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Alterations of telomere length and DNA methylation in hairdressers: A cross-sectional study.

https://arctichealth.org/en/permalink/ahliterature274023
Source
Environ Mol Mutagen. 2016 Mar;57(2):159-67
Publication Type
Article
Date
Mar-2016
Author
Huiqi Li
Gabriella Åkerman
Carola Lidén
Ayman Alhamdow
Tomasz K Wojdacz
Karin Broberg
Maria Albin
Source
Environ Mol Mutagen. 2016 Mar;57(2):159-67
Date
Mar-2016
Language
English
Publication Type
Article
Keywords
Adult
Aging - genetics
Case-Control Studies
Cross-Sectional Studies
Cyclin-Dependent Kinase Inhibitor p16 - genetics
DNA Methylation
DNA Modification Methylases - genetics
DNA Repair Enzymes - genetics
Female
Glutathione S-Transferase pi - genetics
Humans
Middle Aged
Nuclear Proteins - genetics
Occupational Diseases - etiology
Occupational Exposure - adverse effects
Sweden
Telomere
Time Factors
Tumor Suppressor Proteins - genetics
Twist Transcription Factor - genetics
Young Adult
Abstract
Working as hairdressers has been associated with increased risk for cancer, particularly bladder cancer. To evaluate if current hairdressers have elevated risks of adverse health effects, we measured several biomarkers related to cancer-related DNA alterations. We enrolled 295 hairdressers and 92 non-hairdressers (all female non-smokers) from Stockholm and southern Sweden. Questionnaire data were collected for each participant, including work tasks for the hairdressers. We measured telomere length in peripheral blood leucocytes using quantitative PCR and DNA methylation status of genes relevant for bladder cancer using methylation sensitive high resolution melting analysis. The hairdressers had shorter telomeres (ß =?-0.069, P = 0.019) compared with non-hairdressers. Shorter telomeres were found in hairdressers up to 32 years old performing hair waving more than once per week as compared with hairdressers in the same age group performing hair waving less often (ß =?-0.12, P = 0.037). Hair waving was associated with less frequent CDKN2A methylation (odds ratio, OR = 0.19, P = 0.033). Shorter telomeres in hairdressers may indicate a genotoxic effect. Performing hair waving was associated with short telomere length, although the effect was only observed in young hairdressers. No clear patterns were discerned with regard to DNA methylation of bladder cancer-related genes. The observed changes of methylation were not all in the expected direction and warrant further investigation.
PubMed ID
26637967 View in PubMed
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Association between single-nucleotide polymorphisms in hormone metabolism and DNA repair genes and epithelial ovarian cancer: results from two Australian studies and an additional validation set.

https://arctichealth.org/en/permalink/ahliterature93836
Source
Cancer Epidemiol Biomarkers Prev. 2007 Dec;16(12):2557-65
Publication Type
Article
Date
Dec-2007
Author
Beesley Jonathan
Jordan Susan J
Spurdle Amanda B
Song Honglin
Ramus Susan J
Kjaer Suzanne Kruger
Hogdall Estrid
DiCioccio Richard A
McGuire Valerie
Whittemore Alice S
Gayther Simon A
Pharoah Paul D P
Webb Penelope M
Chenevix-Trench Georgia
Author Affiliation
Queensland Institute of Medical Research, Herston, Queensland, Australia.
