| 1. |
|
|
| 2. |
- Ahlbom, Anders, et al.
(författare)
-
Forskning om elöverkänslighet och andra effekter av elektromagnetiska fält; Åttonde årsrapporten
- 2011
-
Rapport (övrigt vetenskapligt/konstnärligt)abstract
- Årets rapport diskuterar några forskningsområden där resultaten är av stor betydelse och som kan förväntas tilldra sig stor uppmärksamhet. Det första avser möjligheterna att skatta exponering och den relativa betydelsen av olika exponeringskällor. Viktigt arbete har där gjorts inom det Schweiziska nationella forskningsprogrammet. Vi har inkluderat en figur som på ett enkelt sätt sammanfattar viktiga och relevanta resultat avseende exponering i den allmänna miljön. Det framgår att basstationer, egen mobiltelefonanvändning och trådlösa hemtelefoner är de viktigaste källorna till exponering (om man bortser från lokal exponering till huvudet under samtal). Nästa område avser sömn och EEG-undersökningar. Det har där visat sig i ett antal undersökningar att elektromagnetiska fält tycks ha effekt på EEG under sömn. Effekterna är måttliga och kan storleksmässigt jämföras med vad som kan erhållas till exempel vid kaffe- eller alkoholintag. De tycks inte vara kopplade till subjektiv sömnkvalitet. Hur dessa effekter uppstår och vad de kan tänkas ha för betydelse är okänt. Men det är klart att det är angeläget att forskningen inom detta område fortsätter så att vi kan få denna effekt bekräftad om den är reell och ytterligare belyst och förstådd. Vi har också beskrivit en del ytterligare epidemiologisk forskning och framför allt slutrapporten från den så kallade Interphone-studien. Det har funnits förhoppningar om att denna studie skulle kunna ge definitivt besked i frågan om mobiltelefonanvändning och hjärntumörrisk. Men det stod redan efter publiceringen av de nationella rapporterna klart att så knappast skulle bli fallet. Rapporten har gett upphov till omfattande metodologiska diskussioner, vilka också varit orsaken till rapportens stora försening. Vår bedömning är att denna rapport inte ändrar våra tidigare bedömningar av risken för hjärntumör vid mobiltelefonanvändning, baserade bland annat på vad som framkommit i de nationella rapporterna. Däremot har denna rapport och andra rapporter från Interphone bidragit med viktiga metodologiska insikter. Vi diskuterar några ytterligare epidemiologiska undersökningar men inte heller de ändrar någonting i våra bedömningar. Slutligen presenterar vi nya riktlinjer för exponering från ”kraftfrekventa elektromagnetiska fält” från ICNIRP. De är baserade på en uppdaterad kunskapsgenomgång och på omfattande principdiskussioner. Bland annat har man nu bedömt att också fotofosfener (ljusblixtar) ska ingå bland kritiska effekter vilket i viss mån har påverkat gränsvärdena numeriskt. Detta har dock ingen praktisk betydelse för allmänhetens exponering därför att nivåerna ändå ligger flera storleksordningar över vad allmänheten normalt exponeras för. Det finns dock arbetsmiljöer där detta kan ha betydelse. En viktiga händelse under 2011 som redan nu kan förutses är att IARC (WHOs cancerforskningsinstitut) i maj ska ha ett så kallat monografimöte och ta ställning till hur sannolikt det är att radiofrekventa elektromagnetiska fält är cancerframkallande.
|
|
| 3. |
- Ahlbom, Anders, et al.
