Dr Stephen Hiscox

Dr Stephen Hiscox

Senior Lecturer

School of Pharmacy and Pharmaceutical Sciences

Email:
hiscoxse1@cardiff.ac.uk
Telephone:
+44 (0)29 2087 0306
Fax:
+44 (0)29 2087 5152

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.

Qualifications

  • PhD, Tumour metastasis, University of Wales College of Medicine (1999)
  • BSc (Hons), Biochemistry, Coventry University (1991)
  • 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

Research interests

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.

Tumour microenvironment

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.

Collaborators

Postdoctoral research associates

  • Dr Nicola Jordan (funded by AstraZeneca)

School of Pharmacy and Pharmaceutical Sciences

  • Professor Robert Nicholson
  • Dr Julia Gee