Source
Cancer Epidemiol Biomarkers Prev. 2007 Dec;16(12):2557-65
Date
Dec-2007
Language
English
Publication Type
Article
Keywords
Australia
Case-Control Studies
DNA Repair - genetics
DNA Repair Enzymes - genetics
Female
Genetic Predisposition to Disease
Genotype
Gonadal Steroid Hormones - genetics - metabolism
Humans
Neoplasms, Glandular and Epithelial - genetics - metabolism
Ovarian Neoplasms - genetics - metabolism
Polymorphism, Single Nucleotide
Reproducibility of Results
Risk factors
Testosterone 5-alpha-Reductase - genetics
Abstract
Although some high-risk ovarian cancer genes have been identified, it is likely that common low penetrance alleles exist that confer some increase in ovarian cancer risk. We have genotyped nine putative functional single-nucleotide polymorphisms (SNP) in genes involved in steroid hormone synthesis (SRD5A2, CYP19A1, HSB17B1, and HSD17B4) and DNA repair (XRCC2, XRCC3, BRCA2, and RAD52) using two Australian ovarian cancer case-control studies, comprising a total of 1,466 cases and 1,821 controls of Caucasian origin. Genotype frequencies in cases and controls were compared using logistic regression. The only SNP we found to be associated with ovarian cancer risk in both of these two studies was SRD5A2 V89L (rs523349), which showed a significant trend of increasing risk per rare allele (P = 0.00002). We then genotyped another SNP in this gene (rs632148; r(2) = 0.945 with V89L) in an attempt to validate this finding in an independent set of 1,479 cases and 2,452 controls from United Kingdom, United States, and Denmark. There was no association between rs632148 and ovarian cancer risk in the validation samples, and overall, there was no significant heterogeneity between the results of the five studies. Further analyses of SNPs in this gene are therefore warranted to determine whether SRD5A2 plays a role in ovarian cancer predisposition.
PubMed ID
18086758 View in PubMed
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[Association of polymorphisms in glutathione-S-transferase and DNA repair genes with ovarian cancer risk in the Russian population].

https://arctichealth.org/en/permalink/ahliterature120602
Source
Genetika. 2012 Jul;48(7):901-4
Publication Type
Article
Date
Jul-2012
Author
D V Khokhrin
A V Khrunin
A A Moiseev
V A Gorbunov
S A Limborskaia
Source
Genetika. 2012 Jul;48(7):901-4
Date
Jul-2012
Language
Russian
Publication Type
Article
Keywords
DNA Repair Enzymes - genetics
Female
Gene Frequency
Genetic Association Studies
Genetic Predisposition to Disease
Genotype
Glutathione Transferase - genetics
Humans
Ovarian Neoplasms - genetics
Polymorphism, Single Nucleotide
Risk factors
Russia
Xeroderma Pigmentosum Group D Protein - genetics
Abstract
Polymorphism ofglutathione-S-transferase (GSTA1, GSTM1, GSTM3, GSTP1, and GSTT1) and DNA repair (ERCC1, ERCC2, and XRCC1) genes in samples of ovarian cancer patients and healthy women of the Russian ethnic group was studied. A trend in the allele frequency variation of ERCC2 gene single nucleotide polymorphism (rs13181, A > C) was revealed. The A allele frequency was higher in the sample of patients (60,6% versus 52,9%, P = 0.058).
PubMed ID
22988779 View in PubMed
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Atypical teratoid rhabdoid tumors (ATRTs): the British Columbia's Children's Hospital's experience, 1986-2006.

https://arctichealth.org/en/permalink/ahliterature128585
Source
Brain Pathol. 2012 Sep;22(5):625-35
Publication Type
Article
Date
Sep-2012
Author
Adam J Fleming
Juliette Hukin
Rod Rassekh
Christopher Fryer
James Kim
Anat Stemmer-Rachamimov
Diane K Birks
Annie Huang
Stephen Yip
Christopher Dunham
Author Affiliation
Division of Hematology, Oncology and Bone Marrow Transplantation, British Columbia Children's Hospital, Vancouver, British Columbia, Canada.
