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Articles by J Hansen
Total Records ( 5 ) for J Hansen
  D Kasperaviciute , C. B Catarino , E. L Heinzen , C Depondt , G. L Cavalleri , L. O Caboclo , S. K Tate , J Jamnadas Khoda , K Chinthapalli , L. M. S Clayton , K. V Shianna , R. A Radtke , M. A Mikati , W. B Gallentine , A. M Husain , S Alhusaini , D Leppert , L. T Middleton , R. A Gibson , M. R Johnson , P. M Matthews , D Hosford , K Heuser , L Amos , M Ortega , D Zumsteg , H. G Wieser , B. J Steinhoff , G Kramer , J Hansen , T Dorn , A. M Kantanen , L Gjerstad , T Peuralinna , D. G Hernandez , K. J Eriksson , R. K Kalviainen , C. P Doherty , N. W Wood , M Pandolfo , J. S Duncan , J. W Sander , N Delanty , D. B Goldstein and S. M. Sisodiya
 

Partial epilepsies have a substantial heritability. However, the actual genetic causes are largely unknown. In contrast to many other common diseases for which genetic association-studies have successfully revealed common variants associated with disease risk, the role of common variation in partial epilepsies has not yet been explored in a well-powered study. We undertook a genome-wide association-study to identify common variants which influence risk for epilepsy shared amongst partial epilepsy syndromes, in 3445 patients and 6935 controls of European ancestry. We did not identify any genome-wide significant association. A few single nucleotide polymorphisms may warrant further investigation. We exclude common genetic variants with effect sizes above a modest 1.3 odds ratio for a single variant as contributors to genetic susceptibility shared across the partial epilepsies. We show that, at best, common genetic variation can only have a modest role in predisposition to the partial epilepsies when considered across syndromes in Europeans. The genetic architecture of the partial epilepsies is likely to be very complex, reflecting genotypic and phenotypic heterogeneity. Larger meta-analyses are required to identify variants of smaller effect sizes (odds ratio <1.3) or syndrome-specific variants. Further, our results suggest research efforts should also be directed towards identifying the multiple rare variants likely to account for at least part of the heritability of the partial epilepsies. Data emerging from genome-wide association-studies will be valuable during the next serious challenge of interpreting all the genetic variation emerging from whole-genome sequencing studies.

  A. E Hoffman , T Zheng , C. H Yi , R. G Stevens , Y Ba , Y Zhang , D Leaderer , T Holford , J Hansen and Y. Zhu
 

As transcriptional regulators, circadian genes have the potential to influence a variety of biological pathways, including many cancer-related processes. Cryptochrome 2 (CRY2) is essential for proper circadian timing and is a key component of the circadian regulatory feedback loop. Here, we report findings from genetic, epigenetic, loss-of-function, and transcriptional profiling analyses of CRY2 in breast cancer. Six single-nucleotide polymorphisms in CRY2 were identified for genotyping in a case-control population (n = 441 cases and n = 479 controls), and three single-nucleotide polymorphisms (rs11038689, rs7123390, and rs1401417) were significantly associated with postmenopausal breast cancer risk, with significant effect modification by menopausal status [dominant model for rs11038689: odds ratio (OR), 0.71; 95% confidence interval (95% CI), 0.51-0.99; P for trend = 0.028; homozygous variants for rs7123390: OR, 0.44; 95% CI, 0.22-0.86; P for trend = 0.028; and rs1401417: OR, 0.44; 95% CI, 0.21-0.92; P for trend = 0.017]. Interestingly, this association was only evident in women with estrogen and progesterone receptor (ER/PR)–negative breast tumors but not with ER/PR-positive tumors. Breast cancer patients also had significantly higher levels of CRY2 promoter methylation relative to controls, which is consistent with tissue array data showing lower levels of CRY2 expression in tumor tissue relative to adjacent normal tissue. Furthermore, in vitro analyses identified several breast cancer–relevant genes that displayed altered expression following CRY2 knockdown. These findings suggest a role for CRY2 in breast tumorigenesis and provide further evidence that the circadian system may be an important modulator of hormone-related cancer susceptibility. Cancer Prev Res; 3(4); 539–48. ©2010 AACR.

