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50bp deletion in the promoter for superoxide dismutase 1 (SOD1) reduces SOD1 expression in vitro and may correlate with increased age of onset of sporadic amyotrophic lateral sclerosis.

https://arctichealth.org/en/permalink/ahliterature156293
Source
Amyotroph Lateral Scler. 2008 Aug;9(4):229-37
Publication Type
Article
Date
Aug-2008
Author
Wendy J Broom
Matthew Greenway
Ghazaleh Sadri-Vakili
Carsten Russ
Kristen E Auwarter
Kelly E Glajch
Nicolas Dupre
Robert J Swingler
Shaun Purcell
Caroline Hayward
Peter C Sapp
Diane McKenna-Yasek
Paul N Valdmanis
Jean-Pierre Bouchard
Vincent Meininger
Betsy A Hosler
Jonathan D Glass
Meraida Polack
Guy A Rouleau
Jang-Ho J Cha
Orla Hardiman
Robert H Brown
Author Affiliation
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA. wendy.broom@gmail.com
Source
Amyotroph Lateral Scler. 2008 Aug;9(4):229-37
Date
Aug-2008
Language
English
Publication Type
Article
Keywords
Age of Onset
Amyotrophic Lateral Sclerosis - enzymology - epidemiology - genetics
Base Sequence
DNA Mutational Analysis
Female
Gene Expression
Genetic Predisposition to Disease
Genotype
Homozygote
Humans
Ireland - epidemiology
Male
Middle Aged
Phenotype
Polymorphism, Genetic
Promoter Regions, Genetic
Quebec - epidemiology
Risk factors
Scotland - epidemiology
Sequence Deletion
Sp1 Transcription Factor - metabolism
Superoxide Dismutase - genetics - metabolism
United States - epidemiology
Abstract
The objective was to test the hypothesis that a described association between homozygosity for a 50bp deletion in the SOD1 promoter 1684bp upstream of the SOD1 ATG and an increased age of onset in SALS can be replicated in additional SALS and control sample sets from other populations. Our second objective was to examine whether this deletion attenuates expression of the SOD1 gene. Genomic DNA from more than 1200 SALS cases from Ireland, Scotland, Quebec and the USA was genotyped for the 50bp SOD1 promoter deletion. Reporter gene expression analysis, electrophoretic mobility shift assays and chromatin immunoprecipitation studies were utilized to examine the functional effects of the deletion. The genetic association for homozygosity for the promoter deletion with an increased age of symptom onset was confirmed overall in this further study (p=0.032), although it was only statistically significant in the Irish subset, and remained highly significant in the combined set of all cohorts (p=0.001). Functional studies demonstrated that this polymorphism reduces the activity of the SOD1 promoter by approximately 50%. In addition we revealed that the transcription factor SP1 binds within the 50bp deletion region in vitro and in vivo. Our findings suggest the hypothesis that this deletion reduces expression of the SOD1 gene and that levels of the SOD1 protein may modify the phenotype of SALS within selected populations.
PubMed ID
18608091 View in PubMed
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Analysis of restriction fragment length polymorphism of cytochrome P450 3A43 gene and evaluation of the incidence of CYP3A43*1B allele in europeoid residents of West Siberia.

https://arctichealth.org/en/permalink/ahliterature81410
Source
Bull Exp Biol Med. 2005 Dec;140(6):726-8
Publication Type
Article
Date
Dec-2005
Author
Shchepotina E G
Nikishina M V
Vavilin V A
Lyakhovich V V
Author Affiliation
Institute of Molecular Biology and Biophysics, Siberian Division of Russian Academy of Medical Sciences, Novosibirsk.
Source
Bull Exp Biol Med. 2005 Dec;140(6):726-8
Date
Dec-2005
Language
English
Publication Type
Article
Keywords
Adolescent
Alleles
Aryl Hydrocarbon Hydroxylases - genetics
Child
Child, Preschool
DNA Mutational Analysis
European Continental Ancestry Group
Female
Gene Frequency
Genetics, Population
Heterozygote
Homozygote
Humans
Infant
Male
Polymorphism, Genetic
Polymorphism, Restriction Fragment Length
Siberia
Abstract
Analysis of restriction fragment length polymorphism is proposed for detecting CYP3A43 gene c1047 > T mutation. The incidence of this mutation (CYP3A43*1B allele) was evaluated in 102 europeoid residents of West Siberia and it was found to be 12.25%.