Source
Brain Pathol. 2012 Sep;22(5):625-35
Date
Sep-2012
Language
English
Publication Type
Article
Keywords
British Columbia - epidemiology
Central Nervous System Neoplasms - epidemiology - genetics - pathology
Child
Child, Preschool
Claudins - genetics
DNA Methylation
DNA Modification Methylases - genetics
DNA Repair Enzymes - genetics
Female
Genetic Testing
Hospitals, Pediatric - statistics & numerical data
Humans
Infant
Male
Mutation - genetics
Retrospective Studies
Rhabdoid Tumor - epidemiology - genetics - pathology
Teratoma - epidemiology - genetics - pathology
Tumor Suppressor Proteins - genetics
Abstract
As "atypical teratoid rhabdoid tumors" (ATRTs) may mimic "small round blue cell tumors" (SRBCT), we reexamined our ATRT experience focusing upon INI-1 immunohistochemistry (IHC). All high-grade pediatric brain tumors occurring from 1986-2006 at our institution underwent INI-1 IHC. Clinicopathologic data from each INI-1 immunonegative case were reviewed. Additional genetic, epigenetic and IHC analyses (including interrogation of INI-1 and CLDN6) were performed on a subset of the INI-1 immunonegative cases. Twelve INI-1 IHC negative tumors were identified retrospectively, of which only two previously carried the diagnosis of ATRT. Overall, the clinicopathologic and genetic data supported the assertion that all 12 cases represented ATRT. Unexpectedly, three long-term survivors (4.2, 7.0 and 8.5 years) were identified. As hypothesized, "teratoid" and "rhabdoid" histologic features were relatively infrequent despite gross total resections in some cases. Methylation specific polymer chain reaction (PCR) (MSP) revealed a uniform methylation pattern across all cases and gene promoters tested (ie, MGMT, HIC1, MLH3 and RASSF1); notably, all cases demonstrated unmethylated MGMT promoters. Our data demonstate that a primitive non-rhabdoid histophenotype is common among ATRTs and highlights the diagnostic importance of INI-1 IHC. Epigenetically, the MGMT promoter is usually unmethylated in ATRT, suggesting that potential temozolomide-based chemotherapy may be of limited efficacy.
PubMed ID
22188464 View in PubMed
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Circulating DNA in the blood of gastric cancer patients.

https://arctichealth.org/en/permalink/ahliterature91762
Source
Ann N Y Acad Sci. 2008 Aug;1137:226-31
Publication Type
Article
Date
Aug-2008
Author
Kolesnikova Elena V
Tamkovich Svetlana N
Bryzgunova Olga E
Shelestyuk Petr I
Permyakova Valentina I
Vlassov Valentin V
Tuzikov Aleksandr S
Laktionov Pavel P
Rykova Elena Y
Author Affiliation
Institute of Chemical Biology and Fundamental Medicine, Siberian Division of the Russian Academy of Sciences, Novosibirsk, 630090 Russia.
Source
Ann N Y Acad Sci. 2008 Aug;1137:226-31
Date
Aug-2008
Language
English
Publication Type
Article
Keywords
Adaptor Proteins, Signal Transducing - genetics
Carrier Proteins - genetics
DNA - blood - diagnostic use - genetics
DNA Methylation
DNA Modification Methylases - genetics
DNA Repair Enzymes - genetics
Female
Humans
Male
Middle Aged
Nuclear Proteins - genetics
Promoter Regions, Genetic
Stomach Neoplasms - blood - diagnosis - genetics
Tumor Suppressor Proteins - genetics
Abstract
The concentration of cell-free DNA and promoter methylation status of the MGMT, p15, and hMLH1 genes were analyzed by a fluorescence-based assay and methylation-specific PCR (MSP) in the blood of gastric cancer patients (n= 20) and healthy subjects (n= 22). Gastric cancer patients were characterized by an increased concentration of circulating DNA in the plasma; the amount of cell-surface-bound DNA was not decreased compared with controls and amounted to 80 +/- 15% of the total circulating DNA. MSP analysis of three genes in the cell-surface-bound DNA permits the detection of gastric cancer patients with a sensitivity of 75% and a specificity of 54%. Thus, the cell-surface-bound DNA is a convenient source of DNA for MSP analysis of cancer-specific markers. The data on the presence of methylated DNA in plasma combined with the analysis of other cancer-related changes in DNA can significantly contribute to cancer diagnostics.
PubMed ID
18837952 View in PubMed
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Deletion of the MGMT gene in familial melanoma.

