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- Johnatty, S. E., et al.
(author)
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No evidence that GATA3 rs570613 SNP modifies breast cancer risk
- 2009
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In: Breast Cancer Research and Treatment. - : Springer. - 0167-6806 .- 1573-7217. ; 117:2, s. 371-379
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Journal article (peer-reviewed)abstract
- GATA-binding protein 3 (GATA3) is a transcription factor that is crucial to mammary gland morphogenesis and differentiation of progenitor cells, and has been suggested to have a tumor suppressor function. The rs570613 single nucleotide polymorphism (SNP) in intron 4 of GATA3 was previously found to be associated with a reduction in breast cancer risk in the Cancer Genetic Markers of Susceptibility project and in pooled analysis of two case-control studies from Norway and Poland (P trend = 0.004), with some evidence for a stronger association with estrogen receptor (ER) negative tumours [Garcia-Closas M et al. (2007) Cancer Epidemiol Biomarkers Prev 16:2269-2275]. We genotyped GATA3 rs570613 in 6,388 cases and 4,995 controls from the Breast Cancer Association Consortium (BCAC) and 5,617 BRCA1 and BRCA2 carriers from the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). We found no association between this SNP and breast cancer risk in BCAC cases overall (ORper-allele = 1.00, 95% CI 0.94-1.05), in ER negative BCAC cases (ORper-allele = 1.02, 95% CI 0.91-1.13), in BRCA1 mutation carriers RRper-allele = 0.99, 95% CI 0.90-1.09) or BRCA2 mutation carriers (RRper-allele = 0.93, 95% CI 0.80-1.07). We conclude that there is no evidence that either GATA3 rs570613, or any variant in strong linkage disequilibrium with it, is associated with breast cancer risk in women.
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- Connolly, John, et al.
(author)
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Using MODIS derived fPAR with ground based flux tower measurements to derive the light use efficiency for two Canadian peatlands
- 2009
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In: Biogeosciences. - : Copernicus GmbH. - 1726-4189. ; 32:6, s. 225-225
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Journal article (peer-reviewed)abstract
- We used satellite remote sensing data; fractionof photosynthetically active radiation absorbed by vegetation(fPAR) from the Moderate Resolution Imaging Spectrora-diometer (MODIS) in combination with tower eddy covari-ance and meteorological measurements to characterise theLight Use Efficiency parameter (ε)variability and the maxi-mumε(εmax)for two contrasting Canadian peatlands. Eight-day MODISfPAR data were acquired for the Mer Bleue(2000 to 2003) and Western Peatland (2004). Flux towereddy covariance and meteorological measurements were in-tegrated to the same eight-day time stamps as the MODISfPAR data. A light use efficiency model: GPP =ε×APAR(where GPP is Gross Primary Productivity and APAR is ab-sorbed photosynthetically active radiation) was used to cal-culateε. Theεmaxvalue for each year (2000 to 2003) at theMer Bleue bog ranged from 0.58 g C MJ−1to 0.78 g C MJ−1and was 0.91 g C MJ−1in 2004, for the Western Peatland.The average growing seasonεfor the Mer Bleue bog forthe four year period was 0.35 g C MJ−1and for the West-ern Peatland in 2004 was 0.57 g C MJ−1. The average snowfree period for the Mer Bleue bog over the four years was 0.27 g C MJ−1and for the Western Peatland in 2004 was0.39 g C MJ−1. Using the light use efficiency method wecalculated theεmaxand the annual variability inεfor twoCanadian peatlands. We determined that temperature was agrowth-limiting factor at both sites Vapour Pressure Deficit(VPD) however was not. MODISfPAR is a useful tool forthe characterization ofεat flux tower sites.
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- Rigopoulos, N., et al.
(author)
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Optically detected extended X-ray absorption fine structure study of InGaN/GaN single quantum wells
- 2007
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In: AIP Conference Proceedings. - : AIP. - 0094-243X. - 9780735403970 ; 893, s. 1503-1504
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Conference paper (peer-reviewed)abstract
- We have investigated the local atomic environment of the Ga atoms in an InxGa1-xN single quantum well structure using Optically Detected Extended X-ray Absorption Fine Structure (OD-EXAFS). A comparison of the OD-EXAFS data with a theoretical model shows the technique to be site selective for this particular structure and reveals that the quantum well emission originates from regions with x=0.15.
