Endocrine Abstracts

An increasing body of evidence demonstrates that growth factor networks are highly interactive with oestrogen receptor (ER) signalling in the pathogenesis of a number of common cancer types, including breast cancer. Thus several growth factor-induced protein kinases are able to target and phosphorylate key regulatory sites within the ER and its co-activating proteins, a process that enables the activity of the ER as a nuclear transcription factor. It is believed that when aberrantly expressed, such growth factor signalling can sensitise developing cancer cells to oestrogen and permit ER signalling in the presence of anti-hormonal drugs to promote endocrine resistant states.

In light of the above, data will be presented that seeks to (i) define the relationship between oestrogen action and growth factor signalling, examining the importance of ER phosphorylation to ligand dependent and independent activation of the ER and (ii) demonstrate that the co-targeting of growth factor signalling elements, alongside the ER, can enhance the quality and duration of response to anti-hormonal drugs, as well as providing novel efficient treatments for de novo and acquired anti-hormone resistant states. Additionally, it is expected that such combination therapies will more effectively limit the actions of oestrogen during cancer development and thus be of increasing value in cancer chemoprevention strategies.