Ellen (Yan Ru) Gao
ANZAC Research Institute
Funding Partner 2010
Rotary Club of Dural and
the David Henning Memorial Foundation
Yan Ru (Ellen) Gao graduated from Otago University, New Zealand in 2005. Ellen has had a long interest in cancer research, and was very enthusiastic about starting her first research position at the Children's Cancer Institute in 2006, where she worked for 18 months. During that time she assisted in examining the cellular mechanisms and gene expression patterns in Medulloblastoma, which is the most common brain tumour of childhood. At the Children’s Cancer Institute she became familiar with all sorts of molecular techniques including PCR, Western blotting, DNA and RNA extraction, immunohistochemistry methods.
In 2007 she joined the Andrology lab at the ANZAC Research Institute where she worked as a research assistant. She expanded her expertise in analysing the androgen actions in various organs including prostate and epididymis. Prostate cancer is androgen dependent in its development and progression, and therefore the work has given her important background for her future research in understanding androgen actions in breast cancer.
Ms Gaos compassion and commitment to cancer patients, however, is not limited to research; Ellen has also contributed by working as a community support worker, helping people with autism and volunteering with the Cancer Council of New South Wales, supporting people with cancer and their families.
SUMMARY OF THE PROJECT:
The role of androgen receptor-mediated actions in breast cancer
Breast cancer is one of the leading causes of cancer death in Australian women, and hence contributes significantly to mortality and public health spending. Androgens are mainly known as male hormones, but also play important roles in female reproductive physiology. All women produce androgens, which can be converted to estrogens, and play a role in puberty and during menstruation. Androgens mediate their actions by bindings to the androgen receptor (AR). High levels of androgen receptor expression (70-90%) in breast tissue, combined with an increased risk of breast cancer in women with high circulating androgen levels, implies a role for androgens via the AR in the origin and/or progression of breast cancer. Although there is some evidence supporting this hypothesis, the specific role of androgens is not well established.
This project aims to provide novel and decisive evidence and specific mechanistic information on androgen actions in mammary carcinogenesis. This will be achieved by utilizing our lab’s novel AR deficient female mouse model, where androgen activity has been blocked, in conjunction with a widely used chemically inducedbreast cancer model to examine the role of AR in breast cancer initiation, progression and therapy.