Jun Yang
St Jude Children�s Research Hospital, USA
Scientific Tracks Abstracts: J Cancer Sci Ther
More than 1.7 million new cases of breast cancer occur every year, 70% of which are estrogen receptor alpha (ER�±) positive. Anti-estrogen therapy to block ER�± function is the most important approach in treatment of ER�± positive patients. However, resistance eventually will develop for various reasons. Previous clinical studies suggest that in vivo tumor environment may play a role in tamoxifen resistance, as hypoxia-inducible factor 1 alpha (HIF-1�±) protein expression is associated with tamoxifen resistance in neoadjuvant, primary therapy of ER�±-positive breast cancers as well as resistance to chemo endocrine therapy. However, whether HIF-1�± plays an autonomous role in modulating endocrine therapy efficacy such as tamoxifen resistance is unknown. It is also puzzling that increased HIF-1�± is associated with ER�± positivity in clinical samples, since ER�± negative breast cancer is more hypoxic. These two important oncogenic transcriptional factors interact has not yet been defined. In this presentation, I will discuss a new signaling pathway between ER�± and HIF-1�±, providing evidence that HIF- 1�± may account for anti-hormone therapy. I will also discuss how HIF-1�± and ER�± cooperate to drive expression of histone demethylase KDM4B in breast cancer and demonstrate KDM4B as a potential therapeutic target.
Jun Yang completed his PhD from Institute of Cancer Research, Sutton, UK, and Post-doctoral studies from Oxford University and St Jude Children’s Research Hospital. He is the Faculty in Department of Surgery, St Jude Children’s Research Hospital. He has published more than 20 papers in reputed journals.
Email: jun.yang2@stjude.org
Cancer Science & Therapy received 3968 citations as per Google Scholar report