PubMed ID
16848237 View in PubMed
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Analysis of the macrophage scavenger receptor 1 gene in Swedish hereditary and sporadic prostate cancer.

https://arctichealth.org/en/permalink/ahliterature17838
Source
Prostate. 2004 May 1;59(2):132-40
Publication Type
Article
Date
May-1-2004
Author
Fredrik Lindmark
Björn-Anders Jonsson
Anders Bergh
Pär Stattin
S Lilly Zheng
Deborah A Meyers
Jianfeng Xu
Henrik Grönberg
Author Affiliation
Department of Radiation Sciences, Oncology, University of Umeå, Umeå, Sweden.
Source
Prostate. 2004 May 1;59(2):132-40
Date
May-1-2004
Language
English
Publication Type
Article
Keywords
Aged
Case-Control Studies
Cell Adhesion Molecules
Chromosomes, Human, Pair 8 - genetics
DNA - analysis
DNA Mutational Analysis
Genotype
Humans
Male
Middle Aged
Pedigree
Polymerase Chain Reaction
Polymorphism, Genetic
Prostatic Neoplasms - genetics
Receptors, Immunologic - genetics
Receptors, Scavenger
Research Support, Non-U.S. Gov't
Risk factors
Scavenger Receptors, Class A
Sweden
Abstract
BACKGROUND: The macrophage scavenger receptor 1 (MSR1) gene on chromosome 8p22 was recently reported as a candidate gene for hereditary prostate cancer (HPC). Here, we further elucidate the role of MSR1 in both Swedish families with HPC and in a cohort of unselected prostate cancer. METHODS: DNA samples from 83 Swedish HPC families and 215 unselected population based cases of prostate cancer as well as 425 age-matched controls were genotyped. RESULTS: A total of 18 variants were identified, including 2 exonic, 7 intronic changes, and 9 changes in the 5'- or 3'-uncoding region. Of the two exonic changes, one previously reported truncation mutation was identified, a R293X nonsense mutation. This mutation was found in 2 of the 83 (2.4%) HPC families. The R293X mutation was found more frequently in men with PC (4.9%) than in unaffected men (2.7%), consistent with previous published results, however our results were not significant (P = 0.16). To additionally test for potential association of common sequence variants and increased risk for the disease, five common polymorphisms (PRO3, INDEL1, IVS5-57, P275A, INDEL7) were genotyped in the group of 215 prostate cancer cases and 425 age-matched controls. No association between any of the five common sequence variants and prostate cancer were found. CONCLUSION: Our results suggest that mutations in MSR1 gene might play a role in prostate cancer susceptibility, particularly the R293X mutation. This study warrants further investigations of the role of MSR1 in prostate cancer etiology.
PubMed ID
15042613 View in PubMed
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APC I1307K increases risk of transition from polyp to colorectal carcinoma in Ashkenazi Jews.

https://arctichealth.org/en/permalink/ahliterature196058
Source
Gastroenterology. 2001 Feb;120(2):392-400
Publication Type
Article
Date
Feb-2001
Author
H S Stern
S. Viertelhausen
A G Hunter
K. O'Rourke
M. Cappelli
H. Perras
K. Serfas
A. Blumenthall
D. Dewar
E. Baumann
A E Lagarde
Author Affiliation
Loeb Health Research Institute, Ottawa Hospital Civic Campus, Ottawa, Ontario, Canada. hartley.stern@orcc.on.ca
Source
Gastroenterology. 2001 Feb;120(2):392-400
Date
Feb-2001
Language
English
Publication Type
Article
Keywords
Adenomatous Polyps - ethnology - genetics
Adult
Aged
Aged, 80 and over
Alleles
Colorectal Neoplasms - ethnology - genetics
Cross-Sectional Studies
DNA Mutational Analysis
Disease Progression
Female
Genes, APC - genetics
Genetic Predisposition to Disease
Heterozygote
Humans
Jews - genetics
Male
Middle Aged
Ontario - epidemiology
Polymorphism, Genetic
Prevalence
Risk factors
Abstract
The I1307K allele of the APC gene has been shown to confer a modestly elevated risk of colorectal cancer in the Ashkenazi Jewish population (relative risk, 1.5-1.7). However, it is unclear whether the alteration predisposes to adenomas and whether the genetic information can be used in clinical practice. To further address the pathogenic significance of I1307K, we offered both a genetic test and a screening program to individuals considered to be at increased risk for colorectal cancer. We compared the prevalence of polyps and their characteristics between carriers and noncarriers.
