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Articles by H. C Shen
Total Records ( 2 ) for H. C Shen
  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.

  P. W Weng , H. C Shen , H. H Lee , S. S Wu and C. H. Lee

Severe glenoid bone loss in recurrent anterior glenohumeral instability is rare and difficult to treat.


The authors present a surgical technique using allogeneic bone grafting for open anatomic glenoid reconstruction in addition to the capsular shift procedure.

Study Design

Case series; Level of evidence, 4.


Nine consecutive patients with a history of recurrent anterior shoulder instability underwent reconstruction of large bony glenoid erosion with a femoral head allograft combined with an anteroinferior capsular shift procedure. Preoperative computed tomographic and arthroscopic evaluation was performed to confirm a ≥120° osseous defect of the anteroinferior quadrant of the glenoid cavity, which had an "inverted-pear" appearance. Patients were followed for at least 4.5 years (range, 4.5–14). Serial postoperative radiographs were evaluated. Functional outcomes were assessed using Rowe scores.


All grafts showed bony union within 6 months after surgery. The mean Rowe score improved to 84 from a preoperative score of 24. The mean loss of external rotation was 7° compared with the normal shoulder. One subluxation and 1 dislocation occurred after grand mal seizures during follow-up. These 2 patients regained shoulder stability after closed reduction. The remaining patients did not report recurrent instability. All patients resumed daily activities without restricted motion.


This technique for open reconstruction is viable for the treatment of recurrent anterior glenohumeral instability with large bony glenoid erosion.

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