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Acute myeloid leukemia with complex hypodiploidy and loss of heterozygosity of 17p in a boy with Fanconi anemia.

https://arctichealth.org/en/permalink/ahliterature101073
Source
Ann Clin Lab Sci. 2011;41(1):66-70
Publication Type
Article
Date
2011
Author
Hye In Woo
Hee-Jin Kim
Soo Hyun Lee
Keon Hee Yoo
Hong Hoe Koo
Sun-Hee Kim
Author Affiliation
Department of Laboratory Medicine & Genetics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Source
Ann Clin Lab Sci. 2011;41(1):66-70
Date
2011
Language
English
Publication Type
Article
Keywords
Child, Preschool
Chromosomes, Human, Pair 17 - genetics
Diploidy
Fanconi Anemia - complications - genetics - pathology
Fatal Outcome
Humans
Karyotyping
Leukemia, Myeloid, Acute - complications - genetics - pathology
Loss of Heterozygosity - genetics
Male
Abstract
Fanconi anemia (FA) is a congenital bone marrow failure syndrome in association with increased susceptibility to malignancy. We report the first in-depth description of a boy with FA who developed acute myeloid leukemia with complex hypodiploidy karyotype after successful stem cell transplantation. Of note, the leukemic cells consistently showed loss of heterozygosity (LOH) of the short arm of chromosome 17 (17p), which harbors the TP53 tumor suppressor gene. The complex hypodiploidy karyotype of the leukemic cells with LOH for 17p may represent a unique karyotypic profile that reflects genomic instability and thereby confers poor prognosis.
PubMed ID
21325258 View in PubMed
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CGH analysis of familial non-BRCA1/BRCA2 breast tumors and mutation screening of a candidate locus on chromosome 17q11.2-12.

https://arctichealth.org/en/permalink/ahliterature16969
Source
Int J Mol Med. 2005 Jul;16(1):135-41
Publication Type
Article
Date
Jul-2005
Author
Paula Maguire
Kerstin Holmberg
Maria Kost-Alimova
Stefan Imreh
Lambert Skoog
Annika Lindblom
Author Affiliation
Department of Molecular Medicine, Karolinska Institute, Stockholm 171 76, Sweden.
Source
Int J Mol Med. 2005 Jul;16(1):135-41
Date
Jul-2005
Language
English
Publication Type
Article
Keywords
BRCA1 Protein - genetics
BRCA2 Protein - genetics
Breast Neoplasms - genetics
Chromosomes, Human, Pair 17 - genetics
DNA Mutational Analysis
Genetic Predisposition to Disease
Genetic Screening
Genomics
Haplotypes
Humans
Mutation - genetics
Nucleic Acid Hybridization
Research Support, Non-U.S. Gov't
Risk factors
Abstract
Mutations in the known predisposing breast cancer genes BRCA1 and BRCA2 account for only a small proportion (
PubMed ID
15942690 View in PubMed
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Chromosome 17q21 gene variants are associated with asthma and exacerbations but not atopy in early childhood.

