BACKGROUND: Although the presence of numerous cell signaling receptors in osteosarcoma is known, their simultaneous characterization has not been performed to date. The current study sought to characterize and quantify the expression of cell surface receptors across a variety of osteosarcoma cell lines. METHODS: Standard (n = 4) and patient‐derived (n = 10) osteosarcoma cell lines were cultured and labeled with antibodies to epidermal growth factor receptor, human epidermal growth factor receptor (HER)‐2, HER‐3, HER‐4, insulin‐like growth factor 1 receptor (IGF‐1R), IGF‐2R, insulin receptor (IR), vascular endothelial growth factor receptor (VEGFR)‐1, VEGFR‐2, VEGFR‐3, c‐Met, fibroblast growth factor receptor (FGFR)‐2, FGFR‐3, and platelet‐derived growth factor receptor (PDGFR)‐β. Cell surface examination was performed using flow cytometry, and the geometric fluorescent mean for each receptor was calculated and compared against a positive control. RESULTS: Significant overexpression of IGF‐2R was shown in all cell lines, with an average geometric mean above the upper expression quartile. A variable expression pattern was seen for c‐Met, PDGFR‐β, IR, IGFR‐1, HER‐2, and VEGFR‐3 with expression values for the remaining receptors mainly in the lower quartile. An apparent association between the expression of IGF‐1R and HER‐2 and between the expression of PDGFR‐β and IR was demonstrated. CONCLUSION: IGF‐2R was consistently overexpressed on the cell surface across all tested osteosarcoma cell lines. Substantial, although variable, expression of c‐Met, HER‐2, IGF‐1R, VEGFR‐3, IR, and PDGFR‐β was demonstrated as well, suggesting that these receptors may contribute to osteosarcoma aggressiveness and biological heterogeneity and may serve as potential targets within a subset of tumors. Associated receptor expression may provide new insight into common regulatory factors or pathways. Targeting either common factors or targeting multiple specific receptors may have therapeutic relevance. Cancer 2012;. © 2011 American Cancer Society.

The findings suggest that surgical reconstruction should aim to reestablish at least the proximal 50% of the UCL ulnar footprint.

Ulnar collateral ligament insufficiency has been shown to result in changes in contact pressure and contact area in the posteromedial elbow. This study used new digital technology to assess the effect of a complete ulnar collateral ligament tear on ulnohumeral contact area, contact pressure, and valgus laxity throughout the throwing motion. Nine elbow cadaveric specimens were tested at 90° and 30° of elbow flexion to simulate the late cocking/early acceleration and deceleration phases of throwing, respectively. A digital sensor was placed in the posteromedial elbow. Each specimen was tested with valgus torque of 2.5 Nm with the anterior band of the ulnar collateral ligament intact and transected. A camera-based motion analysis system was used to measure valgus inclination of the forearm with the applied torque. At 90° of elbow flexion, mean contact area decreased significantly (107.9 mm(2) intact vs 84.9 mm(2) transected, P=.05) and average maximum contact pressure increased significantly (457.6 kPa intact vs 548.6 kPa transected, P<.001). At 30° of elbow flexion, mean contact area decreased significantly (83.9 mm(2) intact vs 65.8 mm(2) transected, P=.01) and average maximum contact pressure increased nonsignificantly (365.9 kPa intact vs 450.7 kPa transected, P=.08). Valgus laxity increased significantly at elbow flexion of 90° (1.1° intact vs 3.3° transected, P=.01) and 30° (1.0° intact vs 1.7° transected, P=.05). Ulnar collateral ligament insufficiency was associated with significant changes in contact area, contact pressure, and valgus laxity during both relative flexion (late cocking/early acceleration phase) and relative extension (deceleration phase) moments during the throwing motion arc.