(författare)
-
Radiofrequency electromagnetic fields and risk of disease and ill health - Research during the last ten years
- 2012
-
Rapport (övrigt vetenskapligt/konstnärligt)abstract
- The focus of this report is electromagnetic fields of the type that occur in connection with mobile telephony, so called radio frequency (RF) fields and the possibility that exposure to such fields poses a risk of disease or ill health. The purpose is to describe what was known ten years ago, what we have learned during the past decade, and where we stand today. TEN YEARS AGOThe mechanism of interaction between RF fields and the human body was established long ago and is increased temperature of exposed tissue (compare microwave ovens). Methods for measurements of the fields in the air were developed early but the data on distribution of the absorbed energy in the human body was still restricted. Data regarding sources and levels of exposure to the population was limited because systematic measurements had not been conducted. A considerable number of provocation studies on exposure to fields of lower frequencies (related to electric power and computer screens) had already been conducted and had not found any evidence of an association to symptoms (headache, vertigo, dizziness, concentration difficulties, insomnia) but the corresponding information about RF fields and occurrence of symptoms was scarce. Few and methodologically limited epidemiological studies had been conducted on RF field exposure and cancer.WHAT WAS LEARNED DURING THE PAST TEN YEARSExtensive research on various aspects of RF fields has been conducted during the last ten years and the knowledge database has increased considerably. Simulation models have improved our knowledge about how the fields and the energy are distributed in the body. Mobile, so called, exposimeters have been developed for use in epidemiological studies. Many more measurements have been conducted to increase our knowledge about sources and level of exposure to the population. More than 15 provocation studies (single or double blind) have been conducted on symptoms attributed to exposure to RF fields. These studies have not been able to demonstrate that people experience symptoms or sensations more often when the fields are turned on than when they are turned off. One longitudinal study has looked at frequency of symptoms in relation to environmental exposure and this study found no association between exposure and symptoms. A considerable number of studies on cancer, and in particular brain tumor, were presented. As a consequence there exist now very useful data including methodological results that can be used in the interpretation of this research. With a small number of exceptions the available results are all negative and taken together with new methodological understandings the overall interpretation is that these do not provide support for an association between mobile telephony and brain tumor risk. In addition, national cancer statistics are very useful sources of information because mobile phone usage has increased so quickly. Had mobile phone use and brain cancer risk been associated it would have been visible as an increasing trend in national cancer statistics. But brain cancer rates are not increasing. WHERE WE STAND TODAYWe now know much more about measurements and absorption of RF fields and also about sources of exposure to the population and levels of exposure. A considerable number of provocation studies on RF exposure and symptoms have been unable to show any association. Overall, the data on brain tumor and mobile telephony do not support an effect of mobile phone use on tumor risk, in particular when taken together with national cancer trend statistics throughout the world. Research on mobile telephony and health started without a biologically or epidemiologically based hypothesis about possible health risks. Instead the inducement was an unspecific concern related to a new and rapidly spreading technology. Extensive research for more than a decade has not detected anything new regarding interaction mechanisms between radiofrequency fields and the human body and has found no evidence for health risks below current exposure guidelines. While absolute certainty can never be achieved, nothing has appeared to suggest that the since long established interaction mechanism of heating would not suffice as basis for health protection.
|
|
| 4. |
- Andersson, Ulrika, et al.
(författare)
-
A comprehensive study of the association between the EGFR and ERBB2 genes and glioma risk
- 2010
-
Ingår i: Acta Oncologica. - : Informa Healthcare. - 0284-186X .- 1651-226X. ; 12, s. 17-17
-
Tidskriftsartikel (refereegranskat)abstract
- Glioma is the most common type of adult brain tumor and glioblastoma, its most aggressive form, has a dismal prognosis. Receptor tyrosine kinases such as the epidermal growth factor receptor (EGFR, ERBB2, ERBB3, ERBB4) family, and the vascular endothelial growth factor receptor (VEGFR), play a central role in tumor progression. We investigated the genetic variants of EGFR, ERBB2, VEGFR and their ligands, EGF and VEGF on glioma and glioblastoma risk. In addition, we evaluated the association of genetic variants of a newly discovered family of genes known to interact with EGFR: LRIG2 and LRIG3 with glioma and glioblastoma risk. Methods. We analyzed 191 tag single nucleotide polymorphisms (SNPs) capturing all common genetic variation of EGF, EGFR, ERBB2, LRIG2, LRIG3, VEGF and VEGFR2 genes. Material from four case-control studies with 725 glioma patients (329 of who were glioblastoma patients) and their 1 610 controls was used. Haplotype analyses were conducted using SAS/Genetics software. Results. Fourteen of the SNPs were significantly associated with glioma risk at p< 0.05, and 17 of the SNPs were significantly associated with glioblastoma risk at p< 0.05. In addition, we found that one EGFR haplotype was related to increased glioblastoma risk at p=0.009, Odds Ratio [OR] = 1.67 (95% confidence interval (CI): 1.14, 2.45). The Bonferroni correction made all p-values non-significant. One SNP, rs4947986 next to the intron/exon boundary of exon 7 in EGFR, was validated in an independent data set of 713 glioblastoma and 2 236 controls, [OR] = 1.42 (95% CI: 1.06,1.91). Discussion. Previous studies show that regulation of the EGFR pathway plays a role in glioma progression but the present study is the first to find that certain genotypes of the EGFR gene may be related to glioblastoma risk. Further studies are required to reinvestigate these findings and evaluate the functional significance.
|
|
| 5. |
- Dobbins, Sara E., et al.
