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Dr Richard Clarkson  -  PhD


Position:Senior Lecturer

Telephone:+44 (0)29 208 70249
Fax:+44 (0)29 208 74116
Extension:70249
Location:European Cancer Stem Cell Research Institute, Cardiff School of Biosciences, Hadyn Ellis Building, Maindy Road, Cathays, Cardiff CF24 4HQ

Research Overview

As animals grow and develop their tissues are re-organised in a highly ordered way. Central to this remodeling is the balance between apoptosis and cell survival/proliferation signals that ultimately determines the composition and size of tissues. Appropriate regulation of these signals is important not only for the efficient removal of supernumerary, potentially harmful, cells but also for the maintenance of pluripotent cells (eg. stem cells) necessary for tissue expansion. The consequences of errors in these cell death/survival signals can be severe, and may lead to major developmental defects, immune diseases or cancer.

My lab focuses on how the aberrant regulation of these processes might contribute to breast cancer.  Using the mouse mammary gland as our principal model, we identified a number of candidate genes that appear to play a role in the re-organisation of different cell types during tissue morphogenesis.  We have since found that some of these genes have disease-modifying effects on the establishment or progression of breast cancers, either by altering the proportion of tumour initiating cells (cancer stem cells) within the tumour or by directly affecting tumour malignancy – such as promoting the migration of cancer cells to other sites within the body. 

Work in our laboratory is directed at using conditional gene technology to regulate these disease modifiers in order to establish whether altering their expression could have beneficial effects on the development and progression of breast cancers.  Our ongoing studies include efforts to identify novel therapeutic and diagnostic strategies that target these novel disease modifiers.  This has led to the development of an experimental pharmacological agent that potently suppresses the spread of tumour cells in pre-clinical models of metastatic breast cancer.

Research Division

Pathophysiology and Repair