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Genomes and Genes | Peter HolmansSummaryAffiliation: Cardiff University Country: UK Publications
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Publications
Statistical methods for pathway analysis of genome-wide data for association with complex genetic traitsPeter Holmans
Biostatistics and Bioinformatics Unit, MRC Centre for Neuropsychiatric Genetics and Genomics, Department of Psychological Medicine and Neurology, Cardiff University School of Medicine, Heath Park, Cardiff, United Kingdom
Adv Genet 72:141-79. 2010..Finally, a list of computer programs for performing pathway analysis on genome-wide association data is provided...
Large-scale linkage analysis of 1302 affected relative pairs with rheumatoid arthritisMarian L Hamshere
Biostatistics and Bioinformatics Unit and Department of Psychological Medicine, Cardiff University, School of Medicine, Heath Park, Cardiff, CF14 4XN, UK
BMC Proc 1:S100. 2007....- Combining linkage data sets for meta-analysis and mega-analysis: the GAW15 rheumatoid arthritis data setRicardo Segurado
Biostatistics and Bioinformatics Unit and Department of Psychological Medicine, Cardiff University, School of Medicine, Heath Park, Cardiff CF14 4XN, UK
BMC Proc 1:S104. 2007..The two approaches were compared, and give strong support to the HLA locus on chromosome 6 as a susceptibility locus. Other regions of interest include loci on chromosomes 11, 2, and 12... 
The effect of linkage disequilibrium on linkage analysis of incomplete pedigreesDouglas F Levinson
Department of Psychiatry, University of Pennsylvania School of Medicine, 353 Market Street, Philadelphia, PA, USA
BMC Genet 6:S6. 2005..Simulation studies on the observed pedigree structures and map can also be used to determine the effect of LD on a particular study...- Covariate linkage analysis of GAW14 simulated data incorporating subclinical phenotype, sex, population, parent-of-origin, and interactionMarian L Hamshere
Biostatistics and Bioinformatics Unit, Cardiff University, Wales College of Medicine, Heath Park, Cardiff CF14 4XN, UK
BMC Genet 6:S45. 2005..Focusing on a randomly chosen replicate (42) we investigated the effect of the 12 subclinical phenotypes, sex, population, and parent-of-origin on the linkage signal from a model-free linkage analysis of Kofendrerd Personality Disorder... 
Genome screen for loci influencing age at onset and rate of decline in late onset Alzheimer's diseasePeter Holmans
Biostatistics and Bioinformatics Unit, Wales College of Medicine, Heath Park, Cardiff, United Kingdom
Am J Med Genet B Neuropsychiatr Genet 135:24-32. 2005..08) and chromosome 9 (max LOD = 3.34). The previously reported genome-wide linkage of AD to chromosome 10 was not influenced by any of the covariates studied...- Gene ontology analysis of GWA study data sets provides insights into the biology of bipolar disorderPeter Holmans
MRC Centre for Neuropsychiatric Genetics and Genomics, Department of Psychological Medicine and Neurology, School of Medicine, Heath Park, CF23 6BQ Cardiff, UK
Am J Hum Genet 85:13-24. 2009..The method was also applied to a meta-analysis of bipolar disorder, and it implicated the modulation of transcription and cellular activity, including that which occurs via hormonal action, as an important player in pathogenesis... - Identification of loci associated with schizophrenia by genome-wide association and follow-upMichael C O'Donovan
Department of Psychological Medicine, School of Medicine, Cardiff University, Cardiff, UK
Nat Genet 40:1053-5. 2008..Meta-analysis provided strongest evidence for association around ZNF804A (P = 1.61 x 10(-7)) and this strengthened when the affected phenotype included bipolar disorder (P = 9.96 x 10(-9))... - Permutation-based approaches do not adequately allow for linkage disequilibrium in gene-wide multi-locus association analysisValentina Moskvina
MRC Centre for Neuropsychiatric Genetics and Genomics, Department of Psychological Medicine and Neurology, School of Medicine, Cardiff University, Cardiff, UK
Eur J Hum Genet 20:890-6. 2012.... - An examination of single nucleotide polymorphism selection prioritization strategies for tests of gene-gene interactionValentina Moskvina
MRC Centre for Neuropsychiatric Genetics and Genomics, Department of Psychological Medicine and Neurology, School of Medicine, Cardiff University, Cardiff, UK
Biol Psychiatry 70:198-203. 2011..Aiming to minimize these statistical and computational burdens, we have explored approaches to prioritize SNPs for interaction analyses... - Genome-wide analysis of copy number variants in attention deficit hyperactivity disorder: the role of rare variants and duplications at 15q13.3Nigel M Williams
