Search our site
Search our site

Dr Terry Gaymes

Senior Lecturer in Haematology and Immunology

About

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 in 2016.

Areas of specialism

  • Leukaemia
  • DNA repair
  • Genomic instability
  • Cancer Biology
  • Telomere biology

Qualifications

  • DPhil Biochemistry (University of Sussex)
  • BSc (Hons) Biomedical sciences (University of Wolverhampton)

Professional membership

Member of the British Society of Haematology

Fellowship of the Higher Education Authority (FHEA)

Research

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

Publications

Number of items: 14.

Article

Gaymes, Terry J., Mohamedali, Azim, Eiliazadeh, Anthony L., Darling, David and Mufti, Ghulam J. (2017) FLT3 and JAK2 mutations in acute myeloid leukemia promote interchromosomal homologous recombination and the potential for copy neutral loss of heterozygosity. Cancer Research, 77(7), pp. 1697-1708. ISSN (print) 0008-5472

Mohamedali, A M, Gaken, J, Ahmed, M, Malik, F, Smith, A E, Best, S, Mian, S, Gaymes, T, Ireland, R, Kulasekararaj, A G and Mufti, G J (2015) High concordance of genomic and cytogenetic aberrations between peripheral blood and bone marrow in myelodysplastic syndrome (MDS). Leukemia, 29(9), pp. 1928-1938. ISSN (print) 0887-6924

Gaymes, Terry J., Mohamedali, Azim M., Patterson, Miranda, Matto, Nazia, Smith, Alexander, Kulasekaraj, Austin, Chelliah, Rajani, Curtin, Nicola, Farzaneh, Farzin, Shall, Sydney and Mufti, Ghulam J. (2013) PARP inhibitor sensitivity in high risk MDS and acute myeloid leukaemia is associated with microsatellite instability dependent frameshift mutations in DNA repair genes. Haematologica, 98(9), pp. 1397-1406. ISSN (print) 0390-6078

Orr, S J, Gaymes, T, Ladon, D, Chronis, C, Czepulkowski, B, Wang, R, Mufti, G J, Marcotte, E M and Thomas, N S B (2010) Reducing MCM levels in human primary T cells during the G0-G1 transition causes genomic instability during the first cell cycle. Oncogene, 29(26), pp. 3803-3814. ISSN (print) 0950-9232

Gaymes, Terry J., Shall, Sydney, MacPherson, Lee J., Twine, Natalie A., Lea, Nicholas C., Farzaneh, Farzin and Mufti, Ghulam J. (2009) Inhibitors of poly ADP-ribose polymerase (PARP) induce apoptosis of myeloid leukemic cells: potential for therapy of myeloid leukemia and myelodysplastic syndromes. Acta Haematologica, 94, pp. 638-646. ISSN (print) 0001-5792

Ranuncolo, Stella Maria, Wang, Ling, Polo, Jose M., Dell'Oso, Tania, Dierov, Jamil, Gaymes, Terry, Rassool, Feyruz, Carroll, Martin and Melnick, Ari (2008) BCL6 mediated attenuation of DNA damage sensing triggers growth arrest and senescence through a 53-dependent pathway in a cell-context dependent manner. The Journal of Biological Chemistry, 283(33), pp. 22565-22572. ISSN (print) 0021-9258

Gaymes, Terry J., Shall, Sydney, Farzaneh, Farzin and Mufti, Ghulam J. (2008) Chromosomal instability syndromes are sensitive to Poly ADP-ribose polymerase inhibitors. Haematologica, 93, pp. 1886-1889. ISSN (print) 0390-6078

Rassool, Feyruz, Gaymes, Terry J., Omidvar, Nader, Brady, Nicola, Buerlet, Stephanie, Pla, Marika, Reboul, Murielle, Lea, Nicholas, Chomienne, Christine, Thomas, Nicholas S.B., Mufti, Ghulam J. and Padua, Rose Ann (2007) Reactive oxygen species, DNA damage, and error-prone repair : a model for genomic instability with progression in myeloid leukemia? Cancer Research, 67(18), pp. 8762-8771. ISSN (print) 0008-5472

Gaymes, Terry J., Padua, Rose Ann, Pla, Marika, Orr, Steven, Omidvar, Nader, Chomienne, Christine, Mufti, Ghulam J. and Rassool, Feyruz V. (2006) Histone Deacetylase Inhibitors (HDI) cause DNA damage in leukemia cells : a mechanism for leukemia-specific HDI-dependent apoptosis? Molecular Cancer Research, 4(8), pp. 563-573. ISSN (print) 1541-7786

Brady, Nicola, Gaymes, Terry J., Cheung, Manyee, Mufti, Ghulam J. and Rassool, Feyruz V. (2003) Increased error-prone NHEJ activity in myeloid leukemias is associated with DNA damage at sites that recruit key nonhomologous end-joining proteins. Cancer Research, 63(8), pp. 1798-1805. ISSN (print) 0008-5472

Gaymes, Terry J., Mufti, Ghulam J. and Rassool, Feyruz V. (2002) Myeloid leukemias have increased activity of the nonhomologous end-joining pathway and concomitant DNA misrepair that is dependent on the Ku70/86 heterodimer. Cancer Research, 62(10), pp. 2791-2797. ISSN (print) 0008-5472

Gaymes, Terry J, North, Phillip S, Brady, Nicola, Hickson, Ian D, Mufti, Ghulam J and Rassool, Feyruz (2001) Increased error-prone non homologous DNA end-joining - a proposed mechanism of chromosomal instability in Bloom's Syndrome. Oncogene, 21, pp. 2525-2533. ISSN (print) 0950-9232

Gaymes, Terry J, Cebrat, Marek, Siemion, Ignacy Z and Kay, John E (1997) Cyclolinopeptide A (CLA) mediates its immunosuppressive activity through cyclophilin-dependent calcineurin inactivation. FEBS Letters, 418(1-2), pp. 224-227. ISSN (print) 0014-5793

Conference or Workshop Item

Gaymes, Terry, Carrett, Neil, Patel, Nishith, Kay, John and Siemion, Iggy (1995) Effects of cyclolinopeptide A on T lymphocyte activation and peptidyl prolyl isomerase activity. In: Biochemical Society Transactions 656th Meeting; 11 - 15 Sep 1995, Dublin, Ireland. (Unpublished)

This list was generated on Fri Nov 24 05:00:43 2017 GMT.
>

Looking for academic staff in the Faculty of Health, Social Care and Education? Visit the Faculty website

Site menu