Invitations to participate in a DNA and colonoscopy screening program were mailed, together with a family questionnaire, to 3540 households forming the Jewish Community in Ottawa. The I1307K variant was analyzed in 242 eligible respondents who were selected because they had a personal or family history of colon cancer. Nearly 80% of these respondents (n = 189; age range, 32-83 years) consented to undergo a single colonoscopic examination.
The overall carrier frequency of I1307K in the study group was 10.3%. A higher proportion of heterozygous gene carriers was found in the subgroup of colon cancer survivors (27%) than among asymptomatic individuals (8%, P 0.5). No significant differences in polyp size, multiplicity, location, degree of villosity, or age-dependent prevalence were found between the 2 groups of participants.
The high frequency of I1307K colorectal cancer patients found in the Ashkenazi Jewish community of Ottawa and the equivalent proportion of carriers and noncarriers who developed adenomatous polyps suggest that in this community, I1307K is associated with a significant predisposition to carcinoma but not adenoma.
PubMed ID
11159880 View in PubMed
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Association between combined properdin and mannose-binding lectin deficiency and infection with Neisseria meningitidis.

https://arctichealth.org/en/permalink/ahliterature29317
Source
Mol Immunol. 2006 Feb;43(5):473-9
Publication Type
Article
Date
Feb-2006
Author
Lise Bathum
Heidi Hansen
Børge Teisner
Claus Koch
Peter Garred
Kirsten Rasmussen
Palle Wang
Author Affiliation
Department of Clinical Biochemistry, Odense University Hospital, Odense, Denmark. l.bathum@ouh.fyns-amt.dk
Source
Mol Immunol. 2006 Feb;43(5):473-9
Date
Feb-2006
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Alleles
Child
Child, Preschool
Chromatography, High Pressure Liquid
Complement Pathway, Alternative
DNA Mutational Analysis
Denmark
Enzyme-Linked Immunosorbent Assay
Epistasis, Genetic
Exons - genetics
Female
Genetic Predisposition to Disease
Humans
Male
Mannose-Binding Lectin - blood - deficiency - genetics
Meningitis, Meningococcal - genetics
Neisseria meningitidis
Pedigree
Polymorphism, Genetic
Promoter Regions (Genetics) - genetics
Properdin - deficiency - genetics
RNA Splice Sites - genetics
Research Support, Non-U.S. Gov't
Risk
Abstract
BACKGROUND: Individuals genetically deficient of properdin are more susceptible to meningococcal disease. Likewise low concentration or decreased biological activity of mannose-binding lectin (MBL) is associated with higher incidence of bacterial infections during childhood. In this study we report our findings in a Danish family with a remarkably high incidence of meningococcal meningitis-in total four cases, one of them fatal. METHODS: Properdin and MBL were quantified by ELISA and the properdin gene was screened for sequence variations using denaturing high-performance liquid chromatography (DHPLC) and subsequent sequencing of abnormal patterns. The MBL gene was genotyped for the three known variant alleles (B, C and D) as well as three promoter polymorphisms (-221Y/X, -550H/L and +4P/Q). RESULTS: Two out of six males with undetectable properdin activity had meningitis. They had also low MBL serum levels or carried an MBL variant allele, whereas high MBL concentrations were measured in three out of four properdin deficient males--without meningitis. A splice site mutation in exon 10 (c.1487-2A>G) was found in the properdin gene and co segregated with biochemically measured properdin deficiency. CONCLUSION: Our results indicate that a combined deficiency of both properdin and MBL increases the risk of infection with Neisseria meningitidis and stress the importance of epistatic genetic interactions in disease susceptibility.