Medical Research Council Centre for Neuropsychiatric Genetics and Genomics, Department of Psychological Medicine and Neurology, and School of Medicine, Cardiff University, Cardiff, UK
Am J Psychiatry 169:195-204. 2012..Because of its multifactorial etiology, however, identifying the genes involved has been difficult. The authors followed up on recent findings suggesting that rare copy number variants (CNVs) may be important for ADHD etiology... - Most genome-wide significant susceptibility loci for schizophrenia and bipolar disorder reported to date cross-traditional diagnostic boundariesHywel J Williams
MRC Centre for Neuropsychiatric Genetics and Genomics, Department of Psychological Medicine and Neurology, School of Medicine, Cardiff University, Cardiff, UK
Hum Mol Genet 20:387-91. 2011..7 × 10(-5)). Including earlier reported data for trans-disorder effects for ZNF804A and CACNA1C, six out of eight of the most robustly associated loci for either disorder show trans-disorder effects... - A comparison of four clustering methods for brain expression microarray dataAlexander L Richards
Department of Psychological Medicine, School of Medicine, University Hospital Wales, Heath Park, Cardiff, Wales, UK
BMC Bioinformatics 9:490. 2008..The results are compared on speed, gene coverage and GO enrichment. The effects of combining the clusters produced by each method are also assessed... - Effects of differential genotyping error rate on the type I error probability of case-control studiesValentina Moskvina
Bioinformatics and Biostatistics Unit, School of Medicine, Wales College of Medicine, Cardiff University, Cardiff, UK
Hum Hered 61:55-64. 2006.... - Convergent evidence that oligodendrocyte lineage transcription factor 2 (OLIG2) and interacting genes influence susceptibility to schizophreniaLyudmila Georgieva
Department of Psychological Medicine, Cardiff University School of Medicine, Heath Park, Cardiff CF14 4XN, United Kingdom
Proc Natl Acad Sci U S A 103:12469-74. 2006..Our data provide strong convergent evidence that variation in OLIG2 confers susceptibility to schizophrenia alone and as part of a network of genes implicated in oligodendrocyte function... - Support for the involvement of large copy number variants in the pathogenesis of schizophreniaGeorge Kirov
Department of Psychological Medicine, Cardiff University, Heath Park, Cardiff, UK
Hum Mol Genet 18:1497-503. 2009..2 and schizophrenia (P = 0.026). This study confirms the involvement of rare CNVs in the pathogenesis of schizophrenia and contributes to the growing list of specific CNVs that are implicated... - Evaluation of an approximation method for assessment of overall significance of multiple-dependent tests in a genomewide association studyValentina Moskvina
MRC Centre for Neuropsychiatric Genetics and Genomics, School of Medicine, Cardiff University, Cardiff, United Kingdom
Genet Epidemiol 35:861-6. 2011..This is particularly relevant at a time of increasing public availability of significantly larger genetic data sets and should go a long way to assist in the rapid analysis of these data sets... - Strong evidence that KIAA0319 on chromosome 6p is a susceptibility gene for developmental dyslexiaNatalie Cope
Department of Psychological Medicine, Wales College of Medicine, Cardiff University, Cardiff, United Kingdom
Am J Hum Genet 76:581-91. 2005..006 in trios; 1-degree-of-freedom tests). Our data strongly implicate KIAA0319 as a susceptibility gene for dyslexia. The gene product is expressed in brain, but its specific function is currently unknown... - Genomewide significant linkage to recurrent, early-onset major depressive disorder on chromosome 15qPeter Holmans
Biostatistics and Bioinformatics Unit, University of Wales College of Medicine, Cardiff, United Kingdom
Am J Hum Genet 74:1154-67. 2004..Chromosome 15q25.3-26.2 deserves further study as a candidate region for susceptibility to MDD... - Streamlined analysis of pooled genotype data in SNP-based association studiesValentina Moskvina
Bioinformatics and Biostatistics Unit, College of Medicine, Cardiff University, United Kingdom
Genet Epidemiol 28:273-82. 2005..By controlling the error rates in the absence of knowledge of the appropriate SNP-specific correction factors, each approach enhances the performance of DNA pooling, while considerably streamlining the method by reducing time and cost... - Analyses of single marker and pairwise effects of candidate loci for rheumatoid arthritis using logistic regression and random forestsBeate Glaser
Biostatistics and Bioinformatics Unit, and Department of Psychological Medicine, Cardiff University, School of Medicine, Heath Park, Cardiff, Wales, CF14 4XN, UK
