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Dr Stephen Hiscox  -  BSc PhD


General

Member of the School's Pharmacology & Physiology Research Discipline

 

Research Interests

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