PubMed ID
16337490 View in PubMed
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The association between headache and Val158Met polymorphism in the catechol-O-methyltransferase gene: the HUNT Study.

https://arctichealth.org/en/permalink/ahliterature82252
Source
J Headache Pain. 2006 Apr;7(2):70-4
Publication Type
Article
Date
Apr-2006
Author
Hagen Knut
Pettersen Elin
Stovner Lars Jacob
Skorpen Frank
Zwart John-Anker
Author Affiliation
Department of Clinical Neuroscience, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway. knut.hagen@ntnu.no
Source
J Headache Pain. 2006 Apr;7(2):70-4
Date
Apr-2006
Language
English
Publication Type
Article
Keywords
Adult
Catechol O-Methyltransferase - genetics
DNA Mutational Analysis - methods
Female
Gene Frequency
Genetic Predisposition to Disease
Genotype
Headache - classification - epidemiology - genetics
Humans
Male
Methionine - genetics
Middle Aged
Norway - epidemiology
Polymorphism, Genetic
Sex Factors
Valine - genetics
Abstract
The catechol-O-methyltransferase (COMT) gene contains a functional polymorphism, Val158Met, that has been found to influence human pain perception, and one study has found that migraine was less likely among those with the Val/Val polymorphism. In the 1995-97 Nord-Trøndelag Health (HUNT) Study, the association between the Val158Met polymorphism and headache was evaluated in a random sample of 2451 individuals. No association between Val158Met polymorphism and migraine was found. Among women, a lower prevalence of non-migrainous headache was found among individuals with the Val/Val genotype than among those with other genotypes (26.2% vs. 33.6%, p = 0.04). That non-migrainous headache was less likely among women with the Val/Val genotype may be an incidental finding, but should be investigated in further studies.
Notes
Comment In: J Headache Pain. 2006 Apr;7(2):6016688409
Comment In: J Headache Pain. 2006 Jun;7(3):165-616767536
PubMed ID
16688411 View in PubMed
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Association of a common allelic polymorphism (C677T) in the methylene tetrahydrofolate reductase gene with a reduced risk of osteoporotic fractures. A case control study in Danish postmenopausal women.

https://arctichealth.org/en/permalink/ahliterature188538
Source
Calcif Tissue Int. 2002 Nov;71(5):386-92
Publication Type
Article
Date
Nov-2002
Author
H L Jørgensen
J S Madsen
B. Madsen
M M A Saleh
B. Abrahamsen
M. Fenger
J B Lauritzen
Author Affiliation
Department of Clinical Biochemistry, Hvidovre University Hospital, Kettegaard Allé 30, 2650 Hvidovre, Denmark. HLJ@Dadlnet.dk
Source
Calcif Tissue Int. 2002 Nov;71(5):386-92
Date
Nov-2002
Language
English
Publication Type
Article
Keywords
Aged
Alleles
Bone Density
Calcaneus - ultrasonography
Case-Control Studies
DNA - analysis
DNA Mutational Analysis
Denmark
Female
Forearm Injuries - diagnosis - enzymology - genetics
Genetic Predisposition to Disease
Hip Fractures - diagnosis - enzymology - genetics
Humans
Methylenetetrahydrofolate Reductase (NADPH2)
Middle Aged
Mutation
Odds Ratio
Osteoporosis, Postmenopausal - diagnosis - enzymology - genetics
Oxidoreductases Acting on CH-NH Group Donors - genetics
Polymerase Chain Reaction
Polymorphism, Genetic
Risk factors
Abstract
Twin studies indicate a substantial genetic component in the development of osteoporosis. One of the latest studied candidate genes is the one coding for methylene tetrahydrofolate reductase (MTHFR) (C677T) in which a point mutation gives rise to a thermolabile variant of MTHFR. The aim of this study was to investigate the influence of this mutation on peripheral measures of bone density and on the odds ratios (OR) for hip and lower forearm fracture in a case control study of Danish postmenopausal women. A total of 74 women with lower forearm fracture, 41 women with hip fracture, and 207 age-matched controls were included. All had broadband ultrasound attenuation (BUA) and speed of sound (SOS) measured at the heel as well as bone mineral density (BMD) measured by dual X-ray absorptiometry at the distal forearm. The MTHFR (C677T) genotypes were determined using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). Only 2 of 21 individuals with the TT genotype had sustained a fracture as opposed to 46 of 142 with the CT genotype and 67 of 159 with the CC genotype (P = 0.007). Using logistic regression, the following odds ratios were found when comparing the individuals homozygotic for the C-allele with those homozygotic for the T-allele: lower forearm fracture OR = 3.93 (1.25; 12.40, P = 0.02), hip fracture OR = 6.99 (l.35; 36.92, P = 0.02) and the fractures combined OR = 4.33 (1.73; 10.81, P = 0.002). In this study, the MTHFR (C677T) genotypes were not significantly associated with BMD at the lower forearm or with ultrasound parameters measured at the calcaneus. However, a significant increase in the odds ratio of fracture was found for the wild-type C-allele.
