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Articles by C. J Burns
Total Records ( 2 ) for C. J Burns
  E. M Schindler , A Hindes , E. L Gribben , C. J Burns , Y Yin , M. H Lin , R. J Owen , G. D Longmore , G. E Kissling , J. S. C Arthur and T. Efimova

Activating Ras mutations occur in a large portion of human tumors. Yet, the signaling pathways involved in Ras-induced tumor formation remain incompletely understood. The mitogen-activated protein kinase pathways are among the best studied Ras effector pathways. The p38 mitogen-activated protein kinase isoforms are important regulators of key biological processes including cell proliferation, differentiation, survival, inflammation, senescence, and tumorigenesis. However, the specific in vivo contribution of individual p38 isoforms to skin tumor development has not been elucidated. Recent studies have shown that p38, a p38 family member, functions as an important regulator of epidermal keratinocyte differentiation and survival. In the present study, we have assessed the effect of p38 deficiency on skin tumor development in vivo by subjecting p38 knockout mice to a two-stage 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate chemical skin carcinogenesis protocol. We report that mice lacking p38 gene exhibited a marked resistance to development of 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate-induced skin papillomas, with increased latency and greatly reduced incidence, multiplicity, and size of tumors compared with wild-type mice. Our data suggest that the underlying mechanism for reduced susceptibility to skin carcinogenesis in p38-null mice involves a defect in proliferative response associated with aberrant signaling through the two major transformation-promoting pathways: extracellular signal-regulated kinase 1/2-activator protein 1 and signal transducer and activator of transcription 3. These findings strongly suggest an in vivo role for p38 in promoting cell proliferation and tumor development in epidermis and may have therapeutic implication for skin cancer. [Cancer Res 2009;69(11):4648–55]

  D. I McBride , C. J Burns , G. P Herbison , N. F Humphry , K Bodner and J. J. Collins

Background Previous studies at the Dow AgroSciences (Formerly Ivon Watkins-Dow) plant in New Plymouth, New Zealand, had raised concerns about the cancer risk in a subset of workers at the site with potential exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. As the plant had been involved in the synthesis and formulation of a wide range of agrochemicals and their feedstocks, we examined the mortality risk for all workers at the site.

Aims To quantify the mortality hazards arising from employment at the Dow AgroSciences agrochemical production site in New Plymouth, New Zealand.

Methods Workers employed between 1 January 1969 and 1 October 2003 were followed up to the end of 2004. Standardized mortality ratios (SMRs) were calculated using national mortality rates by employment duration, sex, period of hire and latency.

Results A total of 1754 employees were followed during the study period and 247 deaths were observed. The all causes and all cancers SMRs were 0.97 (95% CI 0.85–1.10) and 1.01 (95% CI 0.80–1.27), respectively. Mortality due to all causes was higher for short-term workers (SMR 1.23, 95% CI 0.91–1.62) than long-term workers (SMR 0.92, 95% CI 0.80–1.06) and women had lower death rates than men. Analyses by latency and period of hire did not show any patterns consistent with an adverse impact of occupational exposures.

Conclusions The mortality experience of workers at the site was similar to the rest of New Zealand.

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