https://arctichealth.org/en/permalink/ahliterature258546
Source
Genes Chromosomes Cancer. 2014 Aug;53(8):703-11
Publication Type
Article
Date
Aug-2014
Author
Frida Appelqvist
Maria Yhr
Anna Erlandson
Tommy Martinsson
Charlotta Enerbäck
Source
Genes Chromosomes Cancer. 2014 Aug;53(8):703-11
Date
Aug-2014
Language
English
Publication Type
Article
Keywords
DNA Modification Methylases - genetics
DNA Repair Enzymes - genetics
Exons
Gene Deletion
Genetic Predisposition to Disease
Humans
Melanoma - genetics
Polymorphism, Genetic
Promoter Regions, Genetic
Skin Neoplasms - genetics
Sweden
Tumor Suppressor Proteins - genetics
Abstract
The DNA repair gene MGMT (O-6-methylguanine-DNA methyltransferase) is important for maintaining normal cell physiology and genomic stability. Alterations in MGMT play a critical role in the development of several types of cancer, including glioblastoma, lung cancer, and colorectal cancer. The purpose of this study was to explore the function of genetic alterations in MGMT and their connection with familial melanoma (FM). Using multiplex ligation-dependent probe amplification, we identified a deletion that included the MGMT gene in one of 64 families with a melanoma predisposition living in western Sweden. The mutation segregated with the disease as a heterozygous deletion in blood-derived DNA, but a homozygous deletion including the promoter region and exon 1 was seen in tumor tissue based on Affymetrix 500K and 6.0 arrays. By sequence analysis of the MGMT gene in the other 63 families with FM from western Sweden, we identified four common polymorphisms, nonfunctional, as predominantly described in previous studies. We conclude that inherited alterations in the MGMT gene might be a rare cause of FM, and we suggest that MGMT contributes to melanoma predisposition.
PubMed ID
24801985 View in PubMed
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ERCC6 founder mutation identified in Finnish patients with COFS syndrome.

https://arctichealth.org/en/permalink/ahliterature143679
Source
Clin Genet. 2010 Dec;78(6):541-7
Publication Type
Article
Date
Dec-2010
Author
E. Jaakkola
A. Mustonen
P. Olsen
S. Miettinen
T. Savuoja
A. Raams
N G J Jaspers
H. Shao
B L Wu
J. Ignatius
Author Affiliation
Department of Clinical Genetics, Oulu University Hospital, University of Oulu, Oulu, Finland. elisa.jaakkola@ppshp.fi
Source
Clin Genet. 2010 Dec;78(6):541-7
Date
Dec-2010
Language
English
Publication Type
Article
Keywords
Abnormalities, Multiple - genetics
Base Sequence
Cataract - genetics
Child, Preschool
Cockayne Syndrome - genetics
Consanguinity
DNA Helicases - genetics
DNA Mutational Analysis
DNA Repair Enzymes - genetics
Finland
Humans
Male
Microcephaly - genetics
Molecular Sequence Data
Mutation
Phenotype
Syndrome
Abstract
Cerebro-oculo-facio-skeletal (COFS) syndrome is an autosomal recessive disorder characterized by microcephaly, congenital cataracts, facial dysmorphism, neurogenic arthrogryposis, growth failure and severe psychomotor retardation. We report a large consanguineous pedigree from northern Finland with six individuals belonging into four different sibships and affected with typical COFS syndrome phenotype. Two deceased patients have been published previously in 1982 as the first cases exhibiting cerebral calcifications typical for this disorder. Two living and one of the deceased patients were all shown to possess a novel homozygous mutation in the ERCC6 [Cockayne syndrome B (CSB)] gene, thereby confirming the diagnosis on molecular genetic level even for the earlier published cases. Genealogical investigation showed a common ancestor living in a northeastern village in Finland in the 18th century for all six patients implying a founder effect.
PubMed ID
20456449 View in PubMed
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A genome-wide association study identifies CDHR3 as a susceptibility locus for early childhood asthma with severe exacerbations.