BMC Proc 1:S54. 2007..Follow-up analysis, such as by LR, is required since RFs do not indicate high-risk genotype combinations... - Clinical and cognitive characteristics of children with attention-deficit hyperactivity disorder, with and without copy number variantsKate Langley
Department of Psychological Medicine and Neurology, and MRC Centre for Neuropsychiatric Genetics, Cardiff University, Cardiff, UK
Br J Psychiatry 199:398-403. 2011..Submicroscopic, rare chromosomal copy number variants (CNVs) contribute to neurodevelopmental disorders but it is not known whether they define atypical clinical cases... - Rare chromosomal deletions and duplications in attention-deficit hyperactivity disorder: a genome-wide analysisNigel M Williams
MRC Centre in Neuropsychiatric Genetics and Genomics and Department of Psychological Medicine and Neurology, Cardiff University School of Medicine, Cardiff, UK
Lancet 376:1401-8. 2010..We aimed to establish whether burden of CNVs was increased in ADHD, and to investigate whether identified CNVs were enriched for loci previously identified in autism and schizophrenia... - Evidence for novel susceptibility genes for late-onset Alzheimer's disease from a genome-wide association study of putative functional variantsAndrew Grupe
Celera Diagnostics, 1401 Harbor Bay Parkway, Alameda, CA 94502, USA
Hum Mol Genet 16:865-73. 2007..This is a missense mutation in the galanin-like peptide precursor gene (P = 0.00005, OR = 1.2, false positive rate = 0.87)... - Alpha-T-catenin is expressed in human brain and interacts with the Wnt signaling pathway but is not responsible for linkage to chromosome 10 in Alzheimer's diseaseVictoria Busby
Department of Neuroscience, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, United Kingdom
Neuromolecular Med 5:133-46. 2004..None of these SNPs was associated with disease. Although an excellent candidate, we conclude that CTNNA3 is unlikely to account for the AD susceptibility locus on chromosome 10... - Variation in the urokinase-plasminogen activator gene does not explain the chromosome 10 linkage signal for late onset ADAmanda J Myers
Department of Psychiatry, Washington University School of Medicine, St Louis, Missouri, USA
Am J Med Genet B Neuropsychiatr Genet 124:29-37. 2004..Eight polymorphisms spanning the entire gene were examined using case control (CC) and family-based association methods. No association was observed by any method making it unlikely that variation in PLAU explains our linkage data... - Association of ABCA1 with late-onset Alzheimer's disease is not observed in a case-control studyYonghong Li
Celera Diagnostics, Alameda, CA, USA
Neurosci Lett 366:268-71. 2004..Further, we did not observe significant and replicated association of other ABCA1 SNPs we examined with the disease, thus these ABCA1 variants do not appear to influence the risk of LOAD in this study... - Association of late-onset Alzheimer's disease with genetic variation in multiple members of the GAPD gene familyYonghong Li
Celera Diagnostics, Alameda, CA 94502, USA
Proc Natl Acad Sci U S A 101:15688-93. 2004..Our observations raise the possibility that GAPD genes are AD risk factors, a hypothesis that is consistent with the role of GAPD in neuronal apoptosis... - Genetics of recurrent early-onset depression (GenRED): design and preliminary clinical characteristics of a repository sample for genetic linkage studiesDouglas F Levinson
Department of Psychiatry and Center for Neurobiology and Behavior, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 3309, USA
Am J Med Genet B Neuropsychiatr Genet 119:118-30. 2003..This suggests comparability of our cases to those in earlier large family studies. This dataset should prove useful for genetic studies of a highly familial form of major depressive disorder... - Genetic association of the APP binding protein 2 gene (APBB2) with late onset Alzheimer diseaseYonghong Li
Celera Diagnostics, Alameda, California 94502, USA
Hum Mutat 25:270-7. 2005..43 [95% CI: 1.61-3.67]; OR(het)=2.15 [95% CI: 1.46-3.17]; P=0.00006) in the combined sample set. Our data raise the possibility that genetic variations in APBB2 may affect LOAD susceptibility... - A scan of chromosome 10 identifies a novel locus showing strong association with late-onset Alzheimer diseaseAndrew Grupe
Celera Diagnostics, Alameda, CA, USA
Am J Hum Genet 78:78-88. 2006..0165). These results indicate that variants in the RPS3A homologue are associated with LOAD and implicate this gene, adjacent genes, or other functional variants (e.g., noncoding RNAs) in the pathogenesis of this disorder... - Full genome screen for Alzheimer disease: stage II analysisAmanda Myers
Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110, USA