https://arctichealth.org/en/permalink/ahliterature91125
Source
Am J Respir Crit Care Med. 2009 Feb 1;179(3):179-85
Publication Type
Article
Date
Feb-1-2009
Author
Bisgaard Hans
Bønnelykke Klaus
Sleiman Patrick M A
Brasholt Martin
Chawes Bo
Kreiner-Møller Eskil
Stage Malene
Kim Cecilia
Tavendale Roger
Baty Florent
Pipper Christian Bressen
Palmer Colin N A
Hakonarsson Hakon
Author Affiliation
Copenhagen Studies on Asthma in Childhood, The Danish Paediatrics Asthma Centre, Faculty of Health Sciences, University of Copenhagen, Gentofte Hospital, Ledreborg Alle 34, DK-2900 Gentofte, Copenhagen, Denmark. Bisgaard@copsac.dk
Source
Am J Respir Crit Care Med. 2009 Feb 1;179(3):179-85
Date
Feb-1-2009
Language
English
Publication Type
Article
Keywords
Airway Resistance - physiology
Asthma - epidemiology - genetics - physiopathology
Child
Child, Preschool
Chromosomes, Human, Pair 17 - genetics
Denmark - epidemiology
Female
Follow-Up Studies
Forced Expiratory Flow Rates
Genetic Predisposition to Disease
Genetic Variation
Humans
Hypersensitivity, Immediate - epidemiology - genetics - physiopathology
Incidence
Infant
Infant, Newborn
Lung Volume Measurements
Male
Oximetry
Phenotype
Prognosis
Prospective Studies
Recurrence
Risk factors
Time Factors
Abstract
RATIONALE: An asthma predisposition locus on chromosome 17q12-q21 has recently been replicated in different ethnic groups. OBJECTIVES: To characterize the asthma and atopy phenotypes in early childhood that associate with the 17q12-21 locus. METHODS: The single nucleotide polymorphism (SNP), rs7216389, was genotyped in 376 of 411 children from the Copenhagen Prospective Study on Asthma in Childhood (COPSAC) birth cohort born to mothers with asthma together with 305 mothers and 224 fathers. Nineteen additional SNPs in the region were genotyped in the children. Investigator-diagnosed clinical endpoints were based on diary cards and clinic visits every 6 months and at acute symptoms from birth. Lung function, bronchial responsiveness, and sensitization were tested longitudinally from early infancy. MEASUREMENTS AND MAIN RESULTS: rs7216389 was significantly associated with the development of wheeze (hazard ratio 1.64 [1.05-2.59], P value = 0.03), asthma (hazard ratio, 1.88 [1.15-3.07], P = 0.01), and acute severe exacerbations (hazard ratio 2.66 [1.58-4.48], P value = 0.0002). The effect on wheeze and asthma was observed for early onset but not late onset of disease. The increased risk of exacerbations persisted from 1 to 6 years of age (incidence ratio 2.48 [1.42-4.32], P value = 0.001), and increased bronchial responsiveness was present in infancy and at 4 years of age, but not at 6 years. In contrast, rs7216389 conferred no risk of eczema, rhinitis, or allergic sensitization. CONCLUSIONS: Variation at the chromosome 17q12-q21 locus was associated with approximately twofold increased risk of recurrent wheeze, asthma, asthma exacerbations, and bronchial hyperresponsiveness from early infancy to school age but without conferring risk of eczema, rhinitis, or allergic sensitization. These longitudinal clinical data show this locus to be an important genetic determinant of nonatopic asthma in children.
PubMed ID
19029000 View in PubMed
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Clinical and electrophysiological study in French-Canadian population with Charcot-Marie-tooth disease type 1A associated with 17p11.2 duplication.

https://arctichealth.org/en/permalink/ahliterature201127
Source
Can J Neurol Sci. 1999 Aug;26(3):196-200
Publication Type
Article
Date
Aug-1999
Author
N. Dupré
J P Bouchard
L. Cossette
D. Brunet
M. Vanasse
B. Lemieux
G. Mathon
J. Puymirat
Author Affiliation
Laboratoire de Recherche en Génétique Humaine, CHU Laval, Québec, Canada.
Source
Can J Neurol Sci. 1999 Aug;26(3):196-200
Date
Aug-1999
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age of Onset
Aged
Charcot-Marie-Tooth Disease - genetics - physiopathology
Child
Child, Preschool
Chromosomes, Human, Pair 17 - genetics
Disease Progression
Female
Genes, Duplicate - genetics
Humans
Infant
Male
Middle Aged
Quebec
Abstract
The aim of the present study was to examine the frequency and the phenotypic manifestations in a French-Canadian population with a chromosome 17p11.2 duplication (Charcot-Marie-Tooth type 1A, CMT-1A).
Molecular analysis were performed by Southern blot using pVAW409R3a probe. Clinical evaluation was carried out according to the scale defined by the European HMSN Consortium.
The frequency of duplication was found to be similar in the adult (70.8%) and pediatric (72.7%) populations. Onset of symptoms occurred before 20 years of age in 85.7% of adult cases and before the age of 5 in 80% of the pediatric cases. The classical CMT syndrome was observed in 77% of the cases and the syndrome was associated with additional features in 15% of cases in the adult population. All the children presented with classical CMT syndrome with no additional features. There was a significant correlation between the disability score and the duration of the disease but no correlation was found between median nerve conduction velocity and the functional handicap, the age at onset or the duration of the disease. In one family, there was a very conspicuous anticipation over five observed generations.
