As EFNA5 down-regulation is a consistent finding in chondrosarcomas, we presume that it represents another essential alteration in tumorigenesis and tumor progression associated with cell adhesion, in addition to a multitude of other partially unknown biologic functions mediated by bidirectional ephrin/Eph receptor signaling and cross talk.
High expression of Eph receptors in a wide variety of human tumors indicates some roles in tumor progression, which makes these proteins potential targets for anticancer therapy.
Increased expression of Eph receptors and their ephrin ligands has been implicated in promoting angiogenesis and tumour progression in several malignancies.
These findings identify a novel Eph receptor signalling pathway with tumour-suppressor activity and predict that therapeutic intervention to activate EphB4 signalling will inhibit tumour progression.
EPH-A2, or ECK (a receptor for ephrin-A1), is ectopically expressed in most melanoma cell lines; the pathology where this expression is first manifested and the possible role of the receptor in tumor progression are unknown.