https://arctichealth.org/en/permalink/ahliterature106115
Source
Nat Genet. 2014 Jan;46(1):51-5
Publication Type
Article
Date
Jan-2014
Author
Klaus Bønnelykke
Patrick Sleiman
Kasper Nielsen
Eskil Kreiner-Møller
Josep M Mercader
Danielle Belgrave
Herman T den Dekker
Anders Husby
Astrid Sevelsted
Grissel Faura-Tellez
Li Juel Mortensen
Lavinia Paternoster
Richard Flaaten
Anne Mølgaard
David E Smart
Philip F Thomsen
Morten A Rasmussen
Silvia Bonàs-Guarch
Claus Holst
Ellen A Nohr
Rachita Yadav
Michael E March
Thomas Blicher
Peter M Lackie
Vincent W V Jaddoe
Angela Simpson
John W Holloway
Liesbeth Duijts
Adnan Custovic
Donna E Davies
David Torrents
Ramneek Gupta
Mads V Hollegaard
David M Hougaard
Hakon Hakonarson
Hans Bisgaard
Author Affiliation
1] Copenhagen Prospective Studies on Asthma in Childhood, Health Sciences, University of Copenhagen & Danish Pediatric Asthma Center, Copenhagen University Hospital, Gentofte, Denmark. [2] [3].
Source
Nat Genet. 2014 Jan;46(1):51-5
Date
Jan-2014
Language
English
Publication Type
Article
Keywords
Asthma - etiology - genetics
Cadherins - chemistry - genetics - metabolism
Case-Control Studies
Child
Child, Preschool
Chromosomes, Human, Pair 17
DNA Repair Enzymes - genetics
DNA-Binding Proteins - genetics
Denmark
Female
Genetic Predisposition to Disease
Genome-Wide Association Study
Humans
Interleukins - genetics
Male
Membrane Proteins - chemistry - genetics - metabolism
Models, Molecular
Neoplasm Proteins - genetics
Polymorphism, Single Nucleotide
Protein Conformation
Receptors, Cell Surface - genetics
Abstract
Asthma exacerbations are among the most frequent causes of hospitalization during childhood, but the underlying mechanisms are poorly understood. We performed a genome-wide association study of a specific asthma phenotype characterized by recurrent, severe exacerbations occurring between 2 and 6 years of age in a total of 1,173 cases and 2,522 controls. Cases were identified from national health registries of hospitalization, and DNA was obtained from the Danish Neonatal Screening Biobank. We identified five loci with genome-wide significant association. Four of these, GSDMB, IL33, RAD50 and IL1RL1, were previously reported as asthma susceptibility loci, but the effect sizes for these loci in our cohort were considerably larger than in the previous genome-wide association studies of asthma. We also obtained strong evidence for a new susceptibility gene, CDHR3 (encoding cadherin-related family member 3), which is highly expressed in airway epithelium. These results demonstrate the strength of applying specific phenotyping in the search for asthma susceptibility genes.
PubMed ID
24241537 View in PubMed
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Germline mutations in the MYH gene in Swedish familial and sporadic colorectal cancer.

https://arctichealth.org/en/permalink/ahliterature76135
Source
Genet Test. 2005;9(2):147-51
Publication Type
Article
Date
2005
Author
X-L Zhou
T. Djureinovic
B. Werelius
G. Lindmark
X-F Sun
A. Lindblom
Author Affiliation
Department of Molecular Medicine, Karolinska Institutet, S-171 76 Stockholm, Sweden.
