Dr Terry Gaymes
Faculties, deparments and locations
- Faculty of Health, Science, Social Care and Education
- Department of Biomolecular Sciences
- School of Life Sciences, Pharmacy and Chemistry
- Penrhyn Road
Senior lecturer in Haematology and Immunology
- Email:
- t.gaymes@kingston.ac.uk
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 modes of action of novel immunosuppressants. I then worked as a post doctoral researcher at Kings College London (KCL) where I investigated the mechanisms of genomic instability in myeloid malignancies, in particular the adaptations in DNA repair that propagate chromosomal rearrangements in myeloid leukaemia. I took up my position of Lecturer in Haematology and Immunology here at Kingston University in 2016. In my ongoing research, I continue to investigate DNA damage and repair changes biomarkers in leukaemia that can be exploited therapeutically.
Qualifications
- DPhil Biochemistry (University of Sussex)
- BSc (Hons) Biomedical sciences (University of Wolverhampton)
- Fellow of the Higher Education Authority (FHEA)
Domains
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. We 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. Previously, trialled in breast cancer these agents have demonstrated beneficial therapeutic responses in more than 60 clinical trials. 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
A Phase I trial of talazoparib in patients with advanced hematologic malignancies
Gopal, Ajay K, Popat, Rakesh, Mattison, Ryan J, Menne, Tobias, Bloor, Adrian, Gaymes, Terry, Khwaja, Asim, Juckett, Mark, Chen, Ying, Cotter, Matthew J and Mufti, Ghulam J, 2021, International Journal of Hematologic Oncology (10), 3, pp IJH35
FLT3 and JAK2 mutations in acute myeloid leukemia promote interchromosomal homologous recombination and the potential for copy neutral loss of heterozygosity
Gaymes, Terry J., Mohamedali, Azim, Eiliazadeh, Anthony L., Darling, David and Mufti, Ghulam J., 2017, Cancer Research (77), 7, pp 1697-1708
High concordance of genomic and cytogenetic aberrations between peripheral blood and bone marrow in myelodysplastic syndrome (MDS)
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, Leukemia (29), 9, pp 1928-1938
PARP inhibitor sensitivity in high risk MDS and acute myeloid leukaemia is associated with microsatellite instability dependent frameshift mutations in DNA repair genes
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, Haematologica (98), 9, pp 1397-1406
Reducing MCM levels in human primary T cells during the G0-G1 transition causes genomic instability during the first cell cycle
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, Oncogene (29), 26, pp 3803-3814
Inhibitors of poly ADP-ribose polymerase (PARP) induce apoptosis of myeloid leukemic cells: potential for therapy of myeloid leukemia and myelodysplastic syndromes
Gaymes, Terry J., Shall, Sydney, MacPherson, Lee J., Twine, Natalie A., Lea, Nicholas C., Farzaneh, Farzin and Mufti, Ghulam J., 2009, Acta Haematologica (94), pp 638-646
Chromosomal instability syndromes are sensitive to Poly ADP-ribose polymerase inhibitors
Gaymes, Terry J., Shall, Sydney, Farzaneh, Farzin and Mufti, Ghulam J., 2008, Haematologica (93), pp 1886-1889
BCL6 mediated attenuation of DNA damage sensing triggers growth arrest and senescence through a 53-dependent pathway in a cell-context dependent manner
Ranuncolo, Stella Maria, Wang, Ling, Polo, Jose M., Dell'Oso, Tania, Dierov, Jamil, Gaymes, Terry, Rassool, Feyruz, Carroll, Martin and Melnick, Ari, 2008, The Journal of Biological Chemistry (283), 33, pp 22565-22572
Reactive oxygen species, DNA damage, and error-prone repair : a model for genomic instability with progression in myeloid leukemia?
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, Cancer Research (67), 18, pp 8762-8771
Histone Deacetylase Inhibitors (HDI) cause DNA damage in leukemia cells : a mechanism for leukemia-specific HDI-dependent apoptosis?
Gaymes, Terry J., Padua, Rose Ann, Pla, Marika, Orr, Steven, Omidvar, Nader, Chomienne, Christine, Mufti, Ghulam J. and Rassool, Feyruz V., 2006, Molecular Cancer Research (4), 8, pp 563-573
Increased error-prone NHEJ activity in myeloid leukemias is associated with DNA damage at sites that recruit key nonhomologous end-joining proteins
Brady, Nicola, Gaymes, Terry J., Cheung, Manyee, Mufti, Ghulam J. and Rassool, Feyruz V., 2003, Cancer Research (63), 8, pp 1798-1805
Myeloid leukemias have increased activity of the nonhomologous end-joining pathway and concomitant DNA misrepair that is dependent on the Ku70/86 heterodimer
Gaymes, Terry J., Mufti, Ghulam J. and Rassool, Feyruz V., 2002, Cancer Research (62), 10, pp 2791-2797
Increased error-prone non homologous DNA end-joining - a proposed mechanism of chromosomal instability in Bloom's Syndrome
Gaymes, Terry J, North, Phillip S, Brady, Nicola, Hickson, Ian D, Mufti, Ghulam J and Rassool, Feyruz, 2001, Oncogene (21), pp 2525-2533
Cyclolinopeptide A (CLA) mediates its immunosuppressive activity through cyclophilin-dependent calcineurin inactivation
Gaymes, Terry J, Cebrat, Marek, Siemion, Ignacy Z and Kay, John E, 1997, FEBS Letters (418), 1-2, pp 224-227
The use of PARP inhibitors in cancer therapy : use as adjuvant with chemotherapy or radiotherapy ; use as a single agent in susceptible patients ; techniques used to identify susceptible patients
Shall, Sydney, Gaymes, Terry, Farzaneh, Farzin, Curtin, Nicola and Mufti, Ghulam J. (2011). In: Tulin, Alexei V., (ed.), Poly(ADP-Ribose) Polymerase: Methods and Protocols. New York, NY: Springer, pp 239-266
Effects of cyclolinopeptide A on T lymphocyte activation and peptidyl prolyl isomerase activity
Gaymes, Terry, Carrett, Neil, Patel, Nishith, Kay, John and Siemion, Iggy(1995). In: Biochemical Society Transactions 656th Meeting, 11 - 15 Sep 1995 :Dublin, Ireland