Dr Stephen Hiscox
I joined the Metastasis Research Group within the University of Wales College of Medicine as a member of research staff in 1993.
I received the American Association for Cancer Research Young Investigators Award in 1998 and, in 1999, attained my PhD and received a University of Wales College of Medicine Senior Research Fellowship in recognition of my contribution to research within the college.
After spending a further 3 years within this group, I joined the Tenovus Centre for Cancer Research in 2001. In 2007, I was awarded an RCUK Academic Fellowship to enable me to pursue my research and teaching interests in the field of cancer invasion and metastasis within the School of Pharmacy and Pharmaceutical Sciences, Cardiff University. Promotion to Senior Lecturer in the School followed in 2012.
- PhD, Tumour metastasis, University of Wales College of Medicine (1999)
- BSc (Hons), Biochemistry, Coventry University (1991)
I am currently a member of the Executive Committee for the British Association for Cancer Research, a charitable organisation of over 1000 cancer professionals, and a member of the PhD Grants Panel for the Wales Office of Research and Development for Health and Social Care.
Membership of learned bodies
- PH1121 Molecule to patient
- PH1122 The role of the pharmacist in professional practice
- PH1123 Structure and function of cells and microbes
- PH3101 Optimisation of drug design
- PH3110 Optimisation of pharmaceutical care
- PH3202 Research methodology
- PH4116 Pharmacy research or scholarship project
- PH4118 Pharmaceutical sciences, pharmacy practice and the patient
Having previously trained in the field of cancer metastasis, my research interests are concerned with studying how tumour cells develop a metastatic phenotype, how drug resistance contributes to this process and exploring the role of the tumour microenvironment as a modulator of such behaviour. The goal of these studies is to reveal clinical markers of drug response/relapse and clinical targets through which tumour spread can be repressed.
- Breast cancer and acquired drug resistance
- Tumour invasion and metastasis
- Influence of the tumour microenvironment in tumour progression and spread
Acquired drug resistance
My research is concerned with characterisation of the molecular mechanisms associated with resistance to endocrine therapies using in vitro systems modelling relapse on anti-oestrogens. I have a particular interest in studying antihormone-induced alterations in signal transduction pathways which promote an adverse cell phenotype and may contribute to tumour progression in vivo. These studies will reveal potential biomarkers for therapeutic response in addition to highlighting signalling elements which may be targeted alongside existing endocrine therapies to improve response.
Current project include (i) exploring the role of CD44 in anti-hormone resistant breast cancer where it may augment the cells' response to erbB receptor ligands and (ii) the potential of targeting Src alongside the oestrogen receptor as a means to prevent acquired anti-oestrogen resistance.
Tumour invasion and metastasis
Tumour metastasis, a complex series of steps in which cancer cells leave their original site and migrate to other parts of the body via the host circulatory systems, is the single most important factor affecting the survival of a cancer patient. Unfortunately, despite an increasing variety of anticancer agents employed to treat such cancers, they are rarely curative.
My interests are currently concerned with (i) deciphering intracellular signalling pathways which regulate tumour cell adhesion, migration and invasion and enhance the tumour cells' metastatic potential and (ii) identifying key regulatory elements within these pathways which present potential therapeutic targets.
The interplay between tumour cells and their surrounding microenvironment (stromal cells, extracellular matrix) plays an important role in tumour development and progression.
Currently, I am investigating (i) how stromal cells can modulate the angiogenic capacity of tumour cells, (ii) how the c-met receptor, overexpressed in drug-resistant breast cancer, influences the cells' response to stromally-produced HGF/SF and (iii) how the tumour microenvironment can alter cell sensitivity to anticancer drugs.
Postdoctoral research associates
- Dr Nicola Jordan (funded by AstraZeneca)
School of Pharmacy and Pharmaceutical Sciences
- Professor Robert Nicholson
- Dr Julia Gee