PubMed ID
12232679 View in PubMed
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Association of common ATM polymorphism with bilateral breast cancer.

https://arctichealth.org/en/permalink/ahliterature17156
Source
Int J Cancer. 2005 Aug 10;116(1):69-72
Publication Type
Article
Date
Aug-10-2005
Author
Katri Heikkinen
Katrin Rapakko
Sanna-Maria Karppinen
Hannele Erkko
Pentti Nieminen
Robert Winqvist
Author Affiliation
Department of Clinical Genetics, Oulu University Hospital, University of Oulu, Oulu, Finland.
Source
Int J Cancer. 2005 Aug 10;116(1):69-72
Date
Aug-10-2005
Language
English
Publication Type
Article
Keywords
Breast Neoplasms - genetics
Cell Cycle Proteins - genetics
DNA Mutational Analysis
DNA-Binding Proteins - genetics
Family Health
Female
Gene Frequency
Genetic Predisposition to Disease
Humans
Mutation
Ovarian Neoplasms - genetics
Polymorphism, Genetic
Protein-Serine-Threonine Kinases - genetics
Research Support, Non-U.S. Gov't
Tumor Suppressor Proteins - genetics
Abstract
The ATM kinase has an essential role in maintaining genomic integrity. Loss of both ATM alleles results in ataxia-telangiectasia (A-T), a rare autosomal recessive neuroimmunologic disorder associated with cancer susceptibility. Individuals heterozygous for germline ATM mutations have been reported to have an increased risk for malignancy, in particular, female breast cancer. In the current study, a full mutation analysis of the ATM gene was carried out in patients from 121 breast or breast-ovarian cancer families. We discovered that the combination of 5557G-->A in cis position with IVS38-8 T-->C was associated with bilateral breast cancer (OR = 10.2; 95% CI = 3.1-33.8; p = 0.001). As the 5557G-->A change has been reported to affect an exonic splicing enhancer, we hypothesized that the observed composite allele could have some effect on the correct splicing of exon 39. However, no aberrant transcripts were detected, but ATM expression levels of lymphoblast cell lines from heterozygous carriers of this combination allele were lower than from noncarriers (p = 0.09). Lowered gene expression levels may have direct influence on the activities in DNA damage recognition and response pathways, as well as other genome integrity maintenance functions. Based on the results, we propose a cancer risk-modifying effect for the ATM 5557G-->A, IVS38-8T-->C composite allele.
PubMed ID
15756685 View in PubMed
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[Association study of polymorphic markers of F12, PON1, PON2, NOS2, PDE4D, HIF1a, GPIba, CYP11B2 genes with ischemic stroke in Russian patients].

