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Articles by J. L Lee
Total Records ( 2 ) for J. L Lee
  C Yoo , J. E Kim , J. L Lee , J. H Ahn , D. H Lee , J. S Lee , S Na , C. S Kim , J. H Hong , B Hong , C Song and H. Ahn
  Objective

The effects of sunitinib in a broad patient population, especially those of Asian ethnicity, have been rarely investigated. Here, we assessed the efficacy and safety of sunitinib in Korean patients with advanced renal cell carcinoma.

Methods

Between April 2006 and August 2008, 77 Korean patients with advanced renal cell carcinoma were treated with sunitinib. We performed retrospective analysis for efficacy in terms of survival outcomes and response rate. Toxicity profiles were also assessed.

Results

A total of 65 patients, including 39 (60%) patients without previous cytotoxic or immunotherapy, were eligible for the analysis. In 53 patients with measurable lesions, the objective response rate was 43% and disease control was achieved in 46 (86%) patients. The median time to treatment failure, time to progression and overall survival were 7.0, 11.8 and 22.8 months, respectively, with a median follow-up of 26.8 months in surviving patients. The most common treatment-related adverse events were fatigue (81%) and stomatitis (60%). The most common Grade 3 or 4 adverse events were hand–foot syndrome (16%), thrombocytopenia (16%) and stomatitis (10%). Dose reduction was required in 46% of patients.

Conclusions

The efficacy was similar to a previous Phase III trial and a safety profile of sunitinib was manageable in Korean patients with advanced renal cell carcinoma, although the incidence of dose reduction and Grade 3 or 4 adverse events were higher than those of western reports. Future studies should investigate the ethnic differences in toxicity profiles of sunitinib.

  J. L Lee , M. J Wang and J. Y. Chen
 

Expression of the type I transmembrane glycoprotein CD44 has recently been recognized as a signature for cancer stem cells. In this study, we demonstrate that CD44, once engaged, is internalized and translocated to the nucleus, where it binds to various promoters, including that of cyclin D1, leading to cell fate change through transcriptional reprogramming. In regulating cyclin D1 expression, the internalized CD44 forms a complex with STAT3 and p300 (acetyltransferase), eliciting STAT3 acetylation at lysine 685 and dimer formation in a cytokine- and growth factor–independent manner. A bipartite nuclear localization signal (NLS) was mapped to the cytoplasmic tail of CD44, which mediates its nuclear translocation. Expression of CD44(NLS) mutant sequesters STAT3 in cytosol. In the nucleus, the acetylated STAT3 dimer remains associated with CD44 and binds to the cyclin D1 promoter, leading to increased cyclin D1 expression and cell proliferation. This study describes a novel function for CD44 in transcriptional modulation through nuclear translocation of the internalized CD44 and complex formation with transcription factors.

 
 
 
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