This study reveals that the age at onset, the clinical and electrophysiological variability as well as the functional disability variations in a French-Canadian population did not differ from those reported in other populations.
PubMed ID
10451742 View in PubMed
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Fine-mapping the 2q37 and 17q11.2-q22 loci for novel genes and sequence variants associated with a genetic predisposition to prostate cancer.

https://arctichealth.org/en/permalink/ahliterature262670
Source
Int J Cancer. 2015 May 15;136(10):2316-27
Publication Type
Article
Date
May-15-2015
Author
Virpi H Laitinen
Tommi Rantapero
Daniel Fischer
Elisa M Vuorinen
Teuvo L J Tammela
Tiina Wahlfors
Johanna Schleutker
Source
Int J Cancer. 2015 May 15;136(10):2316-27
Date
May-15-2015
Language
English
Publication Type
Article
Keywords
Chromosome Walking
Chromosomes, Human, Pair 17 - genetics
Chromosomes, Human, Pair 2 - genetics
DNA-Binding Proteins - genetics
Finland
Genetic Association Studies
Genetic Predisposition to Disease
Genetic Variation
Humans
Male
Polymorphism, Single Nucleotide
Prostatic Neoplasms - genetics
Quantitative Trait Loci
Sequence Analysis, DNA
Sequence Analysis, RNA
Abstract
The 2q37 and 17q12-q22 loci are linked to an increased prostate cancer (PrCa) risk. No candidate gene has been localized at 2q37 and the HOXB13 variant G84E only partially explains the linkage to 17q21-q22 observed in Finland. We screened these regions by targeted DNA sequencing to search for cancer-associated variants. Altogether, four novel susceptibility alleles were identified. Two ZNF652 (17q21.3) variants, rs116890317 and rs79670217, increased the risk of both sporadic and hereditary PrCa (rs116890317: OR = 3.3-7.8, p = 0.003-3.3 × 10(-5) ; rs79670217: OR = 1.6-1.9, p = 0.002-0.009). The HDAC4 (2q37.2) variant rs73000144 (OR = 14.6, p = 0.018) and the EFCAB13 (17q21.3) variant rs118004742 (OR = 1.8, p = 0.048) were overrepresented in patients with familial PrCa. To map the variants within 2q37 and 17q11.2-q22 that may regulate PrCa-associated genes, we combined DNA sequencing results with transcriptome data obtained by RNA sequencing. This expression quantitative trait locus (eQTL) analysis identified 272 single-nucleotide polymorphisms (SNPs) possibly regulating six genes that were differentially expressed between cases and controls. In a modified approach, prefiltered PrCa-associated SNPs were exploited and interestingly, a novel eQTL targeting ZNF652 was identified. The novel variants identified in this study could be utilized for PrCa risk assessment, and they further validate the suggested role of ZNF652 as a PrCa candidate gene. The regulatory regions discovered by eQTL mapping increase our understanding of the relationship between regulation of gene expression and susceptibility to PrCa and provide a valuable starting point for future functional research.
