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Association of functional variants of PTPN22 and tp53 in psoriatic arthritis: a case-control study.

https://arctichealth.org/en/permalink/ahliterature170485
Source
Arthritis Res Ther. 2006;8(1):R27
Publication Type
Article
Date
2006
Author
Christopher Butt
Lynette Peddle
Celia Greenwood
Sean Hamilton
Dafna Gladman
Proton Rahman
Author Affiliation
Memorial University of Newfoundland, Hospital for Sick Children, Department of Public Health Sciences, University of Toronto, Toronto, Canada. cbutt@mun.ca
Source
Arthritis Res Ther. 2006;8(1):R27
Date
2006
Language
English
Publication Type
Article
Keywords
Adult
Arginine
Arthritis, Psoriatic - genetics
Case-Control Studies
Cohort Studies
European Continental Ancestry Group - genetics
Female
Gene Frequency
Genetic Predisposition to Disease
Genetic Variation
Genotype
Humans
Male
Newfoundland and Labrador
Ontario
Protein Tyrosine Phosphatase, Non-Receptor Type 22
Protein Tyrosine Phosphatases - genetics
Risk
Tryptophan
Tumor Suppressor Protein p53 - genetics
Abstract
Recent studies have implicated PTPN22 and tp53 in susceptibility to several autoimmune diseases, including rheumatoid arthritis, suggesting that these genes are important in maintaining immune homeostasis. Because autoimmune diseases may share similar susceptibility loci, investigation of these genes in psoriatic arthritis (PsA) is of potential relevance. As a result we investigated known coding polymorphisms in PTPN22 and tp53 in a homogenous Caucasian PsA cohort from Newfoundland, Canada and an admixed Caucasian PsA cohort from Toronto, Canada. We observed a moderate association of the R620W variant of PTPN22 with PsA in the Toronto population only. Because of the conflicting findings reported regarding the association of PTPN22 with PsA, further studies in other PsA populations are warranted.
Notes
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PubMed ID
16507123 View in PubMed
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Association of interleukin-23 receptor variants with ankylosing spondylitis.

https://arctichealth.org/en/permalink/ahliterature157934
Source
Arthritis Rheum. 2008 Apr;58(4):1020-5
Publication Type
Article
Date
Apr-2008
Author
Proton Rahman
Robert D Inman
Dafna D Gladman
Jeff P Reeve
Lynette Peddle
Walter P Maksymowych
Author Affiliation
Memorial University, St. John's, Newfoundland, Canada. prahman@mun.ca
Source
Arthritis Rheum. 2008 Apr;58(4):1020-5
Date
Apr-2008
Language
English
Publication Type
Article
Keywords
Adult
Canada
Case-Control Studies
Female
Genetic Predisposition to Disease
Haplotypes
Humans
Inflammatory Bowel Diseases - genetics
Male
Middle Aged
Polymorphism, Single Nucleotide - genetics
Psoriasis - genetics
Receptors, Interleukin - genetics
Spondylitis, Ankylosing - genetics
Abstract
Recent studies have shown that a nonsynonymous single-nucleotide polymorphism (SNP) (Arg381Gln; rs11209026) in the interleukin-23 receptor (IL-23R) gene on chromosome 1p31 is associated with Crohn's disease and psoriasis. Given the clinical and immunologic overlap between ankylosing spondylitis (AS) and these diseases, and the potential function of this candidate SNP, this study was undertaken to examine the association of IL-23R variants with AS in multiple Canadian populations.
We examined 3 cohorts of AS patients from established rheumatic disease centers in Canada. The majority of AS patients were Caucasians of northern European descent, and all patients satisfied the modified New York classification criteria for AS or for juvenile spondylarthritis. We examined 424 AS probands and 401 controls from Alberta, 251 AS probands and 122 controls from Toronto, and 121 AS probands and 219 controls from Newfoundland. Ten IL-23R SNPs were genotyped, 9 of which were incorporated in the haplotype analysis. Allele and haplotype associations were calculated using the WHAP software package. P values for haplotype associations were calculated using a permutation test.
The primary SNP of interest in a previous study of inflammatory bowel disease (IBD) (Arg381Gln; rs11209026) was found to be protective against AS in the Newfoundland population (P=0.04) and in the Toronto population (P=0.04) in single-marker univariate analysis. The strongest association, however, was with SNP rs11465804 (P=0.007 for the Newfoundland population and P=0.0007 for the Toronto population). A 3-marker sliding window omnibus test revealed a significant association with markers rs10489629, rs2201841, and rs11465804 in both the Newfoundland population (P=0.04) and the Alberta population (P=0.034). Our results were independent of the IBD and psoriasis status of the AS patients.
This concurrent analysis of 3 distinct AS populations and their regional controls demonstrates a disease association with the IL-23R locus and implicates the same polymorphisms associated with IBD and psoriasis.
PubMed ID
18383363 View in PubMed
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Association of interleukin 23 receptor variants with psoriatic arthritis.