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- Bickerton, A. S. T., et al.
(author)
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Adipose tissue fatty acid metabolism in insulin-resistant men
- 2008
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In: Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 51:8, s. 1466-1474
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Journal article (peer-reviewed)abstract
- Aims/hypothesis Increased NEFA production and concentrations may underlie insulin resistance. We examined systemic and adipose tissue NEFA metabolism in insulin-resistant overweight men (BM1 25-35 kg/m(2)). Methods In a cohort study we examined NEFA concentrations in men in the upper quartile of fasting insulin (n = 124) and in men with fasting insulin below the median (n 159). In a metabolic study we examined NEFA metabolism in the fasting and postprandial states, in ten insulin-resistant men and ten controls. Results In the cohort study, fasting NEFA concentrations were not significantly different between the two groups (median values: insulin-resistant men, 410 mu mol/l; controls, 445 2 mu mol/l). However, triacylglycerol concentrations differed markedly (1.84 vs 1.18 mmol/l respectively, p<0.001). In the metabolic study, arterial NEFA concentrations again did not differ between groups, whereas triacylglycerol concentrations were significantly higher in insulin-resistant men. Systemic NEFA production and the release of NEFA from subcutaneous adipose tissue, expressed per unit of fat mass, were both reduced in insulin-resistant men compared with controls (fasting values by 32%, p=0.02, and 44%, p=0.04 respectively). 3-Hydroxybutyrate concentrations, an index of hepatic fat oxidation and ketogenesis, were lower (p=0.03). Conclusions/interpretation Adipose tissue NEFA output is not increased (per unit weight of tissue) in insulin resistance. On the contrary, it appears to be suppressed by high fasting insulin concentrations. Alterations in triacylglycerol metabolism are more marked than those in NEFA metabolism. and are indicative of altered metabolic partitioning of fatty acids (decreased oxidation, increased esterification) in the liver.
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- Garcia-Closas, Montserrat, et al.
(author)
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Heterogeneity of breast cancer associations with five susceptibility loci by clinical and pathological characteristics
- 2008
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In: PLoS genetics. - : Public Library of Science (PLoS). - 1553-7404. ; 4:4, s. e1000054-
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Journal article (peer-reviewed)abstract
- A three-stage genome-wide association study recently identified single nucleotide polymorphisms (SNPs) in five loci (fibroblast growth receptor 2 (FGFR2), trinucleotide repeat containing 9 (TNRC9), mitogen-activated protein kinase 3 K1 (MAP3K1), 8q24, and lymphocyte-specific protein 1 (LSP1)) associated with breast cancer risk. We investigated whether the associations between these SNPs and breast cancer risk varied by clinically important tumor characteristics in up to 23,039 invasive breast cancer cases and 26,273 controls from 20 studies. We also evaluated their influence on overall survival in 13,527 cases from 13 studies. All participants were of European or Asian origin. rs2981582 in FGFR2 was more strongly related to ER-positive (per-allele OR (95%CI) = 1.31 (1.27-1.36)) than ER-negative (1.08 (1.03-1.14)) disease (P for heterogeneity = 10(-13)). This SNP was also more strongly related to PR-positive, low grade and node positive tumors (P = 10(-5), 10(-8), 0.013, respectively). The association for rs13281615 in 8q24 was stronger for ER-positive, PR-positive, and low grade tumors (P = 0.001, 0.011 and 10(-4), respectively). The differences in the associations between SNPs in FGFR2 and 8q24 and risk by ER and grade remained significant after permutation adjustment for multiple comparisons and after adjustment for other tumor characteristics. Three SNPs (rs2981582, rs3803662, and rs889312) showed weak but significant associations with ER-negative disease, the strongest association being for rs3803662 in TNRC9 (1.14 (1.09-1.21)). rs13281615 in 8q24 was associated with an improvement in survival after diagnosis (per-allele HR = 0.90 (0.83-0.97). The association was attenuated and non-significant after adjusting for known prognostic factors. Our findings show that common genetic variants influence the pathological subtype of breast cancer and provide further support for the hypothesis that ER-positive and ER-negative disease are biologically distinct. Understanding the etiologic heterogeneity of breast cancer may ultimately result in improvements in prevention, early detection, and treatment.
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