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Articles by K. J Chang
Total Records ( 3 ) for K. J Chang
  C. H Lin , J. Y Liau , Y. S Lu , C. S Huang , W. C Lee , K. T Kuo , Y. C Shen , S. H Kuo , C Lan , J. M Liu , W. H Kuo , K. J Chang and A. L. Cheng
 

Background: In the past two decades, the incidence of breast cancer in young Taiwanese females has been rapidly increasing, approaching the risk level of western countries. As a first step to investigate the possible etiology, we examined the molecular subtypes of female breast cancer in Taiwan.

Methods: This study included 1,028 consecutive patients with breast cancer diagnosed in National Taiwan University Hospital between 2004 and 2006. Estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor-2, cytokeratin 5/6, and epidermal growth factor receptor expression and/or gene amplification were analyzed.

Results: Younger (≤50 years) breast cancer patients had a higher prevalence of luminal A (67% versus 57%; P < 0.001) and a lower prevalence of basal-like subtype (9% versus 17%; P < 0.001) compared with older (>50 years) patients. The higher prevalence of luminal A subtype was mainly attributed to a higher ER (75% versus 63%; P < 0.001) and PR (47% versus 33%; P < 0.001) expression rate in younger patients than older patients. Tumors with histologic grade 3 were less prevalent in younger patients than in older patients (23% versus 30%; P = 0.01). For very young (<35 years) patients, the molecular subtype distribution, ER and/or PR expression rate, and histologic grade were not significantly different from those of less young (35-50 years) patients.

Conclusions: Young breast cancer patients in Taiwan are characterized by a high prevalence of luminal A subtype and low prevalence of histologic grade 3 tumor and/or basal-like subtype. These features are distinct from young breast cancer patients in western countries. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1807–14)

  S. T Chiu , K. J Chang , C. H Ting , H. C Shen , H Li and F. J. Hsieh
 

Receptor tyrosine kinase EphB3 is expressed in cells in the bottom of intestinal crypts near stem cell niches. Loss of Ephb3 has recently been reported to produce invasive colorectal carcinoma in ApcMin/+ mice and EphB-mediated compartmentalization was demonstrated to be a mechanism suppressing colorectal cancer progression; however, it is unknown whether other factors contribute to EphB-mediated tumor suppression. EphA4–ephrin-A and EphB4–ephrin-B2 signaling have been reported to promote mesenchymal-to-epithelial transition (MET). Here, we examine whether EphB3–ephrin-B interaction has a similar effect and investigate its role in tumor suppression. We found in a clinical cohort that EphB3 expression was significantly reduced in advanced Dukes’ stage tumor specimens, so we over-expressed EphB3 in HT-29 cells by stable transfection. EphB3 over-expression inhibited HT-29 growth in monolayer cultures, anchorage-independent growth in soft agar and xenograft growth in nude mice and initiated morphological, behavioral and molecular changes consistent with MET. Specifically, EphB3 over-expression re-organized cytoskeleton (converting spreading cells to a cobble-like epithelial morphology, patterning cortical actin cytoskeleton and polarizing E-cadherin and ZO-1), induced functional changes favoring MET (decreased transwell migration, increased apoptosis and Ca2+-dependent cell–cell adhesion), decreased mesenchymal markers (fibronectin and nuclear β-catenin), increased epithelial markers (ZO-1, E-cadherin and plakoglobin) and inactivated CrkL–Rac1, a known epithelial-to-mesenchymal transition signaling pathway. Additionally, cross talk from Wnt signaling potentiated the restoration of epithelial cell polarity. Noteworthily, the same factors contributing to MET, owing to EphB3 signaling, also facilitated tumor suppression. We conclude that EphB3–ephrin-B interaction promotes MET by re-establishing epithelial cell–cell junctions and such an MET-promoting effect contributes to EphB3-mediated tumor suppression.

  Y. Y Shao , K. T Kuo , F. C Hu , Y. S Lu , C. S Huang , J. Y Liau , W. C Lee , C Hsu , W. H Kuo , K. J Chang , C. H Lin and A. L. Cheng
  Objective

We studied tau and excision repair cross-complementing 1 expression to evaluate their predictive values in advanced breast carcinoma patients.

Methods

Patients treated with paclitaxel and cisplatin as the first-line chemotherapy for locally advanced or metastatic breast cancer were enrolled. The expression levels of tau and excision repair cross-complementing 1 were assessed by immunohistochemistry and examined for their associations with treatment response and survival.

Results

Fifty-four patients were included in this study. Despite the strong association between tau expression and lower histological grade and estrogen receptor expression, tau expression remained an independent predictor for a lower response rate in multivariate analysis (odd ratio = 0.24, P = 0.02). However, tau expression was a predictor for longer overall survival in both univariate analysis (median, 57.5 vs. 30.4 months, P = 0.02) and multivariate analysis (hazard ratio = 0.36, P = 0.008). Excision repair cross-complementing 1 was not associated with treatment response or overall survival.

Conclusions

Tau expression but not excision repair cross-complementing 1 in advanced breast cancer predicts poor response to combination chemotherapy of paclitaxel and cisplatin. However, tau expression is significantly associated with longer overall survival.

 
 
 
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