https://arctichealth.org/en/permalink/ahliterature153999
Source
J Rheumatol. 2009 Jan;36(1):137-40
Publication Type
Article
Date
Jan-2009
Author
Proton Rahman
Robert D Inman
Walter P Maksymowych
Jeff P Reeve
Lynette Peddle
Dafna D Gladman
Author Affiliation
Department of Medicine, Memorial University, 154 Le Marchant Road, St. John's, NL, Canada, A1C 5B8. prahman@mun.ca
Source
J Rheumatol. 2009 Jan;36(1):137-40
Date
Jan-2009
Language
English
Publication Type
Article
Keywords
Adult
Arthritis, Psoriatic - genetics
Canada
Cohort Studies
Crohn Disease - genetics
Female
Gene Frequency
Genetic Predisposition to Disease
Genetic Variation
Haplotypes
Humans
Interleukin-23 - genetics
Male
Middle Aged
Polymorphism, Single Nucleotide
Abstract
A recent genome-wide pooling study noted a significant association of interleukin 23 receptor (IL-23R) and psoriasis. Overxpression of IL-23 has been detected in lesional psoriatic skin, and induces epidermal proliferation. Given the interplay between psoriasis and PsA, we examined the association of IL-23R variants in 2 independent Canadian Caucasian cohorts of patients with psoriatic arthritis (PsA).
We examined 496 PsA probands and 476 controls. Cases and controls were genotyped for a panel of 11 single-nucleotide polymorphisms (SNP) in IL-23R. Allele and haplotype associations were calculated using WHAP software. P values for haplotype associations were calculated using a permutation test.
The 381Gln allele of the coding SNP Arg381Gln (rs11209026) was found to be protective in the Canadian population (p=0.004; corrected p=0.044). A 2-marker haplotype from SNP rs7530511 and rs11209026 was associated with PsA (p=0.011). All 3-marker sliding windows containing SNP rs11209026 were associated with PsA (p=0.02 for all 3 windows). The magnitude of effect of IL-23R association in PsA appears to be similar to that reported in uncomplicated psoriasis.
Significant associations between Arg381Gln SNP and haplotypes encoding this variant were noted in PsA. It remains to be determined what contribution of this association, if any, is specifically due to the inflammatory arthritis (PsA) rather than psoriasis.
PubMed ID
19040306 View in PubMed
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Association of the IL1 gene cluster with susceptibility to ankylosing spondylitis: an analysis of three Canadian populations.

https://arctichealth.org/en/permalink/ahliterature170470
Source
Arthritis Rheum. 2006 Mar;54(3):974-85
Publication Type
Article
Date
Mar-2006
Author
Walter P Maksymowych
Proton Rahman
Jeff P Reeve
Dafna D Gladman
Lynette Peddle
Robert D Inman
Author Affiliation
University of Alberta, Edmonton, Alberta, Canada. walter.maksymowych@ualberta.ca
Source
Arthritis Rheum. 2006 Mar;54(3):974-85
Date
Mar-2006
Language
English
Publication Type
Article
Keywords
Adult
Aged
Alberta - epidemiology
Case-Control Studies
Female
Genetic Predisposition to Disease - genetics
Humans
Interleukin-1 - genetics
Male
Middle Aged
Multigene Family
Newfoundland and Labrador - epidemiology
Ontario - epidemiology
Polymorphism, Single Nucleotide
Spondylitis, Ankylosing - epidemiology - genetics
Abstract
To examine the association between the IL1 gene cluster and susceptibility to ankylosing spondylitis (AS) in 3 independent case-control cohorts.
We analyzed 394 patients and 446 controls from Alberta, Newfoundland, and Toronto, Canada. Samples were genotyped using a panel of 38 single-nucleotide polymorphism (SNP) markers within the IL1 gene cluster. Data from 20 informative and nonredundant SNP markers were analyzed using several association test strategies. First, we used the program WHAP to identify single-marker associations. Second, we used WHAP to analyze "sliding windows" of 3 contiguous markers along the entire extent of the IL1 gene cluster in order to identify haplotypic associations. Third, we used the linkage disequilibrium mapping program DMLE to estimate the posterior probability distribution of a disease locus.
A total of 14 SNP markers showed significant single-locus disease associations, the most significant being rs3783526 (IL1A) (P = 0.0009 in the Alberta cohort, P = 0.04 in the Newfoundland cohort) and rs1143627 (IL1B) (P = 0.0005 in the Alberta cohort, P = 0.02 in the Newfoundland cohort). Analysis of 3-marker sliding windows revealed significant and consistent associations with all of the haplotypes in the IL1A and IL1B loci in the Alberta cohort and with IL1B in the Newfoundland cohort, especially haplotypes rs1143634/rs1143630/rs3917356 and rs1143630/rs3917356/rs3917354 (P = 0.006-0.0001). With DMLE, a strong peak in the probability distribution was estimated near IL1A in both the Alberta and the Newfoundland populations.
These results indicate that the IL1 locus, or a locus close to IL1, is associated with susceptibility to AS.
PubMed ID
16508980 View in PubMed
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Association of TNF-alpha polymorphisms in Crohn disease.

