个人简介
I received a BSc (Hons) in 1985 in Physiological Sciences from the University of Newcastle-Upon-Tyne and was awarded the University's Physiology prize for that year. I then undertook a Medical Research Council-funded PhD studentship at the University of Wales College of Medicine in the then Tenovus Institute (breast cancer laboratory, PhD awarded 1991).
I held 3 consecutive postdoctoral positions in the Tenovus Institute between 1991-2000 (including one with Dept. Surgery, University of Wales College of Medicine), becoming a Senior Researcher in 1995.
Between 2000-April 2007, I took up the position of Senior Research Associate & Research Co-ordinator for the Tenovus Centre for Cancer Research within the School of Pharmacy and Pharmaceutical Sciences, where the programme of work focussed around anti‑hormone resistance and progression in breast cancer. Alongside contributing to the management of (and defining research strategies for) the Tenovus group, my role was to oversee the Clinical Immunocytochemistry Team, extending to analysing signalling elements using activation-specific antibodies in several phase II breast cancer trials.
I also lead the group's Gene Discovery Team applying microarrays and bioinformatics to reveal new signalling in resistant breast cancer, and receiving a gold medal in this area at the 9th World Congress on Advances in Oncology/7th International Symposium on Molecular Medicine. I was subsequently funded until Sept. 2010 as Principal Investigator on a Tenovus Charity programme grant investigating and targeting anti‑hormone-induced signalling during the drug responsive phase of ER+ breast cancer.
Most recently, I successfully secured a prestigious 5-year Breast Cancer Campaign-funded Senior Scientific Fellowship (2010-2015), based in the School of Pharmacy and Pharmaceutical Sciences, to examine the impact of prolonged antihormone exposure on the acquired resistant phenotype in ER+ disease to define targets potentially relevant following adjuvant antihormone relapse in the clinic.
Alongside defining research strategies for further funding bids, my current role extends to formulating new hypotheses and contributing to management and implementing projects, development and strategic planning for our research group. I am also responsible for securing supportive external grant funding and for sustaining various existing (and securing new) collaborations with key academic groups and pharmaceutical companies.
研究领域
Anti‑hormone-induced signalling in ER + breast cancer.
Mechanisms of anti‑hormone and anti-growth factor resistant breast cancer growth and progression.
Novel target discovery and evaluation of new therapies using breast cancer cells in vitro.
(Signal transduction and biomarker studies in clinical cancer.
My research interests have principally been directed towards gaining a fuller appreciation of breast cancer biology, mechanisms of failure of anti‑hormonal agents and the associated gain of poorer prognosis. In my PhD, I used electron microscopy and immunocytochemistry to examine the impact of anti‑oestrogens on the normal breast. The studentship included optimising novel immunocytochemical procedures to monitor oestrogen receptor in breast cancer, a protein now routinely measured in the clinic. My subsequent postdoctoral positions focussed around monitoring signal transduction deregulation in clinical DCIS, and then in my position as Senior Research Associate for the Tenovus Centre for Cancer Research within invasive breast cancer, determining growth factor signal transduction underlying resistance to anti‑hormones and anti-growth factors in experimental models and clinical disease. The aim of these latter studies was not only to reveal novel drug failure biomarkers, but also new therapeutic targets including providing landmark data demonstrating the success of anti-EGFR therapy alongside anti‑hormones in ER+ breast cancer in vitro.
More recently, I have been interested in deciphering and evaluating targeting of oncogenic signalling induced by anti-hormones during the drug responsive phase of ER+ breast cancer that may limit maximal initial growth-inhibitory response. This novel research area, pioneered by our group, stemmed from our studies demonstrating compensatory induction of erbB signalling by antihormones and landmark data demonstrating the value of co-targeting induced EGFR alongside such agents in ER+ breast cancer. Our in vitro findings using multiple breast cancer models indicate the immense potential for targeting of compensatory signalling such as EGFR, HER2 and Src irrespective of genetic background, potentially further influenced by paracrine environment. Through such studies the aim is to reveal new signalling targets for pharmacological inhibitors that can be used in "intelligent" treatment combination strategies with anti-hormones to improve initial response and delay/prevent resistance. My Fellowship will now consider the ability of extended antihormonal exposure to radically re-programme ER+ breast cancer and will encompass in vitro and clinical breast cancer studies. As part of the Fellowship, I will also undertake training with Dr. Graham Ball, Reader in Bioinformatics at Nottingham Trent University. The Fellowship will deepen my resistance knowledge, enhance my bioinformatics skills, allow me to further flourish as an independent researcher in breast cancer and consolidate my team's reputation at the forefront of translational research in breast cancer.
近期论文
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Milevskiy, M.et al. 2016. Long-range regulators of the lncRNAHOTAIR enhance its prognostic potential in breast cancer. Human Molecular Genetics , article number: ddw177. (10.1093/hmg/ddw177) pdf
Bellerby, R.et al. 2016. Overexpression of specific CD44 isoforms is associated with aggressive cell features in acquired endocrine resistance. Frontiers in Oncology 6, article number: 145. (10.3389/fonc.2016.00145) pdf
Agrawal, A.et al. 2016. Biological effects of fulvestrant on estrogen receptor positive human breast cancer: short, medium and long-term effects based on sequential biopsies. International Journal of Cancer 138(1), pp. 146-159. (10.1002/ijc.29682) pdf
Abdulkareem, Z.et al. 2016. Knockdown of the small conductance Ca2+-activated K+ channels is potently cytotoxic in breast cancer cell lines. British Journal of Pharmacology 173(1), pp. 177-190. (10.1111/bph.13357) pdf
Hynes, N.et al. 2015. ELF5 drives lung metastasis in luminal breast cancer through recruitment of Gr1+ CD11b+ myeloid-derived suppressor cells. PLoS Biology 13(12), article number: e1002330. (10.1371/journal.pbio.1002330) pdf
Simões, B.et al. 2015. Anti-estrogen resistance in human breast tumors is driven by JAG1-NOTCH4-dependent cancer stem cell activity. Cell Reports 12(12), pp. 1968-1977. (10.1016/j.celrep.2015.08.050) pdf
Stone, A.et al. 2015. DNA methylation of oestrogen-regulated enhancers defines endocrine sensitivity in breast cancer. Nature Communications 6, article number: 7758. (10.1038/ncomms8758) pdf
Gee, J.et al. 2015. A new cell panel to study oestrogen receptor loss in acquired endocrine resistant breast cancer. Cancer Research 75(9), article number: P3-05-19. pdf
Robertson, J.et al. 2014. A good drug made better: the Fulvestrant Dose Response Story. Clinical Breast Cancer 14(6), pp. 381-389. (10.1016/j.clbc.2014.06.005) pdf
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