Skip to main content

Dr Terence Davis

Research Fellow

School of Medicine

+44 292068 8102
Cochrane Building, Heath Park, Cardiff, CF14 4YU


I am a Lecturer in the Division of Medical Education.


Career Overview

2020 - present:   Lecturer, School of Medicine, Cardiff University, UK

2006 -  2019:   Research Fellow, School of Medicine, Cardiff University, UK

2002 - 2006:    BBSRC Recognised Researcher, Cardiff University School of Medicine, UK

1999 - 2006:    Research Associate, Pathology Department, Cardiff University School of Medicine, UK (UWCM until 2004)

1997 - 1999:    Assistant Researcher, CCRT, University of Hawaii, USA

1996:               Research Associate, Imperial College, University of London, UK

1992 - 1995:    Research Associate, Biology Dept, University of Sussex, UK

1991:               Research Assistant, Genetics Dept, University of Glasgow, UK

1985 - 1990:    Research Assistant, Genetics Dept, University of Cambridge, UK

Education and Qualifications

Ph.D.               Biochemistry, University of Glasgow, 1984

B.Sc. (Hons:2i)             Biochemistry, University of Dundee, 1980

Professional memberships

Fellow of The Royal Society of Biology

Member of the British Society for Research into Ageing

Member of The Genetical Society


We are currently unable to retrieve the list of publications. Visit our institutional repository.


My current teaching role includes:

Case-Based Learning Educational Lead for Yr 2

Facilitator for Case-Based Learning for both Yr1 and Yr 2 modules

Facilitator for Platform for Clinical Science modules

Facilittator for Various Turtorial groups

SSC Yr1 Critical Literature Review

Various assessements including Yr1 Practise Research Exercises

Prior to moving to the Division of Medical Education my research investigated the mechanisms by which human cells enter a state called "sensecence" - a stable non dividing state.

It is thought that senescent cells accumulate during the ageing process in humans and contribute to "age-related frailty." Senescent cells appear not to be removed from ageing individuals and, as they no longer appear to maintain their normal functions, they interfere detrimentally with tissue maintenance. They may do this in several ways, 1) reduce ability to replace damaged cells in division competent tissues, 2) secrete pro-inflammatory cytokines and tissue degrading enzymes that actively damage surrounding healthy tissues, 3) induce cancer development of surrounding tissues.

Senescent cells are thought to underly the pathology of much age-related illness, including atherosclerosis, osteoporosis, type II diabetes, cancer and others. This is supported by the recent data showing that these diseases can be alleviated in mouse models by actively killing the senescent cells. Very preliminary human clinical trials have now started to test this.

As part of my research I used Human progeroid syndromes (where humans age more quickly than normal). These included Werner syndrome and Hutchinson-Gilford Progeria.

In my final years as researcher I investigated whether the molecular signalling pathways that lead to cellular senescence might play a role in resistance of cancer cells to chemotherapy through a process called "therapy induced senescence". As chemotherapy is a DNA damaging stress on cells a natural response is for the cell to enter a sensecent state. When the therapy is concluded these cells then have the possibility to re-enter division leading to relapse. This therapy induced senescence is of growing interest in the field of chemotherapy.  My work in this area looked at lung cancer cells.

If these ideas are correct, then developing therapeutics that either prevent, or remove, senescent cells may prove useful in alleviating the increasing burdens of age-related frailty and cancer. As part of my teaching profile I am attempting to introduce these ideas.