https://arctichealth.org/en/permalink/ahliterature176841
Source
Hum Immunol. 2005 Jan;66(1):56-9
Publication Type
Article
Date
Jan-2005
Author
Katrin Zipperlen
Lynette Peddle
Bill Melay
Donna Hefferton
Proton Rahman
Author Affiliation
Newfound Genomics, Memorial University of Newfoundland, Newfoundland, Canada.
Source
Hum Immunol. 2005 Jan;66(1):56-9
Date
Jan-2005
Language
English
Publication Type
Article
Keywords
Crohn Disease - etiology - genetics
DNA Primers - genetics
Genetic Linkage
Genetic Predisposition to Disease
Humans
Newfoundland and Labrador
Polymorphism, Single Nucleotide
Tumor Necrosis Factor-alpha - genetics
Abstract
Clinical and molecular studies implicate tumor necrosis factor alpha (TNF-alpha) as a key mediator in the initiation and propagation of Crohn disease (CD). Genetic associations have been documented between promoter polymorphisms of TNF-alpha and CD; however, these associations have not been universally replicated. In this study, we set out to examine the association of five promoter TNF-alpha polymorphisms in CD subjects from a founder population. In total, 128 CD subjects and 103 ethnically matched healthy controls were genotyped with time-of-flight mass spectrometry for the following five single nucleotide polymorphisms (SNPs) in the 5' flanking region of TNF-alpha gene: -1031 (T-->C), -863 (C-->A), -857 (C-->T), -308 (G-->A), and -238 (G-->A). Primer sequences, termination mixes, and multiplexing were determined with Sequenom SpectroDESIGNER software v1.3.4. The minor allele frequency for the TNF-alpha SNPs in subjects with CD and healthy controls, respectively, were -238 (5.5% vs. 5.3%); -308 (17.6% vs. 18.9%); -857 (5.1% vs. 7.8%); -863 (19.1% vs. 17.5%), and -1031 (24.6% vs. 22.8%). Thus, none of the TNF-alpha variants was associated with CD. Furthermore, no genotype/phenotype correlations were observed for the mutant allele of the TNF-alpha variants and selected clinical outcomes. In conclusion, there was no significant association for any of the TNF-alpha promoter polymorphism tested and CD in the Newfoundland population.
PubMed ID
15620462 View in PubMed
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A cost effectiveness analysis of thiopurine methyltransferase testing for guiding 6-mercaptopurine dosing in children with acute lymphoblastic leukemia.