(författare)
-
Common variation at 10p12.31 near MLLT10 influences meningioma risk
- 2011
-
Ingår i: Nature Genetics. - London : Nature America, Inc.. - 1061-4036 .- 1546-1718. ; 43:9, s. 825-827
-
Tidskriftsartikel (refereegranskat)abstract
- To identify susceptibility loci for meningioma, we conducted a genome-wide association study of 859 affected individuals (cases) and 704 controls with validation in two independent sample sets totaling 774 cases and 1,764 controls. We identified a new susceptibility locus for meningioma at 10p12.31 (MLLT10, rs11012732, odds ratio = 1.46, P(combined) = 1.88 x 10(-14)). This finding advances our understanding of the genetic basis of meningioma development.
|
|
| 6. |
- Jacobs, Kevin B, et al.
(författare)
-
Detectable clonal mosaicism and its relationship to aging and cancer.
- 2012
-
Ingår i: Nature Genetics. - New York : Nature Publishing Group. - 1061-4036 .- 1546-1718. ; 44:6, s. 651-658
-
Tidskriftsartikel (refereegranskat)abstract
- In an analysis of 31,717 cancer cases and 26,136 cancer-free controls from 13 genome-wide association studies, we observed large chromosomal abnormalities in a subset of clones in DNA obtained from blood or buccal samples. We observed mosaic abnormalities, either aneuploidy or copy-neutral loss of heterozygosity, of >2 Mb in size in autosomes of 517 individuals (0.89%), with abnormal cell proportions of between 7% and 95%. In cancer-free individuals, frequency increased with age, from 0.23% under 50 years to 1.91% between 75 and 79 years (P = 4.8 × 10(-8)). Mosaic abnormalities were more frequent in individuals with solid tumors (0.97% versus 0.74% in cancer-free individuals; odds ratio (OR) = 1.25; P = 0.016), with stronger association with cases who had DNA collected before diagnosis or treatment (OR = 1.45; P = 0.0005). Detectable mosaicism was also more common in individuals for whom DNA was collected at least 1 year before diagnosis with leukemia compared to cancer-free individuals (OR = 35.4; P = 3.8 × 10(-11)). These findings underscore the time-dependent nature of somatic events in the etiology of cancer and potentially other late-onset diseases.
|
|
| 7. |
- Melin, Beatrice, et al.
(författare)
-
Known glioma risk loci are associated with glioma with a family history of brain tumours : a case-control gene association study
- 2013
-
Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 132:10, s. 2464-2468
-
Tidskriftsartikel (refereegranskat)abstract
- Familial cancer can be used to leverage genetic association studies. Recent genome-wide association studies have reported independent associations between seven single nucleotide polymorphisms (SNPs) and risk of glioma. The aim of this study was to investigate whether glioma cases with a positive family history of brain tumours, defined as having at least one first- or second-degree relative with a history of brain tumour, are associated with known glioma risk loci. One thousand four hundred and thirty-one glioma cases and 2,868 cancer-free controls were identified from four casecontrol studies and two prospective cohorts from USA, Sweden and Denmark and genotyped for seven SNPs previously reported to be associated with glioma risk in casecontrol designed studies. Odds ratios were calculated by unconditional logistic regression. In analyses including glioma cases with a family history of brain tumours (n = 104) and control subjects free of glioma at baseline, three of seven SNPs were associated with glioma risk: rs2736100 (5p15.33, TERT), rs4977756 (9p21.3, CDKN2A-CDKN2B) and rs6010620 (20q13.33, RTEL1). After Bonferroni correction for multiple comparisons, only one marker was statistically significantly associated with glioma risk, rs6010620 (ORtrend for the minor (A) allele, 0.39; 95% CI: 0.250.61; Bonferroni adjusted ptrend, 1.7 x 104). In conclusion, as previously shown for glioma regardless of family history of brain tumours, rs6010620 (RTEL1) was associated with an increased risk of glioma when restricting to cases with family history of brain tumours. These findings require confirmation in further studies with a larger number of glioma cases with a family history of brain tumours.
|
|
| 8. |
- Rajaraman, Preetha, et al.
