fredrik / Gronberg, Henrik / Haiman, Christopher A / Schleutker, Johanna / Nordestgaard, Børge G / Travis, Ruth C / Donovan, Jenny L / Pashayan, Nora /

Khaw, Kay-Tee / Stanford, Janet L / Blot, William J / Thibodeau, Stephen N / Maier, Christiane / Kibel, Adam S / Cybulski, Cezary / Cannon-Albright, Lisa / Brenner, Hermann / Park, Jong / Kaneva, Radka / Batra, Jyotsna / Teixeira, Manuel R / Pandha, Hardev / Zheng, Wei

British journal of cancer

2016 Band 115, Heft 5, Seite(n) 624–631

Abstract: Background: Prostate cancer is a common cancer worldwide with no established modifiable lifestyle factors to guide prevention. The associations between polyunsaturated fatty acids (PUFAs) and prostate cancer risk have been inconsistent. Using Mendelian ... ...

Abstract	Background: Prostate cancer is a common cancer worldwide with no established modifiable lifestyle factors to guide prevention. The associations between polyunsaturated fatty acids (PUFAs) and prostate cancer risk have been inconsistent. Using Mendelian randomisation, we evaluated associations between PUFAs and prostate cancer risk. Methods: We used individual-level data from a consortium of 22 721 cases and 23 034 controls of European ancestry. Externally-weighted PUFA-specific polygenic risk scores (wPRSs), with explanatory variation ranging from 0.65 to 33.07%, were constructed and used to evaluate associations with prostate cancer risk per one standard deviation (s.d.) increase in genetically-predicted plasma PUFA levels using multivariable-adjusted unconditional logistic regression. Results: No overall association was observed between the genetically-predicted PUFAs evaluated in this study and prostate cancer risk. However, risk reductions were observed for short-chain PUFAs, linoleic (ORLA=0.95, 95%CI=0.92, 0.98) and α-linolenic acids (ORALA=0.96, 95%CI=0.93, 0.98), among men <62 years; whereas increased risk was found among men ⩾62 years for LA (ORLA=1.04, 95%CI=1.01, 1.07). For long-chain PUFAs (i.e., arachidonic, eicosapentaenoic, and docosapentaenoic acids), increased risks were observed among men <62 years (ORAA=1.05, 95%CI=1.02, 1.08; OREPA=1.04, 95%CI=1.01, 1.06; ORDPA=1.05, 95%CI=1.02, 1.08). Conclusion: Results from this study suggest that circulating ω-3 and ω-6 PUFAs may have a different role in the aetiology of early- and late-onset prostate cancer.
Mesh-Begriff(e)	Fatty Acids, Unsaturated/metabolism ; Genome-Wide Association Study ; Humans ; Male ; Prostatic Neoplasms/epidemiology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Risk Factors
Chemische Substanzen	Fatty Acids, Unsaturated
Sprache	Englisch
Erscheinungsdatum	2016-08-04
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/bjc.2016.228
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Alcohol consumption and prostate cancer incidence and progression: A Mendelian randomisation study.

Brunner, Clair / Davies, Neil M / Martin, Richard M / Eeles, Rosalind / Easton, Doug / Kote-Jarai, Zsofia / Al Olama, Ali Amin / Benlloch, Sara / Muir, Kenneth / Giles, Graham / Wiklund, Fredrik / Gronberg, Henrik / Haiman, Christopher A / Schleutker, Johanna / Nordestgaard, Børge G / Travis, Ruth C / Neal, David / Donovan, Jenny / Hamdy, Freddie C /

Pashayan, Nora / Khaw, Kay-Tee / Stanford, Janet L / Blot, William J / Thibodeau, Stephen / Maier, Christiane / Kibel, Adam S / Cybulski, Cezary / Cannon-Albright, Lisa / Brenner, Hermann / Park, Jong / Kaneva, Radka / Batra, Jyotsna / Teixeira, Manuel R / Pandha, Hardev / Zuccolo, Luisa

International journal of cancer

2016 Band 140, Heft 1, Seite(n) 75–85

Abstract: Prostate cancer is the most common cancer in men in developed countries, and is a target for risk reduction strategies. The effects of alcohol consumption on prostate cancer incidence and survival remain unclear, potentially due to methodological ... ...

