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Articles by C Johansen
Total Records ( 4 ) for C Johansen
  C Johansen , C Vestergaard , K Kragballe , G Kollias , M Gaestel and L. Iversen
 

The association between inflammation and tumorigenesis is well recognized. Mitogen-activated protein kinase-activated protein kinase-2 (MK2) is known to play a pivotal role in inflammatory processes. Here, we studied the effect of MK2-deficiency and tumor necrosis factor (TNF)--deficiency on skin tumor development in mice using the two-stage chemical carcinogenesis model. We found that MK2–/– mice developed significantly fewer skin tumors compared with both TNF-–/– and wild-type mice when induced by initiation with 7,12-dimethylbenz[a]anthracene (DMBA) and by promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA). The TPA-induced inflammatory response was reduced in both, TNF-–/– mice and MK2–/– mice, but most pronounced in TNF-–/– mice, indicating that a reduced inflammatory response was not the only explanation for the inhibited tumorigenesis seen in MK2–/– mice. Interestingly, increased numbers of apoptotic cells were detected in the epidermis of MK2–/– mice compared with TNF-–/– and wild-type mice, suggesting an additional role of MK2 in the regulation of apoptosis. This was further supported by: (i) increased levels of the tumor suppressor protein p53 in MK2–/– mice after DMBA/TPA treatment compared with controls, (ii) reduced phosphorylation (activation) of the negative p53 regulator, murine double minute 2 in MK2/ mouse keratinocytes in vitro and (iii) a significant decrease in the DMBA/TPA induced apoptosis in cultured MK2–/– keratinocytes transfected with p53 small interfering RNA. Taken together, these findings demonstrate a dual role of MK2 in the early stages of tumor promotion through regulation of both the inflammatory response and apoptosis of DNA-damaged cells. These results also identify MK2 as a putative target for future skin carcinoma therapy.

  I Deltour , C Johansen , A Auvinen , M Feychting , L Klaeboe and J. Schuz
 

In Denmark, Finland, Norway, and Sweden, the use of mobile phones increased sharply in the mid-1990s; thus, time trends in brain tumor incidence after 1998 may provide information about possible tumor risks associated with mobile phone use. We investigated time trends in the incidence of glioma and meningioma in Denmark, Finland, Norway, and Sweden from 1974 to 2003, using data from national cancer registries. We used joinpoint regression models to analyze the annual incidence rates of glioma and meningioma. During this period, 59 984 men and women aged 20–79 years were diagnosed with brain tumors in a population of 16 million adults. All statistical tests were two-sided. From 1974 to 2003, the incidence rate of glioma increased by 0.5% per year (95% confidence interval [CI] = 0.2% to 0.8%) among men and by 0.2% per year (95% CI = –0.1% to 0.5%) among women and that of meningioma increased by 0.8% per year (95% CI = 0.4% to 1.3%) among men, and after the early 1990s, by 3.8% per year (95% CI = 3.2% to 4.4%) among women. No change in incidence trends were observed from 1998 to 2003, the time when possible associations between mobile phone use and cancer risk would be informative about an induction period of 5–10 years.

  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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