New molecular targets in bone metastases
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2019, Journal of Bone OncologyCitation Excerpt :Inhibition of the receptor not only prevents migration of MM cells, but also sensitizes malignant tumor cells to therapeutic agents [86]. Tumor Growth Factor-β (TGF-ß) and RANKL are two prominent soluble factors involved in stimulation of pro-osteoclast formation [87]. RANKL activates osteoclast-mediated bone resorption and subsequently promotes the release of matrix growth factors such as TGF-ß, further inducing tumor growth in a positive feedback mechanism [87].
3D printing hydrogel with graphene oxide is functional in cartilage protection by influencing the signal pathway of Rank/Rankl/OPG
2018, Materials Science and Engineering CCitation Excerpt :One essential characteristic of GO-np is their hydrophobic domains within the core, which are substantially ionized along the edges and then GO-np can have large specific surface area, strong ion exchange capacity, therefore, having a high drug-loading capacity [20,21]. Presenting itself as a candidate for osteoclastogenesis, rank plays a central role in the pathway of Rank/Rankl/OPG, they can regulate OPG and Rankl via direct interaction in the Rank/Rankl/OPG system [22,23]. Rank is also known as TNF-related activation-induced cytokine receptor since its signaling plays a critical role in osteoclastogenesis [23].
Assessing response to treatment of bone metastases from breast cancer: What should be the standard of care?
2015, Annals of OncologyCitation Excerpt :The bone marrow also provides an ideal milieu with low partial pressures of oxygen and pH as well as high levels of extracellular calcium which promote residence and dormancy of DTCs [4, 5]. Once metastatic colonization from CICs is initiated, the normal balanced homeostatic mechanisms of bone formation and resorption, the RANK-RANKL homeostatic loop between osteoblasts and osteoclasts, becomes disrupted [6]. The binding of these two tumour necrosis factor proteins drives bone resorption by osteoclasts; this binding is regulated by the expression of the decoy receptor osteoprotegerin (OPG) [7].