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Frances V Fuller-pace


Cancer
Dundee University
Belgium

Biography

Frances Fuller-Pace carried out her PhD studies with Professor Noreen Murray, firstly at EMBL Heidelberg, and subsequently at the University of Edinburgh. After post-doctoral fellowships in Dr Peter Southern’s lab at the Scripps Research Institute in San Diego, California, and in Dr Clive Dickson’s lab at the Imperial Cancer Research Fund (now CRUK) in London, she joined Prof. Sir David Lane’s lab at Dundee to work on the DEAD box family of RNA helicases. She was awarded an MRC Senior Fellowship on 1992, which allowed her to set up an independent research group and which she renewed in 1997. Frances was elected a Fellow of the Higher Education Academy in 2007 and a Fellow of the Royal Society of Biologists in 2010. Work in the Fuller-Pace lab focuses on the role of RNA helicases in breast cancer development and progression and on factors that influence the response to chemotherapy and endocrine therapy, and is supported by Breast Cancer Now and Tenovus Scotland.

Research Interest

My group's main research interests are in the factors underlying breast cancer progression and chemotherapy/endocrine therapy resistance, with a focus on the role of the multi-functional RNA helicases p68 (DDX5) and p72 (DDX17) and their interactions with the tumour suppressor p53 and with nuclear hormone receptors in this process.  Together with our clinical colleagues we are also interested in exploring the importance of the peri-tumoral stroma in the response to neoadjuvant therapy in breast cancer. This is a collaboration that combines gene expression and functional analysis of tumoral and peri-tumoral fibroblasts (our own work) combined with Magnetic Resonance Imaging (MRI) and Shear Wave Elastography of breast cancers (clinical radiologists) and Pathology with the long-term view of predicting response to neoadjuvant chemotherapy. Our main research aims: ·         Understanding how the function of p68 and p72 as transcriptional co-regulators modulates the p53 response to DNA damage. ·         Analysis of cross talk between p68/p72 and nuclear hormone receptors, and their impact on the development of therapy resistance. ·         Understanding the role of differences in gene expression patterns in breast tumoral and peri-tumoral fibroblasts, both in the response to neoadjuvant chemotherapy and in tumour cell migration/invasion. To address these questions we are using a combination of molecular and cell culture techniques together with analysis of patient tumour material.

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