Abstract	Prostate cancer is the most common cancer in men in developed countries, and is a target for risk reduction strategies. The effects of alcohol consumption on prostate cancer incidence and survival remain unclear, potentially due to methodological limitations of observational studies. In this study, we investigated the associations of genetic variants in alcohol-metabolising genes with prostate cancer incidence and survival. We analysed data from 23,868 men with prostate cancer and 23,051 controls from 25 studies within the international PRACTICAL Consortium. Study-specific associations of 68 single nucleotide polymorphisms (SNPs) in 8 alcohol-metabolising genes (Alcohol Dehydrogenases (ADHs) and Aldehyde Dehydrogenases (ALDHs)) with prostate cancer diagnosis and prostate cancer-specific mortality, by grade, were assessed using logistic and Cox regression models, respectively. The data across the 25 studies were meta-analysed using fixed-effect and random-effects models. We found little evidence that variants in alcohol metabolising genes were associated with prostate cancer diagnosis. Four variants in two genes exceeded the multiple testing threshold for associations with prostate cancer mortality in fixed-effect meta-analyses. SNPs within ALDH1A2 associated with prostate cancer mortality were rs1441817 (fixed effects hazard ratio, HR
Mesh-Begriff(e)	Aged ; Aged, 80 and over ; Alcohol Drinking/adverse effects ; Alcohol Drinking/genetics ; Aldehyde Dehydrogenase/genetics ; Aldehyde Dehydrogenase 1 Family ; Aldehyde Dehydrogenase, Mitochondrial ; Case-Control Studies ; Disease Progression ; Humans ; Incidence ; Linkage Disequilibrium ; Male ; Middle Aged ; Neoplasm Grading ; Polymorphism, Single Nucleotide ; Prostatic Neoplasms/epidemiology ; Prostatic Neoplasms/mortality ; Prostatic Neoplasms/pathology ; Regression Analysis ; Retinal Dehydrogenase/genetics ; Survival Analysis
Chemische Substanzen	Aldehyde Dehydrogenase 1 Family (EC 1.2.1) ; ALDH1B1 protein, human (EC 1.2.1.3) ; Aldehyde Dehydrogenase (EC 1.2.1.3) ; Aldehyde Dehydrogenase, Mitochondrial (EC 1.2.1.3) ; ALDH1A2 protein, human (EC 1.2.1.36) ; Retinal Dehydrogenase (EC 1.2.1.36)
Sprache	Englisch
Erscheinungsdatum	2016-10-08
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Meta-Analysis
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.30436
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Investigating the possible causal role of coffee consumption with prostate cancer risk and progression using Mendelian randomization analysis.

Taylor, Amy E / Martin, Richard M / Geybels, Milan S / Stanford, Janet L / Shui, Irene / Eeles, Rosalind / Easton, Doug / Kote-Jarai, Zsofia / Amin Al Olama, Ali / Benlloch, Sara / Muir, Kenneth / Giles, Graham G / Wiklund, Fredrik / Gronberg, Henrik / Haiman, Christopher A / Schleutker, Johanna / Nordestgaard, Børge G / Travis, Ruth C / Neal, David /

Pashayan, Nora / Khaw, Kay-Tee / Blot, William / Thibodeau, Stephen / Maier, Christiane / Kibel, Adam S / Cybulski, Cezary / Cannon-Albright, Lisa / Brenner, Hermann / Park, Jong / Kaneva, Radka / Batra, Jyotsna / Teixeira, Manuel R / Pandha, Hardev / Donovan, Jenny / Munafò, Marcus R

International journal of cancer

2016 Band 140, Heft 2, Seite(n) 322–328

Abstract: Coffee consumption has been shown in some studies to be associated with lower risk of prostate cancer. However, it is unclear if this association is causal or due to confounding or reverse causality. We conducted a Mendelian randomisation analysis to ... ...

