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Articles by H Sugiura
Total Records ( 9 ) for H Sugiura
  S Togo , X Liu , X Wang , H Sugiura , K Kamio , S Kawasaki , T Kobayashi , R. F Ertl , Y Ahn , O Holz , H Magnussen , K Fredriksson , C. M Skold and S. I. Rennard
 

Fibrotic diseases are characterized by the accumulation of extracellular matrix together with distortion and disruption of tissue architecture. Phosphodiesterase (PDE)4 inhibitors, by preventing the breakdown of cAMP, can inhibit fibroblast functions and may be able to mitigate tissue remodeling. Transforming growth factor (TGF)-β1, a mediator of fibrosis, can potentially modulate cAMP by altering PGE2 metabolism. The present study assessed whether PDE4 inhibitors functionally antagonize the profibrotic activity of fibroblasts stimulated by TGF-β1. The PDE4 inhibitors roflumilast and rolipram both inhibited fibroblast-mediated contraction of three-dimensional collagen gels and fibroblast chemotaxis toward fibronectin in the widely studied human fetal lung fibroblast strain HFL-1 and several strains of fibroblasts from adult human lung. Roflumilast was ~10-fold more potent than rolipram. There was a trend for PDE4 inhibitors to inhibit more in the presence of TGF-β1 (0.05 < P < 0.08). The effect of the PDE4 inhibitors was mediated through cAMP-stimulated protein kinase A (PKA), although a PKA-independent effect on gel contraction was also observed. The effect of PDE4 inhibitors depended on fibroblast production of PGE2 and TGF-β1-induced PGE2 production. PDE4 inhibitors together with TGF-β1 resulted in augmented PGE2 production together with increased expression of COX mRNA and protein. The present study supports the concept that PDE4 inhibitors may attenuate fibroblast activities that can lead to fibrosis and that PDE4 inhibitors may be particularly effective in the presence of TGF-β1-induced fibroblast stimulation.

  T Toyama , H Yamashita , H Sugiura , N Kondo , H Iwase and Y. Fujii
  Objective

The CYP2D6 enzyme plays a major role in converting tamoxifen to its active metabolites. We investigated whether there is an association between the CYP2D6*10 allele and clinical outcome in node-negative Japanese breast cancer patients.

Methods

CYP2D6 genotyping was performed in 154 node-negative breast cancer patients who had received adjuvant tamoxifen treatment alone. The CYP2D6 genotypes were determined using the TaqMan Allelic Discrimination Assay.

Results

Eighteen percent (28 of 154) of the patients carried the CYP2D6*10/*10 genotype, 40% the CYP2D6 wild-type (wt)/*10 genotype and 42% the CYP2D6 wt/wt genotype. There were no discernible correlations between clinicopathologic parameters and the CYP2D6*10 genotype. Next, we determined whether there was a correlation between the CYP2D6*10 genotype and survival and found that the clinical outcome for patients carrying the CYP2D6*10/*10 genotype was similar to those with other genotypes.

Conclusions

Our results suggest that the CYP2D6*10 genotype is unlikely to have any clinical significance for prognosis of node-negative Japanese breast cancer patients receiving adjuvant tamoxifen alone.

 
 
 
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