Notes
Cites: Nat Methods. 2010 Apr;7(4):248-920354512
Cites: Annu Rev Biochem. 2006;75:69-9216756485
Cites: Nat Methods. 2010 Aug;7(8):575-620676075
Cites: Nucleic Acids Res. 2011 Jan;39(Database issue):D980-520880996
Cites: Nucleic Acids Res. 2011 Jan;39(Database issue):D945-5020952405
Cites: Mol Cancer Res. 2006 Sep;4(9):655-6516966434
Cites: Prostate. 2007 Mar 1;67(4):410-517192958
Cites: Hum Genet. 2007 Mar;121(1):49-5517120048
Cites: Nat Genet. 2007 Aug;39(8):977-8317603485
Cites: Am J Hum Genet. 2007 Sep;81(3):559-7517701901
Cites: Nat Genet. 2007 Oct;39(10):1217-2417873874
Cites: Nat Genet. 2008 Mar;40(3):316-2118264097
Cites: PLoS Biol. 2008 Jul 22;6(7):e18418651794
Cites: Bioinformatics. 2009 May 1;25(9):1105-1119289445
Cites: J Biol Chem. 2010 Jan 8;285(2):1393-40319887448
Cites: Oncol Rep. 2010 Apr;23(4):1045-5220204290
Cites: Nucleic Acids Res. 2011 Jan;39(Database issue):D876-8220959295
Cites: Nucleic Acids Res. 2011 Jan;39(Database issue):D685-9021071392
Cites: Genome Biol. 2010;11(10):R10620979621
Cites: Oncogene. 2011 May 12;30(19):2207-1821242980
Cites: Nat Genet. 2011 Jun;43(6):570-321602798
Cites: Biometrics. 2005 Mar;61(1):55-6315737078
Cites: Am J Hum Genet. 2005 Aug;77(2):219-2915988677
Cites: PLoS One. 2010;5(5):e1069320502693
Cites: Int J Cancer. 2011 Nov 15;129(10):2400-721207418
Cites: J Cell Biochem. 2011 Oct;112(10):2742-721678463
Cites: Cancer Res. 2012 Jan 1;72(1):13-722180494
Cites: N Engl J Med. 2012 Jan 12;366(2):141-922236224
Cites: Ann Oncol. 2012 Mar;23(3):707-1321652578
Cites: Genome Biol. 2011;12(9):R9421955854
Cites: Nat Genet. 2012 Jun;44(6):685-922610119
Cites: Hum Mutat. 2012 Aug;33(8):1166-7422505138
Cites: Clin Cancer Res. 2012 Aug 15;18(16):4291-30222723371
Cites: Genome Res. 2012 Sep;22(9):1790-722955989
Cites: Nature. 2012 Sep 6;489(7414):57-7422955616
Cites: Nucleic Acids Res. 2013 Jan;41(Database issue):D48-5523203987
Cites: Oncogene. 2013 Jan 3;32(1):70-722349817
Cites: Cancer Lett. 2013 Apr 28;330(2):217-2423219899
Cites: Cancer Epidemiol Biomarkers Prev. 2013 Mar;22(3):452-6023292082
Cites: Nat Genet. 2013 Apr;45(4):385-91, 391e1-223535732
Cites: APMIS. 2013 Jul;121(7):626-3323216165
Cites: Eur Urol. 2013 Oct;64(4):567-7623759327
Cites: Nucleic Acids Res. 2000 Jan 1;28(1):27-3010592173
Cites: J Biol Chem. 2000 Mar 3;275(9):6195-20010692412
Cites: Clin Cancer Res. 2000 Dec;6(12):4810-511156239
Cites: Biochem Biophys Res Commun. 2002 Dec 13;299(4):581-612459178
Cites: J Biol Chem. 2002 Dec 13;277(50):48965-7512388557
Cites: Nat Cell Biol. 2004 Feb;6(2):97-10514743216
Cites: Eur Urol. 2004 Mar;45(3):382-9; author reply 38915036687
PubMed ID
25335771 View in PubMed
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[Genome-wide association study of bronchial asthma in the Volga-Ural region of Russia].