Abstract	Coffee consumption has been shown in some studies to be associated with lower risk of prostate cancer. However, it is unclear if this association is causal or due to confounding or reverse causality. We conducted a Mendelian randomisation analysis to investigate the causal effects of coffee consumption on prostate cancer risk and progression. We used two genetic variants robustly associated with caffeine intake (rs4410790 and rs2472297) as proxies for coffee consumption in a sample of 46,687 men of European ancestry from 25 studies in the PRACTICAL consortium. Associations between genetic variants and prostate cancer case status, stage and grade were assessed by logistic regression and with all-cause and prostate cancer-specific mortality using Cox proportional hazards regression. There was no clear evidence that a genetic risk score combining rs4410790 and rs2472297 was associated with prostate cancer risk (OR per additional coffee increasing allele: 1.01, 95% CI: 0.98,1.03) or having high-grade compared to low-grade disease (OR: 1.01, 95% CI: 0.97,1.04). There was some evidence that the genetic risk score was associated with higher odds of having nonlocalised compared to localised stage disease (OR: 1.03, 95% CI: 1.01, 1.06). Amongst men with prostate cancer, there was no clear association between the genetic risk score and all-cause mortality (HR: 1.00, 95% CI: 0.97,1.04) or prostate cancer-specific mortality (HR: 1.03, 95% CI: 0.98,1.08). These results, which should have less bias from confounding than observational estimates, are not consistent with a substantial effect of coffee consumption on reducing prostate cancer incidence or progression.
Mesh-Begriff(e)	Aged ; Alleles ; Coffee/adverse effects ; Disease Progression ; Genetic Variation/genetics ; Humans ; Male ; Mendelian Randomization Analysis/methods ; Middle Aged ; Prostatic Neoplasms/etiology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Risk Factors
Chemische Substanzen	Coffee
Sprache	Englisch
Erscheinungsdatum	2016-10-26
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.30462
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: AA9int: SNP interaction pattern search using non-hierarchical additive model set.

Lin, Hui-Yi / Huang, Po-Yu / Chen, Dung-Tsa / Tung, Heng-Yuan / Sellers, Thomas A / Pow-Sang, Julio M / Eeles, Rosalind / Easton, Doug / Kote-Jarai, Zsofia / Amin Al Olama, Ali / Benlloch, Sara / Muir, Kenneth / Giles, Graham G / Wiklund, Fredrik / Gronberg, Henrik / Haiman, Christopher A / Schleutker, Johanna / Nordestgaard, Børge G / Travis, Ruth C /

Hamdy, Freddie / Neal, David E / Pashayan, Nora / Khaw, Kay-Tee / Stanford, Janet L / Blot, William J / Thibodeau, Stephen N / Maier, Christiane / Kibel, Adam S / Cybulski, Cezary / Cannon-Albright, Lisa / Brenner, Hermann / Kaneva, Radka / Batra, Jyotsna / Teixeira, Manuel R / Pandha, Hardev / Lu, Yong-Jie / Park, Jong Y

Bioinformatics (Oxford, England)

2018 Band 34, Heft 24, Seite(n) 4141–4150

Abstract: Motivation: The use of single nucleotide polymorphism (SNP) interactions to predict complex diseases is getting more attention during the past decade, but related statistical methods are still immature. We previously proposed the SNP Interaction Pattern ...

Abstract	Motivation: The use of single nucleotide polymorphism (SNP) interactions to predict complex diseases is getting more attention during the past decade, but related statistical methods are still immature. We previously proposed the SNP Interaction Pattern Identifier (SIPI) approach to evaluate 45 SNP interaction patterns/patterns. SIPI is statistically powerful but suffers from a large computation burden. For large-scale studies, it is necessary to use a powerful and computation-efficient method. The objective of this study is to develop an evidence-based mini-version of SIPI as the screening tool or solitary use and to evaluate the impact of inheritance mode and model structure on detecting SNP-SNP interactions. Results: We tested two candidate approaches: the 'Five-Full' and 'AA9int' method. The Five-Full approach is composed of the five full interaction models considering three inheritance modes (additive, dominant and recessive). The AA9int approach is composed of nine interaction models by considering non-hierarchical model structure and the additive mode. Our simulation results show that AA9int has similar statistical power compared to SIPI and is superior to the Five-Full approach, and the impact of the non-hierarchical model structure is greater than that of the inheritance mode in detecting SNP-SNP interactions. In summary, it is recommended that AA9int is a powerful tool to be used either alone or as the screening stage of a two-stage approach (AA9int+SIPI) for detecting SNP-SNP interactions in large-scale studies. Availability and implementation: The 'AA9int' and 'parAA9int' functions (standard and parallel computing version) are added in the SIPI R package, which is freely available at https://linhuiyi.github.io/LinHY_Software/. Supplementary information: Supplementary data are available at Bioinformatics online.
Mesh-Begriff(e)	Algorithms ; Computational Biology ; Computer Simulation ; Polymorphism, Single Nucleotide ; Software ; Statistics as Topic
Sprache	Englisch
Erscheinungsdatum	2018-06-07
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/bty461
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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