(författare)
-
Genome-wide association study of glioma and meta-analysis
- 2012
-
Ingår i: Human Genetics. - : SPRINGER. - 0340-6717 .- 1432-1203. ; 131:12, s. 1877-1888
-
Tidskriftsartikel (refereegranskat)abstract
- Gliomas account for approximately 80 % of all primary malignant brain tumors and, despite improvements in clinical care over the last 20 years, remain among the most lethal tumors, underscoring the need for gaining new insights that could translate into clinical advances. Recent genome-wide association studies (GWAS) have identified seven new susceptibility regions. We conducted a new independent GWAS of glioma using 1,856 cases and 4,955 controls (from 14 cohort studies, 3 case-control studies, and 1 population-based case-only study) and found evidence of strong replication for three of the seven previously reported associations at 20q13.33 (RTEL), 5p15.33 (TERT), and 9p21.3 (CDKN2BAS), and consistent association signals for the remaining four at 7p11.2 (EGFR both loci), 8q24.21 (CCDC26) and 11q23.3 (PHLDB1). The direction and magnitude of the signal were consistent for samples from cohort and case-control studies, but the strength of the association was more pronounced for loci rs6010620 (20q,13.33; RTEL) and rs2736100 (5p15.33, TERT) in cohort studies despite the smaller number of cases in this group, likely due to relatively more higher grade tumors being captured in the cohort studies. We further examined the 85 most promising single nucleotide polymorphism (SNP) markers identified in our study in three replication sets (5,015 cases and 11,601 controls), but no new markers reached genome-wide significance. Our findings suggest that larger studies focusing on novel approaches as well as specific tumor subtypes or subgroups will be required to identify additional common susceptibility loci for glioma risk.
|
|
| 9. |
- Wang, Zhaoming, et al.
(författare)
-
Imputation and subset-based association analysis across different cancer types identifies multiple independent risk loci in the TERT-CLPTM1L region on chromosome 5p15.33
- 2014
-
Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 23:24, s. 6616-6633
-
Tidskriftsartikel (refereegranskat)abstract
- Genome-wide association studies (GWAS) have mapped risk alleles for at least 10 distinct cancers to a small region of 63 000 bp on chromosome 5p15.33. This region harbors the TERT and CLPTM1L genes; the former encodes the catalytic subunit of telomerase reverse transcriptase and the latter may play a role in apoptosis. To investigate further the genetic architecture of common susceptibility alleles in this region, we conducted an agnostic subset-based meta-analysis (association analysis based on subsets) across six distinct cancers in 34 248 cases and 45 036 controls. Based on sequential conditional analysis, we identified as many as six independent risk loci marked by common single-nucleotide polymorphisms: five in the TERT gene (Region 1: rs7726159, P = 2.10 × 10(-39); Region 3: rs2853677, P = 3.30 × 10(-36) and PConditional = 2.36 × 10(-8); Region 4: rs2736098, P = 3.87 × 10(-12) and PConditional = 5.19 × 10(-6), Region 5: rs13172201, P = 0.041 and PConditional = 2.04 × 10(-6); and Region 6: rs10069690, P = 7.49 × 10(-15) and PConditional = 5.35 × 10(-7)) and one in the neighboring CLPTM1L gene (Region 2: rs451360; P = 1.90 × 10(-18) and PConditional = 7.06 × 10(-16)). Between three and five cancers mapped to each independent locus with both risk-enhancing and protective effects. Allele-specific effects on DNA methylation were seen for a subset of risk loci, indicating that methylation and subsequent effects on gene expression may contribute to the biology of risk variants on 5p15.33. Our results provide strong support for extensive pleiotropy across this region of 5p15.33, to an extent not previously observed in other cancer susceptibility loci.
|
|