https://arctichealth.org/en/permalink/ahliterature127434
Source
Mol Biol (Mosk). 2011 Nov-Dec;45(6):992-1003
Publication Type
Article
Author
A S Karunas
B B Iunusbaev
Iu Iu Fedorova
G F Gimalova
N N Ramazanova
L L Gur'eva
L A Mukhtarova
Sh Z Zagidullin
E I Etkina
E K Khusnutdinova
Source
Mol Biol (Mosk). 2011 Nov-Dec;45(6):992-1003
Language
Russian
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Asthma - genetics
Case-Control Studies
Child
Child, Preschool
Chromosomes, Human, Pair 17 - genetics
Egg Proteins - genetics
Female
Gene Expression
Gene Frequency
Genetic Predisposition to Disease
Genome-Wide Association Study
Humans
Introns - genetics
Male
Membrane Proteins - genetics
Middle Aged
Neoplasm Proteins - genetics
Polymorphism, Single Nucleotide
Russia
Abstract
Bronchial asthma is a chronic inflammatory respiratory disease that is caused by the complex interaction of environmental influences and genetic susceptibility. The first genome-wide association study of bronchial asthma discovered a significant association between SNPs within 17q12-21 genomic region and childhood bronchial asthma in individuals of European descent. Association with this genomic region was then replicated in a number of independent samples of European and Asian descent. Here we report results of the first genome-wide association study of bronchial asthma in the Volga-Ural region of Russia. The present study includes 358 unrelated patients with physician-diagnosed bronchial asthma and 369 disease-free control subjects of different ethnic origin (Russians, Tatars and Bashkirs). Genotyping of DNA samples was carried out using the Illumina Human610 quad array as a part of GABRIEL project (contract from the EC No LSHB-CT-2006-018996). After QC filtering procedures, a final set of 550915 SNPs genotyped in 330 cases and 348 controls was tested for association with bronchial asthma. Five markers on chromosome 17q12-21 showed statistically significant association with bronchial asthma (p
PubMed ID
22295569 View in PubMed
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Genomewide scan of multiple sclerosis in Finnish multiplex families.

https://arctichealth.org/en/permalink/ahliterature207172
Source
Am J Hum Genet. 1997 Dec;61(6):1379-87
Publication Type
Article
Date
Dec-1997
Author
S. Kuokkanen
M. Gschwend
J D Rioux
M J Daly
J D Terwilliger
P J Tienari
J. Wikström
J. Palo
L D Stein
T J Hudson
E S Lander
L. Peltonen
Author Affiliation
Department of Human Molecular Genetics, National Public Health Institute, Helsinki, Finland.
Source
Am J Hum Genet. 1997 Dec;61(6):1379-87
Date
Dec-1997
Language
English
Publication Type
Article
Keywords
Autoimmune Diseases - epidemiology - genetics
Chromosome Mapping
Chromosomes, Human - genetics
Chromosomes, Human, Pair 17 - genetics
Disease Susceptibility
Ethnic Groups - genetics
Female
Finland - epidemiology
Gene Frequency
Genetic markers
Genome, Human
Haplotypes - genetics
Humans
Lod Score
Male
Multiple Sclerosis - epidemiology - ethnology - genetics
Pedigree
Abstract
Multiple sclerosis (MS) is a neurological, demyelinating disorder with a putative autoimmune etiology. It is thought to be a multifactorial disease with a complex mode of inheritance. Here we report the results of a two-stage genomewide scan for loci predisposing to MS. The first stage of the screen, with a low-resolution map, was performed in a selection of 16 pedigrees collected from an isolated Finnish population. Multipoint, non-parametric linkage analysis of the 328 markers did not reveal statistically significant results. However, 10 slightly interesting regions (P = .1-.15) emerged, including our previous findings of the HLA complex on 6p21 and a putative locus on 5p14-p12. Eight of these novel regions were further analyzed by use of denser marker maps, in the second stage of the scan. For the chromosomal regions 4cen, 11tel, and 17q, the statistical significance increased, but not conclusively; for 2q32 and 10q21, the statistical significance did not change. Accordingly, genotyping of the high-density markers in these regions was performed, and the data were analyzed by use of two-point, parametric linkage analysis using the complete pedigree information of the 21 Finnish multiplex families. We detected suggestive evidence for a predisposing locus on chromosomal region 17q22-q24. Several markers on 17q22-q24 yielded positive LOD scores, with the maximum LOD score (Zmax) occurring with D17S807 (Zmax = 2.8, theta = .04; dominant model). Interestingly, a suggestive linkage between MS and the markers on 17q22-q24 was also revealed by a recent genomewide scan in MS families from the United Kingdom.
