Finally, top-line results from the ’147 trial (Study on Prolonging Bone Metastasis-Free Survival in Men With Hormone Refractory Prostate Cancer) suggest that denosumab can help prevent bone metastases in prostate cancer, an ability not yet shown by zoledronate.”
“Objective: Repair approaches for the non-vascular meniscus are rarely developed. Recent strategies use scaffold-based techniques and inducing factors. The aim of the study was the investigation of
cell recruitment and re-differentiation inducing factors for a scaffold-based meniscus repair approach.
Method: 3D cultivation of in vitro expanded human meniscus-derived cells was performed in high-density cultures supplemented with 25% hyaluronic acid (HA), 10% human serum (HS) or 10 ng/ml transforming growth factor (TGF-beta 3) compared to untreated controls. The in vitro cell recruitment potential of different HS concentrations GSK690693 was tested by chemotaxis assay. Analysis of chondrocytic markers (type I, II, IX collagen and proteoglycans) was performed on protein and gene expression level.
Results: Cells were attracted by 1-20% HS. 3D cultures supplemented with 10% HS and 25% HA showed meniscus-like gene expression profiles at day 7 with significantly increased cartilage oligomeric matrix protein (COMP) and aggrecan expression levels in the HS group and
a slightly increased profile Etomoxir ic50 in the HA group compared to control. The TGF-beta 3 group showed an additional GSK923295 induction of gene expression levels for type II and type IX collagen. Histological findings confirmed these results by proteoglycan and type I collagen staining in all groups and type II collagen staining only in the TGF-beta 3 group.
Conclusion: This study demonstrates that human meniscus cells are attracted by HS and allow for meniscal matrix formation in 3D culture in the presence of HA and HS, whereas TGF-beta 3 additive does not initiate meniscal tissue. Regarding non-vascular meniscus repair, results
of this study encourage scaffold-based repair approaches. (C) 2013 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.”
“Erlotinib is a low molecular weight, orally active, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor. Inhibition of EGFR tyrosine kinase results in the disruption of processes involved in cancer growth and development, including cell migration, proliferation, angiogenesis, and apoptosis.
In the well designed, phase III SATURN study, oral erlotinib 150 mg/day as maintenance treatment prolonged progression-free survival (PFS) in patients with non-small-cell lung cancer (NSCLC) who had not progressed after four cycles of first-line platinum doublet chemotherapy.