  M Morant , C Ekstrom , P Ulvskov , C Kristensen , M Rudemo , C. E Olsen , J Hansen , K Jorgensen , B Jorgensen , B. L Moller and S. Bak
 

Auxin homeostasis is pivotal for normal plant growth and development. The superroot2 (sur2) mutant was initially isolated in a forward genetic screen for auxin overproducers, and SUR2 was suggested to control auxin conjugation and thereby regulate auxin homeostasis. However, the phenotype was not uniform and could not be described as a pure high auxin phenotype, indicating that knockout of CYP83B1 has multiple effects. Subsequently, SUR2 was identified as CYP83B1, a cytochrome P450 positioned at the metabolic branch point between auxin and indole glucosinolate metabolism. To investigate concomitant global alterations triggered by knockout of CYP83B1 and the countermeasures chosen by the mutant to cope with hormonal and metabolic imbalances, 10-day-old mutant seedlings were characterized with respect to their transcriptome and metabolome profiles. Here, we report a global analysis of the sur2 mutant by the use of a combined transcriptomic and metabolomic approach revealing pronounced effects on several metabolic grids including the intersection between secondary metabolism, cell wall turnover, hormone metabolism, and stress responses. Metabolic and transcriptional cross-talks in sur2 were found to be regulated by complex interactions between both positively and negatively acting transcription factors. The complex phenotype of sur2 may thus not only be assigned to elevated levels of auxin, but also to ethylene and abscisic acid responses as well as drought responses in the absence of a water deficiency. The delicate balance between these signals explains why minute changes in growth conditions may result in the non-uniform phenotype. The large phenotypic variation observed between and within the different surveys may be reconciled by the complex and intricate hormonal balances in sur2 seedlings decoded in this study.

  L Calvio , M Feuerstein , J Hansen and G. M. Luff
 

Background Occupationally active malignant brain tumour survivors (MBTS) are rarely studied. However, cognitive limitations with the potential to impact work are commonly reported in MBTS.

Aims To obtain a better understanding of factors that are associated with cognitive limitations in employed MBTS.

Methods The study was performed by means of a web-based survey. Occupationally active MBTS (n = 113) and a non-cancer comparison group (n = 123) were recruited. While accounting for demographics, medical factors, health behaviours and problem-solving orientation, the relationship among measures of symptom burden (fatigue, depression and anxiety) and cognitive limitations were investigated.

Results MBTS (average 4 years post-diagnosis) reported higher levels of physical fatigue (P < 0.001), depression (P < 0.001) and anxiety (P < 0.01). MBTS reported more overall cognitive limitations (P < 0.001), memory (P < 0.001), executive function (P < 0.001) and attention (P < 0.001) deficits. Education (B = –3.4, 95% CI = –6.7 to 0.1), ethnicity (B = 5.2, 95% CI = 0.6–9.8), job stress (B = 3.9, 95% CI = 1.5–6.4), depressive symptoms (B = 0.7, 95% CI = 0.1–1.3) and negative problem solving (B = 4.2, 95% CI = 1.5–7.0) were also associated with higher levels of cognitive limitations in both groups.

Conclusions Occupationally active MBTS report higher levels of cognitive limitations. However, modifiable factors were related to cognitive limitations in both groups and should be considered when developing approaches to improve cognitive limitations in the workplace.

  M Agostini , G Ferro , A Olsson , I Burstyn , F De Vocht , J Hansen , C Funch Lassen , C Johansen , K Kjaerheim , S Langard , I Stucker , W Ahrens , T Behrens , M. L Lindbohm , P Heikkila , D Heederik , L Portengen , J Shaham , P Boffetta and H. Kromhout
 

Objective: Development of a method for retrospective assessment of exposure to bitumen fume, bitumen condensate, organic vapour, polycyclic aromatic hydrocarbons, and co-exposures to known or suspected lung carcinogens for a nested case–control study of lung cancer mortality among European asphalt workers.

Methods: Company questionnaires and structured questionnaires used in interviews and industry-specific job-exposure matrices (JEMs) were elaborated and applied. Three sources of information were eventually used for exposure assessment and assignment: (i) data obtained in cohort phase, (ii) data from living subjects, next-of-kin, and fellow-workers questionnaires, and (iii) JEMs for bitumen exposure by inhalation and via skin and co-exposures to known or suspected lung carcinogens within and outside cohort companies. Inhalation and dermal exposure estimates for bitumen were adjusted for time trends, time spent in a job, and other determinants of exposure (e.g. oil gravel paving). Clothing patterns, personal protective devices, and personal hygiene were taken into consideration while estimating dermal exposure.

Results: Occupational exposures could be assessed for 433 cases and 1253 controls for relevant time periods. Only 43% of work histories were spent inside original asphalt and construction companies. A total of 95.8% of job periods in cohort companies could be coded at a more detailed level. Imputation of work time and ‘hygienic behaviour’ multipliers was needed for <10% of work history years. Overall, downward trends in exposure were present and differences existed between countries and companies. As expected, correlations were strongest (r > 0.7) among bitumen-related agents, while correlations between coal tar, bitumen-related agents, and established lung carcinogens were weaker (r < 0.4).

Conclusions: A systematic and detailed approach was developed to estimate inhalation and dermal exposure for a nested case–control study among asphalt workers.

 
 
 
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