Notes
Cites: Nat Genet. 1995 Nov;11(3):241-77581446
Cites: Nature. 1995 Sep 14;377(6545):150-17675080
Cites: Am J Hum Genet. 1996 Jun;58(6):1347-638651312
Cites: Lancet. 1996 Jun 22;347(9017):1728-308656905
Cites: Nat Genet. 1996 Aug;13(4):464-88696343
Cites: Nat Genet. 1996 Aug;13(4):472-68696345
Cites: Nat Genet. 1996 Aug;13(4):477-808696346
Cites: Acta Neurol Scand. 1975 Mar;51(3):173-831146497
Cites: Neurology. 1981 Sep;31(9):1138-427196536
Cites: Ann Neurol. 1983 Mar;13(3):227-316847134
Cites: Acta Neurol Scand. 1983 May;67(5):255-626880604
Cites: Proc Natl Acad Sci U S A. 1984 Jun;81(11):3443-66587361
Cites: N Engl J Med. 1986 Dec 25;315(26):1638-423785335
Cites: Am J Med Genet. 1988 Mar;29(3):533-413376997
Cites: J Neuroimmunol. 1989 Jan;21(1):59-662562801
Cites: Cell. 1989 Jun 30;57(7):1095-1002567636
Cites: J Neuroimmunol. 1991 May;32(2):141-71672869
Cites: Tissue Antigens. 1991 Jul;38(1):1-151926129
Cites: Ann Neurol. 1991 Sep;30(3):402-101683213
Cites: Lancet. 1992 Oct 24;340(8826):987-911383661
Cites: J Neurol Neurosurg Psychiatry. 1992 Oct;55(10):883-61431951
Cites: Lancet. 1993 May 8;341(8854):1179-817683738
Cites: Am J Hum Genet. 1993 Jul;53(1):252-638317490
Cites: J Med Genet. 1993 Oct;30(10):857-658230163
Cites: Hum Hered. 1994 Jan-Feb;44(1):44-518163291
Cites: J Neuroimmunol. 1994 Jun;52(1):97-97515903
Cites: Hum Hered. 1994 Jul-Aug;44(4):225-378056435
Cites: Eur J Hum Genet. 1993;1(4):257-688081940
Cites: Science. 1994 Sep 30;265(5181):2049-548091227
Cites: J Neurol Neurosurg Psychiatry. 1994 Oct;57(10):1191-47523603
Cites: J Neurol. 1994 Oct;241(10):615-97530769
Cites: Am J Hum Genet. 1995 Mar;56(3):777-877887434
Cites: Nat Genet. 1995 Jul;10(3):313-77545492
Cites: Nature. 1996 Mar 14;380(6570):152-48600387
PubMed ID
9399895 View in PubMed
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A genome-wide study of panic disorder suggests the amiloride-sensitive cation channel 1 as a candidate gene.

https://arctichealth.org/en/permalink/ahliterature132493
Source
Eur J Hum Genet. 2012 Jan;20(1):84-90
Publication Type
Article
Date
Jan-2012
Author
Noomi Gregersen
Hans A Dahl
Henriette N Buttenschøn
Mette Nyegaard
Anne Hedemand
Thomas D Als
August G Wang
Sofus Joensen
David Pd Woldbye
Pernille Koefoed
Ann S Kristensen
Torben A Kruse
Anders D Børglum
Ole Mors
Author Affiliation
Centre for Psychiatric Research, Aarhus University Hospital, Risskov, Aarhus, Denmark. noomigregersen@mac.com
Source
Eur J Hum Genet. 2012 Jan;20(1):84-90
Date
Jan-2012
Language
English
Publication Type
Article
Keywords
Acid Sensing Ion Channels
Alleles
Case-Control Studies
Chromosome Mapping
Chromosomes, Human, Pair 17 - genetics
Degenerin Sodium Channels
Denmark - epidemiology - ethnology
Epithelial Sodium Channels - genetics
Ethnic Groups - genetics
Genome-Wide Association Study
Genotype
Humans
Microsatellite Repeats
Nerve Tissue Proteins - genetics
Panic Disorder - diagnosis - epidemiology - genetics
Polymorphism, Single Nucleotide
Population Groups - genetics
Abstract
Panic disorder (PD) is a mental disorder with recurrent panic attacks that occur spontaneously and are not associated to any particular object or situation. There is no consensus on what causes PD. However, it is recognized that PD is influenced by environmental factors, as well as genetic factors. Despite a significant hereditary component, genetic studies have only been modestly successful in identifying genes of importance for the development of PD. In this study, we conducted a genome-wide scan using microsatellite markers and PD patients and control individuals from the isolated population of the Faroe Islands. Subsequently, we conducted a fine mapping, which revealed the amiloride-sensitive cation channel 1 (ACCN1) located on chromosome 17q11.2-q12 as a potential candidate gene for PD. The further analyses of the ACCN1 gene using single-nucleotide polymorphisms (SNPs) revealed significant association with PD in an extended Faroese case-control sample. However, analyses of a larger independent Danish case-control sample yielded no substantial significant association. This suggests that the possible risk alleles associated in the isolated population are not those involved in the development of PD in a larger outbred population.