Source
Genet Test. 2005;9(2):147-51
Date
2005
Language
English
Publication Type
Article
Keywords
Amino Acid Substitution
Colorectal Neoplasms - genetics
DNA Repair - genetics
DNA Repair Enzymes - genetics
Humans
Mutation, Missense
Polymorphism, Single Nucleotide
Sweden
Abstract
Biallelic germline mutations in the base excision repair gene MYH have been shown to predispose to a proportion of multiple colorectal adenomas and cancer. To evaluate the contribution of MYH mutations to non- FAP, non-HNPCC familial colorectal cancer, 84 unrelated Swedish individuals affected with colorectal cancer from such families were screened for germline mutations in the coding sequence of the gene. None of the cases was found to carry any pathogenic sequence change. We then determined the prevalence of the two most common pathogenic MYH mutations found in Caucasians, Y165C and G382D, in 450 Swedish sporadic colorectal cancer cases and 480 Swedish healthy controls. The frequency of both variants in Swedish cases and controls was similar to those previously reported. In addition, we found that previously unknown sequence variations at the position of amino acid 423 (R423Q, R423P, and R423R) appear to occur more frequently in cases than in controls (p = 0.02), a finding that warrants future studies.
PubMed ID
15943555 View in PubMed
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Identification of Lynch syndrome among patients with colorectal cancer.

https://arctichealth.org/en/permalink/ahliterature119784
Source
JAMA. 2012 Oct 17;308(15):1555-65
Publication Type
Article
Date
Oct-17-2012
Author
Leticia Moreira
Francesc Balaguer
Noralane Lindor
Albert de la Chapelle
Heather Hampel
Lauri A Aaltonen
John L Hopper
Loic Le Marchand
Steven Gallinger
Polly A Newcomb
Robert Haile
Stephen N Thibodeau
Shanaka Gunawardena
Mark A Jenkins
Daniel D Buchanan
John D Potter
John A Baron
Dennis J Ahnen
Victor Moreno
Montserrat Andreu
Maurizio Ponz de Leon
Anil K Rustgi
Antoni Castells
Author Affiliation
Department of Gastroenterology, Hospital Clínic, Centro de Investigación Biomédica en Red en Enfermedades Hepáticas y Digestivas, Institut d’Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Barcelona, Spain.
Source
JAMA. 2012 Oct 17;308(15):1555-65
Date
Oct-17-2012
Language
English
Publication Type
Article
Keywords
Adult
Aged
Cohort Studies
Colorectal Neoplasms, Hereditary Nonpolyposis - diagnosis - genetics
DNA Mismatch Repair - genetics
DNA Repair Enzymes - genetics
Family
Female
Finland
Genetic Testing - standards
Humans
Male
Middle Aged
Multivariate Analysis
Ohio
Registries - statistics & numerical data
Sensitivity and specificity
Abstract
Lynch syndrome is the most common form of hereditary colorectal cancer (CRC) and is caused by germline mutations in DNA mismatch repair (MMR) genes. Identification of gene carriers currently relies on germline analysis in patients with MMR-deficient tumors, but criteria to select individuals in whom tumor MMR testing should be performed are unclear.
To establish a highly sensitive and efficient strategy for the identification of MMR gene mutation carriers among CRC probands.
Pooled-data analysis of 4 large cohorts of newly diagnosed CRC probands recruited between 1994 and 2010 (n = 10,206) from the Colon Cancer Family Registry, the EPICOLON project, the Ohio State University, and the University of Helsinki examining personal, tumor-related, and family characteristics, as well as microsatellite instability, tumor MMR immunostaining, and germline MMR mutational status data.
Performance characteristics of selected strategies (Bethesda guidelines, Jerusalem recommendations, and those derived from a bivariate/multivariate analysis of variables associated with Lynch syndrome) were compared with tumor MMR testing of all CRC patients (universal screening).
Of 10,206 informative, unrelated CRC probands, 312 (3.1%) were MMR gene mutation carriers. In the population-based cohorts (n = 3671 probands), the universal screening approach (sensitivity, 100%; 95% CI, 99.3%-100%; specificity, 93.0%; 95% CI, 92.0%-93.7%; diagnostic yield, 2.2%; 95% CI, 1.7%-2.7%) was superior to the use of Bethesda guidelines (sensitivity, 87.8%; 95% CI, 78.9%-93.2%; specificity, 97.5%; 95% CI, 96.9%-98.0%; diagnostic yield, 2.0%; 95% CI, 1.5%-2.4%; P
Notes
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PubMed ID
23073952 View in PubMed
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12 records – page 1 of 2.