Am J Med Genet 114:235-44. 2002..Of the seven markers we tested in family-based and case control samples, the only nominally positive association we found was with the 167 bp allele of marker D10S1217 (chi-square=7.11, P=0.045, df=1)... - Ubiquilin 1 polymorphisms are not associated with late-onset Alzheimer's diseaseScott Smemo
Department of Psychiatry, Washington University School of Medicine, 660 S Euclid Street, St Louis, MO 63110, USA
Ann Neurol 59:21-6. 2006..We did not find any evidence that this single nucleotide polymorphism, or any of six others tested in UBQLN1, increases risk for LOAD... - Genetics of recurrent early-onset major depression (GenRED): final genome scan reportPeter Holmans
Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 701A Welch Rd, Suite 3325, Palo Alto, CA 94304 5797, USA
Am J Psychiatry 164:248-58. 2007.... - Genetics of recurrent early-onset major depression (GenRED): significant linkage on chromosome 15q25-q26 after fine mapping with single nucleotide polymorphism markersDouglas F Levinson
Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 701A Welch Rd, Suite 3325, Palo Alto, CA 94304 5797, USA
Am J Psychiatry 164:259-64. 2007.... - Genomewide linkage scan in schizoaffective disorder: significant evidence for linkage at 1q42 close to DISC1, and suggestive evidence at 22q11 and 19p13Marian L Hamshere
Department of Psychological Medicine, School of Medicine, Cardiff University, Wales
Arch Gen Psychiatry 62:1081-8. 2005..Follow-up of this region should use samples enriched for cases of schizoaffective disorder. Our findings have similar implications for the search for genetic variation on chromosome 22q11 that influences susceptibility to psychosis... - Investigating the role of p11 (S100A10) sequence variation in susceptibility to major depressionRanjana Verma
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Am J Med Genet B Neuropsychiatr Genet 144:1079-82. 2007..2%, P = 0.15). None of the tag SNPs showed any evidence of association. Our results do not support a major role for either common or rare p11 SNPs with MDD. Several limitations of the study are discussed... - Bipolar affective puerperal psychosis: genome-wide significant evidence for linkage to chromosome 16Ian Jones
Department of Psychological Medicine, Henry Wellcome Building, Wales School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN UK
Am J Psychiatry 164:1099-104. 2007..The authors conducted a search by systematic whole genome linkage scan for loci influencing vulnerability to bipolar affective puerperal psychosis... - Evidence that common variation in NEDD9 is associated with susceptibility to late-onset Alzheimer's and Parkinson's diseaseYonghong Li
Celera, 1401 Harbor Bay Parkway, Alameda, CA 94502, USA
Hum Mol Genet 17:759-67. 2008..These data implicate NEDD9 as a novel susceptibility gene for LOAD and possibly PD... - Linkage disequilibrium mapping of a chromosome 15q25-26 major depression linkage region and sequencing of NTRK3Ranjana Verma
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Biol Psychiatry 63:1185-9. 2008..Here we present initial linkage-disequilibrium (LD) fine mapping of this signal and sequence analysis of NTRK3 (neurotrophic receptor kinase-3), a biologically plausible candidate gene... - Association studies between risk for late-onset Alzheimer's disease and variants in insulin degrading enzymePetra Nowotny
Department of Psychiatry, Washington University School of Medicine, St Louis, MO 63110, USA
Am J Med Genet B Neuropsychiatr Genet 136:62-8. 2005..Although our results are not universally negative, we were unable to replicate the results of previous studies and conclude that common variants or haplotypes of these variants in IDE are not major risk factors for LOAD... - Detecting gene-gene interactions using affected sib pair analysis with covariatesPeter Holmans
MRC Biostatistics Unit, Cambridge, UK
Hum Hered 53:92-102. 2002..If disease-associated genotypes are available, it may be worth re-analysing the whole genome... - A survey of genetic human cortical gene expressionAmanda J Myers
Laboratory of Neurogenetics, National Institute on Aging, Porter Neuroscience Building, National Institutes of Health Main Campus, Bethesda, Maryland 20892, USA
Nat Genet 39:1494-9. 2007.... - Multiple testing in the genomics era: findings from Genetic Analysis Workshop 15, Group 15Lisa J Martin
Department of Pediatrics, Cincinnati Children s Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA
Genet Epidemiol 31:S124-31. 2007..We show that while each approach may have certain advantages, adequate error control is largely dependent upon the question under consideration and often requires the use of multiple analytic strategies...