Notes
Cites: Nat Genet. 1999 Dec;23(4):397-40410581024
Cites: Depress Anxiety. 2010 Aug;27(8):716-3020112245
Cites: Curr Psychiatry Rep. 2001 Apr;3(2):131-711276408
Cites: Trends Genet. 2001 Sep;17(9):502-1011525833
Cites: Am J Psychiatry. 2001 Oct;158(10):1568-7811578982
Cites: Am J Med Genet. 2002 Mar 8;114(2):245-5211857589
Cites: Eur J Hum Genet. 2002 Jun;10(6):381-712080390
Cites: Hum Mol Genet. 2002 Oct 1;11(20):2507-1512351587
Cites: J Neurosci. 2003 Jul 2;23(13):5496-50212843249
Cites: Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3621-614988500
Cites: Hum Genet. 2004 Jun;115(1):19-2815083358
Cites: Arch Gen Psychiatry. 1983 Oct;40(10):1085-96625857
Cites: Nat Genet. 1994 Dec;8(4):380-67894490
Cites: Ann Hum Genet. 1995 Jan;59(Pt 1):97-1057762987
Cites: Science. 1996 Oct 25;274(5287):536-98928008
Cites: Psychiatry Res. 1997 Jan 15;66(1):69-719061805
Cites: Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1170-29989995
Cites: Nat Genet. 2005 Jan;37(1):90-515608637
Cites: Bioinformatics. 2005 Jan 15;21(2):263-515297300
Cites: Mol Psychiatry. 2006 Jan;11(1):37-4616205737
Cites: Eur J Hum Genet. 2006 Apr;14(4):497-50416434998
Cites: Arch Gen Psychiatry. 2006 Apr;63(4):415-2416585471
Cites: Psychiatr Genet. 2006 Jun;16(3):99-10416691127
Cites: Am J Med Genet B Neuropsychiatr Genet. 2006 Jul 5;141B(5):524-3316741940
Cites: Biol Psychiatry. 2006 Aug 15;60(4):388-40116919526
Cites: Mol Psychiatry. 2006 Dec;11(12):1126-3816924267
Cites: Hum Mol Genet. 2007 Mar 15;16(6):704-1517376794
Cites: Mol Psychiatry. 2010 Nov;15(11):1101-1119786960
Cites: Lancet. 2010 Oct 23;376(9750):1401-820888040
Cites: Am J Hum Genet. 2010 Nov 12;87(5):618-3021055719
Cites: Mol Psychiatry. 2011 Jun;16(6):647-6320368705
Cites: Am J Hum Genet. 2007 Sep;81(3):559-7517701901
Cites: Psychiatr Genet. 2008 Apr;18(2):73-918349698
Cites: Genome Biol. 2008;9(8):10918771588
Cites: J Hum Genet. 2009 Feb;54(2):122-619165232
Cites: J Anxiety Disord. 2009 Jun;23(5):600-819233608
Cites: Epidemiol Psichiatr Soc. 2009 Jan-Mar;18(1):23-3319378696
Cites: Cell. 2009 Nov 25;139(5):1012-2119945383
Cites: Depress Anxiety. 2009;26(12):1165-7119842165
Cites: Am J Med Genet B Neuropsychiatr Genet. 2010 Mar 5;153B(2):582-9119693800
Cites: Psychiatr Genet. 2010 Apr;20(2):59-6420023595
Cites: Genetics. 2000 Jun;155(2):945-5910835412
PubMed ID
21811305 View in PubMed
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23 records – page 1 of 3.