https://arctichealth.org/en/permalink/ahliterature136779
Source
Pediatr Blood Cancer. 2011 Aug;57(2):231-9
Publication Type
Article
Date
Aug-2011
Author
Jennifer R Donnan
Wendy J Ungar
Maria Mathews
Rebecca L Hancock-Howard
Proton Rahman
Author Affiliation
Department of Health Policy, Management & Evaluation, University of Toronto, Toronto, Ontario, Canada.
Source
Pediatr Blood Cancer. 2011 Aug;57(2):231-9
Date
Aug-2011
Language
English
Publication Type
Article
Keywords
6-Mercaptopurine - administration & dosage - adverse effects
Antimetabolites, Antineoplastic - administration & dosage - adverse effects
Bone Marrow Diseases - chemically induced - prevention & control
Child, Preschool
Clinical Enzyme Tests - economics
Cost-Benefit Analysis
Decision Trees
Drug Dosage Calculations
Genetic Testing - economics
Genotype
Humans
Methyltransferases - deficiency - genetics
Models, Econometric
Ontario
Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy - enzymology - genetics
Sensitivity and specificity
Survival Analysis
Abstract
An increased understanding of the genetic basis of disease creates a demand for personalized medicine and more genetic testing for diagnosis and treatment. The objective was to assess the incremental cost-effectiveness per life-month gained of thiopurine methyltransferase (TPMT) genotyping to guide doses of 6-mercaptopurine (6-MP) in children with acute lymphoblastic leukemia (ALL) compared to enzymatic testing and standard weight-based dosing.
A cost-effectiveness analysis was conducted from a health care system perspective comparing costs and consequences over 3 months. Decision analysis was used to evaluate the impact of TPMT tests on preventing myelosuppression and improving survival in ALL patients receiving 6-MP. Direct medical costs included laboratory tests, medications, physician services, pharmacy and inpatient care. Probabilities were derived from published evidence. Survival was measured in life-months. The robustness of the results to variable uncertainty was tested in one-way sensitivity analyses. Probabilistic sensitivity analysis examined the impact of parameter uncertainty and generated confidence intervals around point estimates.
Neither of the testing interventions showed a benefit in survival compared to weight-based dosing. Both test strategies were more costly compared to weight-based dosing. Incremental costs per child (95% confidence interval) were $277 ($112, $442) and $298 ($392, $421) for the genotyping and phenotyping strategies, respectively, compared to weight-based dosing.
The present analysis suggests that screening for TPMT mutations using either genotype or enzymatic laboratory tests prior to the administration of 6-MP in pediatric ALL patients is not cost-effective.
Notes
Comment In: Pediatr Blood Cancer. 2011 Dec 15;57(7):124721796762
PubMed ID
21344614 View in PubMed
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Current challenges in the genetics of psoriatic arthritis: a report from the GRAPPA 2009 annual meeting.

https://arctichealth.org/en/permalink/ahliterature101822
Source
J Rheumatol. 2011 Mar;38(3):564-6
Publication Type
Article
Date
Mar-2011
Author
Proton Rahman
Author Affiliation
St. Clare's Mercy Hospital, St. John's, Newfoundland A1C 5B8, Canada. prahman@mun.ca
Source
J Rheumatol. 2011 Mar;38(3):564-6
Date
Mar-2011
Language
English
Publication Type
Article
Keywords
Arthritis, Psoriatic - genetics
Congresses as topic
Genetic Predisposition to Disease
Genome-Wide Association Study
Humans
Psoriasis - genetics
Sweden
Abstract
Psoriasis and psoriatic arthritis (PsA) are heterogeneous diseases. While both have a strong genetic basis, it is strongest for PsA, where fewer investigators are studying its genetics. Over the last year the number of independent genetic loci associated with psoriasis has substantially increased, mostly due to completion of multiple genome-wide association studies (GWAS) in psoriasis. At least 2 GWAS efforts are now under way in PsA to identify novel genes in this disease; a metaanalysis of genome-wide scans and further studies must follow to examine the genetics of disease expression, epistatic interaction, and gene-environment interaction. In the long term, it is anticipated that genome-wide sequencing is likely to generate another wave of novel genes in PsA. At the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) in Stockholm, Sweden, in 2009, members discussed issues and challenges regarding the advancement of the genetics of PsA; results of those discussions are summarized here.
PubMed ID
21362789 View in PubMed
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Effectiveness and safety of etanercept in patients with psoriatic arthritis in a Canadian clinical practice setting: the REPArE trial.

