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Articles by G. E Kissling
Total Records ( 2 ) for G. E Kissling
  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]

  S. C Hewitt , J. E O'Brien , J. L Jameson , G. E Kissling and K. S. Korach
 

In vitro models have been used to demonstrate that estrogen receptors (ERs) can regulate estrogen-responsive genes either by directly interacting with estrogen-responsive element (ERE) DNA motifs or by interacting with other transcription factors such as AP1. In this study, we evaluated estrogen (E2)-dependent uterine gene profiles by microarray in the KIKO mouse, an in vivo knock-in mouse model that lacks the DNA-binding function of ER and is consequently restricted to non-ERE-mediated responses. The 2- or 24-h E2-mediated uterine gene responses were distinct in wild-type (WT), KIKO, and ERKO genotypes, indicating that unique sets of genes are regulated by ERE and non-ERE pathways. After 2 h E2 treatment, 38% of the WT transcripts were also regulated in the KIKO, demonstrating that the tethered mechanism does operate in this in vivo model. Surprisingly, 1438 E2-regulated transcripts were unique in the KIKO mouse and were not seen in either WT or ERKO. Pathway analyses revealed that some canonical pathways, such as the Jak/Stat pathway, were affected in a similar manner by E2 in WT and KIKO. In other cases, however, the WT and KIKO differed. One example is the Wnt/β-catenin pathway; this pathway was impacted, but different members of the pathway were regulated by E2 or were regulated in a different manner, consistent with differences in biological responses. In summary, this study provides a comprehensive analysis of uterine genes regulated by E2 via ERE and non-ERE pathways.

 
 
 
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