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Faculty of Science, Engineering and Computing.
Penrhyn Road
Kingston upon Thames
Surrey KT1 2EE

Tel: +44 (0)20 8417 9000

Dr Terry Gaymes

School/Department: Life Sciences, Pharmacy & Chemistry
Position: Lecturer In Immunology & Haematology


I graduated from the University of Wolverhampton with a Biomedical Sciences degree and went on to study for A DPhil in Biochemistry at the University of Sussex. My DPhil research investigated the efficacy and mode of action of novel immunosuppressants. I then worked as a post doctoral researcher at Kings College London (KCL) under the supervision of Dr. Feyruz Rassool. At Kings, I investigated the mechanisms of genomic instability in myeloid malignancies, in particular the adaptations in DNA repair that propagate chromosomal rearrangements in myeloid leukaemia. When Dr. Rassool took up a position at the University of Maryland, USA, I became lead investigator. Having worked at KCL for more than 15 years, I took up my position of Lecturer in Haematology and Immunology here at Kingston University.

Educational and Professional Qualifications

  • 1993 - 1997 DPhil Biochemistry (Sussex)
  • 1989 - 1993 BSc Biomedical sciences (Wolverhampton)

Research Interests

DNA is continually exposed to exogenous and endogenous insults. Genomic integrity is maintained in the cell by a number of well-defined repair mechanisms including the double strand break (DSB) repair pathways of homologous recombination and non-homologous end-joining (NHEJ). However, defects in DNA repair can result in the improper repair of DNA damage and an increased propensity to cancer.

I have previously showed that myeloid leukaemic cells and chromosomal instability syndromes demonstrated up-regulated and erroneous NHEJ repair activity as a result of constitutive DNA damage.

If the breakdown in DNA damage repair is the basis of chromosomal instability, then the particular factors responsible for giving survival advantages to the leukaemia clone are in fact targets for therapy. We and others have realised that genetic defects in the pathways of DSB DNA repair and other DNA damage response pathways would render tumour cells sensitive to DNA repair inhibitors such as Poly ADP ribose polymerase (PARP)inhibitors.

As lead investigator at KCL, we demonstrated that a cohort of myeloid leukaemia patients were sensitive to PARP inhibitors. Previously, trialled in breast cancer these agents have demonstrated beneficial therapeutic responses in more than 60 clinical trials. With the backing of the US pharmaceutical, Biomarin Inc, the very first ever clinical trial of PARP inhibitors in myeloid malignancy was stated at KCL in 2010.

The future aims are to investigate and identify biomarkers in Leukaemia that would identify patients for PARP inhibitor therapy. Furthermore, could one further exploit DNA repair anomalies with other agents in Leukaemia for therapeutic intervention

Teaching Area

LS5008 - Infection and Immunity LS6003 - Chemotherapy of Infectious and neoplastic disease. LS6005 - Clinical Chemistry and Haematology (Blood Sciences) LS7002 - Immunology and the Biology of Disease LS7005 - Anaemia, haemostasis and blood transfusion LS7006 - Haematological Malignancy LS7007 - Cancer Diagnosis and Therapy

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