https://arctichealth.org/en/permalink/ahliterature134507
Source
J Rheumatol. 2011 Jul;38(7):1355-62
Publication Type
Article
Date
Jul-2011
Author
Dafna D Gladman
Claire Bombardier
Carter Thorne
Boulos Haraoui
Majed Khraishi
Proton Rahman
William Bensen
Jerry Syrotuik
Melanie Poulin-Costello
Author Affiliation
Toronto Western Hospital (University of Toronto) and University Health Network, Toronto, Ontario, Canada. dafna.gladman@utoronto.ca
Source
J Rheumatol. 2011 Jul;38(7):1355-62
Date
Jul-2011
Language
English
Publication Type
Article
Keywords
Adult
Antirheumatic Agents - adverse effects - therapeutic use
Arthritis, Psoriatic - drug therapy - physiopathology
Canada
Disability Evaluation
Efficiency - physiology
Fatigue - epidemiology - physiopathology
Female
Health status
Humans
Immunoglobulin G - adverse effects - therapeutic use
Incidence
Interviews as Topic
Longitudinal Studies
Male
Middle Aged
Receptors, Tumor Necrosis Factor - therapeutic use
Treatment Outcome
Tumor Necrosis Factor-alpha - antagonists & inhibitors
Abstract
To describe the longterm effectiveness and safety of etanercept in Canadian patients with psoriatic arthritis (PsA), treated over 24 months in clinical practice.
Patients with active PsA (= 3 tender and = 3 swollen joints) were recruited from 22 centers. Etanercept was administered at 50 mg/week subcutaneously. In addition to clinical assessment of skin and joint disease, conducted at baseline and at Months 6, 12, 18, and 24, regular patient interviews were conducted by telephone. Patient responses related to health status, disability, and work productivity were scored using the patient global assessment tool, the Health Assessment Questionnaire (HAQ), the Health and Labour Questionnaire (HLQ), and the Fatigue Severity Scale.
Out of 110 patients, 71 (65%) maintained etanercept treatment through the end of our study. All clinical measures of disease severity, including joint tenderness/pain, joint swelling, and Psoriasis Area and Severity Index score, improved significantly between baseline and Month 6 of etanercept treatment and remained constant thereafter. By the end of our study, 79% of patients achieved a Psoriatic Arthritis Response Criteria response, and 56% of patients achieved a 0.5-point improvement on HAQ, indicating clinically significant improvement in disability; 14% of patients finished our study free of disability (HAQ = 0). Patients' work productivity and fatigue improved significantly in parallel with these clinical and functional improvements.
Continuous treatment with etanercept over 2 years in a clinical setting improved clinical symptoms of PsA while reducing fatigue, improving work productivity, and ameliorating or eliminating disability.
PubMed ID
21572156 View in PubMed
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Evaluation for psoriatic arthritis in dermatology clinics.

https://arctichealth.org/en/permalink/ahliterature148206
Source
J Cutan Med Surg. 2009 Sep-Oct;13 Suppl 2:S88-92
Publication Type
Article
Author
Darren D O'Rielly
Proton Rahman
Author Affiliation
Faculty of Medicine and Division of Rhematology, Memorial University, St. John's, NeL.
Source
J Cutan Med Surg. 2009 Sep-Oct;13 Suppl 2:S88-92
Language
English
Publication Type
Article
Keywords
Arthritis, Psoriatic - classification - epidemiology - etiology
Canada - epidemiology
Dermatology - methods
Hospitals, Special
Humans
Incidence
Prevalence
Psoriasis - complications - epidemiology
PubMed ID
19799831 View in PubMed
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Genetic structure of the Newfoundland and Labrador population: founder effects modulate variability.

https://arctichealth.org/en/permalink/ahliterature284662
Source
Eur J Hum Genet. 2016 Jul;24(7):1063-70
Publication Type
Article
Date
Jul-2016
Author
Guangju Zhai
Jiayi Zhou
Michael O Woods
Jane S Green
Patrick Parfrey
Proton Rahman
Roger C Green
Source
Eur J Hum Genet. 2016 Jul;24(7):1063-70
Date
Jul-2016
Language
English
Publication Type
Article
Keywords
Consanguinity
Founder Effect
Genome, Human
Genotype
Humans
Newfoundland and Labrador
Polymorphism, Single Nucleotide
Population - genetics
Abstract
The population of the province of Newfoundland and Labrador (NL) has been a resource for genetic studies because of its historical isolation and increased prevalence of several monogenic disorders. Controversy remains regarding the genetic substructure and the extent of genetic homogeneity, which have implications for disease gene mapping. Population substructure has been reported from other isolated populations such as Iceland, Finland and Sardinia. We undertook this study to further our understanding of the genetic architecture of the NL population. We enrolled 494 individuals randomly selected from NL. Genome-wide SNP data were analyzed together with that from 14 other populations including HapMap3, Ireland, Britain and Native American samples from the Human Genome Diversity Project. Using multidimensional scaling and admixture analysis, we observed that the genetic structure of the NL population resembles that of the British population but can be divided into three clusters that correspond to religious/ethnic origins: Protestant English, Roman Catholic Irish and North American aboriginals. We observed reduced heterozygosity and an increased inbreeding coefficient (mean=0.005), which corresponds to that expected in the offspring of third-cousin marriages. We also found that the NL population has a significantly higher number of runs of homozygosity (ROH) and longer lengths of ROH segments. These results are consistent with our understanding of the population history and indicate that the NL population may be ideal for identifying recessive variants for complex diseases that affect populations of European origin.
Notes
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PubMed ID
26669659 View in PubMed
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18 records – page 1 of 2.