https://arctichealth.org/en/permalink/ahliterature123677
Source
Zh Nevrol Psikhiatr Im S S Korsakova. 2012;112(2):51-4
Publication Type
Article
Date
2012
Author
M A Avdonina
T V Nasedkina
A Iu Ikonnikova
E V Bondarenko
P A Slominskii
N A Shamalov
I M Shetova
S A Limborskaia
A S Zasedatelev
V I Skvortsova
Source
Zh Nevrol Psikhiatr Im S S Korsakova. 2012;112(2):51-4
Date
2012
Language
Russian
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Aldosterone Synthase - genetics
Aryldialkylphosphatase - genetics
Cyclic Nucleotide Phosphodiesterases, Type 3 - genetics
DNA Mutational Analysis
Factor XII - genetics
Female
Genetic markers
Genome-Wide Association Study
Humans
Hypoxia-Inducible Factor 1, alpha Subunit - genetics
Male
Membrane Glycoproteins - genetics
Middle Aged
Nitric Oxide Synthase Type II - genetics
Polymorphism, Genetic
Russia - epidemiology
Stroke - epidemiology - genetics
Abstract
Allele and genotype frequencies of 10 single nucleotide polymorphisms in F12, PON1, PON2, NOS2, PDE4D, HIF1a,GPIba, CYP11B2 genes were studied in a group of Russian patients with ischemic stroke (IS) from central regions of the Russian Federation and healthy donors matched for sex, age and ethnicity. The genotyping procedure included the amplification of selected DNA sequences with the following hybridization of fluorescently-labeled regions with allele-specific DNA-probes immobilized on a biochip. An analysis of allele and genotype frequencies for each gene in IS patients and controls did not reveal any significant differences. The pair-wise comparison of genes demonstrated that the frequency of the combination PON1A/-x PON2 GG was higher in the group of patients (p=0.044, OR=3.4 95% CI 1.06 - 10.4) compared to the controls and, thus, was associated with the higher risk for stroke.
PubMed ID
22677666 View in PubMed
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ATM variants and cancer risk in breast cancer patients from Southern Finland.

https://arctichealth.org/en/permalink/ahliterature167890
Source
BMC Cancer. 2006;6:209
Publication Type
Article
Date
2006
Author
Johanna Tommiska
Laila Jansen
Outi Kilpivaara
Hege Edvardsen
Vessela Kristensen
Anitta Tamminen
Kristiina Aittomäki
Carl Blomqvist
Anne-Lise Børresen-Dale
Heli Nevanlinna
Author Affiliation
Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Helsinki, Finland. johanna.tommiska@helsinki.fi
Source
BMC Cancer. 2006;6:209
Date
2006
Language
English
Publication Type
Article
Keywords
Ataxia Telangiectasia Mutated Proteins
Breast Neoplasms - genetics
Cell Cycle Proteins - genetics
DNA Mutational Analysis
DNA-Binding Proteins - genetics
Female
Finland
Genetic Predisposition to Disease
Humans
Polymorphism, Genetic
Protein-Serine-Threonine Kinases - genetics
Tumor Suppressor Proteins - genetics
Abstract
Individuals heterozygous for germline ATM mutations have been reported to have an increased risk for breast cancer but the role for ATM genetic variants for breast cancer risk has remained unclear. Recently, a common ATM variant, ATMivs38 -8T>C in cis with the ATMex39 5557G>A (D1853N) variant, was suggested to associate with bilateral breast cancer among familial breast cancer patients from Northern Finland. We have here evaluated the 5557G>A and ivs38-8T>C variants in an extensive case-control association analysis. We also aimed to investigate whether there are other ATM mutations or variants contributing to breast cancer risk in our population.
Two common ATM variants, 5557G>A and ivs38-8T>C, previously suggested to associate with bilateral breast cancer, were genotyped in an extensive set of 786 familial and 884 unselected breast cancer cases as well as 708 healthy controls. We also screened the entire coding region and exon-intron boundaries of the ATM gene in 47 familial breast cancer patients and constructed haplotypes of the patients. The identified variants were also evaluated for increased breast cancer risk among additional breast cancer cases and controls.
Neither of the two common variants, 5557G>A and ivs38-8T>C, nor any haplotype containing them, was significantly associated with breast cancer risk, bilateral breast cancer or multiple primary cancers in any of the patient groups or subgoups. Three rare missense alterations and one intronic change were each found in only one patient of over 250 familial patients studied and not among controls. The fourth missense alteration studied further was found with closely similar frequencies in over 600 familial cases and controls.
Altogether, our results suggest very minor effect, if any, of ATM genetic variants on familial breast cancer in Southern Finland. Our results do not support association of the 5557G>A or ivs38-8T>C variant with increased breast cancer risk or with bilateral breast cancer.
Notes
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PubMed ID
16914028 View in PubMed
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58 records – page 1 of 6.