Liverpool Head & Neck Centre

Jason Parsons

Jason Parsons

Dr Parsons is a Senior Lecturer/Research Group Leader at the University of Liverpool, and Honorary Lead for Radiobiology Research at the Clatterbridge Cancer Centre. As a radiation biologist, his Group's research is focussed on the biochemistry, molecular and cellular biology of ionising radiation (radiotherapy). His main interests are on examining the biology of radiation of different ionisation densities, particularly proton beam therapy and other high-linear energy transfer (LET) radiation in comparison to low-LET photons, and largely its impact on the signalling and processing of DNA damage. Research is centred on models of head and neck squamous cell carcinoma (HNSCC), but also on other radioresistant cancers including glioblastoma, and on identifying optimal strategies including combination with targeted drugs/inhibitors to enhance sensitivity of these cancers to low/high-LET radiotherapy.

  • The Parsons Lab is a vibrant and active research group focussing on radiation biology, particularly in cell models of head and neck cancer. The Group is located at the University of Liverpool, and part of the Institute for Systems, Molecular and Integrative Biology.

    The Principal Investigator, Dr Jason Parsons, is currently a Senior Lecturer at the University of Liverpool and Honorary Lead for Radiobiology Research at the Clatterbridge Cancer Centre. Dr Parsons has accumulated over 20 years of experience in studying the biological effects of ionising radiation, particularly the impact on DNA damage and repair. A particular interest is in examining the radiobiology of proton beam therapy (at Clatterbridge) and how this compares to conventional (x-ray) radiotherapy. The long term goal is to identify optimal treatment strategies using radiotherapy for patients with head and neck cancer.

    Dr Parsons has published over 60 peer-reviewed publications and reviews on radiation biology and DNA damage repair related work. Research is currently funded by grants from the National Institutes of Health (NIH), the Medical Research Council (MRC) and North West Cancer Research (NWCR).

  • The Radiobiology of Proton Beam Therapy

    Whilst radiotherapy using conventional x-ray radiation is utilised in the treatment of ~50 % of human cancers, proton beam therapy (PBT) is increasingly being utilised as an alternative, cutting-edge precision targeted technique. This is due to the fact that unlike x-rays, the radiation dose can be precisely targeted to the tumour and limits unnecessary irradiation of the surrounding normal tissues and organs at risk, and therefore reduces adverse side effects. However, PBT displays changes in energy along with increases in linear energy transfer (LET) leading to differences in the biological effectiveness. In particular, PBT causes changes in the DNA damage profile compared to x-rays and leads to increases in levels of complex DNA damage (CDD), containing several lesions in close proximity within DNA. Consequently, there are still significant biological uncertainties regarding the optimal treatment strategies using PBT, compared to other radiotherapy modalities, in specific tumours.

    Our research is focussed on examining the radiobiology of protons (using the 60 MeV cyclotron at the Clatterbridge Cancer Centre, Bebington) versus conventional x-ray irradiation on radioresistant tumour cell models, particularly those of the head and neck but also of the adult brain (glioblastoma). A particular interest is in the induction and repair of CDD induced by PBT, but then to identify specific enzymes and pathways that respond to the DNA damage and therefore control tumour cell radiosensitivity. We are furthermore investigating the effect of oxygenation (hypoxia) and delivery of radiotherapy at ultra-high dose rates (FLASH) on the radiobiology of tumour cells and the appropriate normal cell models. Our goal is to improve our basic understanding of the radiobiology of protons versus x-rays, and ultimately in the identification of optimal strategies using these radiotherapy techniques for the treatment of head and neck cancers and glioblastoma.

    Optimising the Radiosensitivity of Head and Neck Cancer Cells

    Head and neck squamous cell carcinoma (HNSCC) is the 6th most common cancer worldwide, with nearly 600,000 new cases per year reported. The incidence of HNSCC in the North West region of the UK in particular is at least three times higher than the national average. There has also been a rapid increase in the incidence of human papillomavirus type 16 (HPV)-associated HNSCC, specifically of the oropharynx, in the last few decades. However interestingly, there are improved prognosis and survival rates for patients with HPV-positive tumours treated with radiotherapy and chemotherapy in comparison to their HPV-negative counterparts whose outcome is very poor. However, the molecular mechanisms which underlie this differential survival and radiosensitivity is unclear. Our research is also centred on glioblastoma, the most common primary brain tumour in adults where survival rates are poor, and where conventional (x-ray) radiotherapy has limited effectiveness.

    We are currently investigating the key cellular pathways, particularly those involved in DNA damage repair, that control the response of HNSCC and glioblastoma cell models to radiotherapy (x-rays and proton beam therapy). This is achieved utilising tumour cells grown as monolayers (in 2D) and more importantly those in 3D (spheroids and patient-derived organoids), which more accurately reflect the structure and environment of the original tumour and how this responds to treatment. We are specifically examining the effect of targeted drugs/inhibitors, as well as using siRNA/drug screening approaches, to identify those that can enhance tumour cell killing in response to radiotherapy, and therefore which may be translated into the clinic for future benefit of patients with HNSCC and glioblastoma.

    The Biochemistry of DNA Damage Repair

    Our cellular DNA is under constant attack from both endogenous and exogenous mutagens which can lead to the development of human diseases, such as premature aging, neurodegenerative diseases and cancer. Conversely, ionising radiation (radiotherapy) is a key cancer treatment that acts through the induction of DNA damage in the tumour cells. Our cells contain efficient DNA repair mechanisms that respond to damaged DNA bases, DNA single and double strand breaks of varying complexity that can prevent human disease development, although conversely in tumours this can create cells that are resistant to radiotherapy and chemotherapy. Therefore, it is important that we have a detailed understanding of the mechanisms and regulation of DNA damage repair pathways.

    We have a particular interest in the base excision repair (BER) pathway, which plays a vital role in repairing damaged DNA bases and DNA single strand breaks co-ordinated through the actions of specific enzymes. We have pioneered ongoing novel research demonstrating that post-translational modifications, particularly ubiquitylation, perform a key role in controlling the stability of BER proteins and therefore controls the response of cells to DNA damaging agents, such as radiotherapy. Indeed, we have identified specific enzymes (E3 ubiquitin ligases and deubiquitylation enzymes) that modulate ubiquitylation-dependent proteasomal degradation of key BER proteins, and therefore play vital roles in the cellular DNA damage response, and in the maintenance of genome stability. We aim to use this knowledge to further understand how these mechanisms control the onslaught of the damage to our DNA and which is important for disease prevention, but also whether enzymes within these pathways in tumour cells can be targeted with drugs/inhibitors to enhance the response to treatment, particularly radiotherapy.

  • Peer-reviewed articles

    1.      Nickson, C.M., Fabbrizi, M.R., Carter, R.J., Hughes, J.R., Kacperek, A., Hill, M.A., and Parsons, J.L. (2021) USP9X is required to maintain cell survival in response to high-LET radiation. Front. Oncol., 11:671431. doi: 10.3389/fonc.2021.671431.

    2.      Clifford, R.E., Govindarajah, N., Bowden, D., Sutton, P., Glenn, M., Darvish-Damavandi, M., Buczacki, S., McDermott, U., Szulc, Z., Ogretmen, B., Parsons, J.L., and Vimalachandran, D. (2020) Targeting acid ceramidase to improve the radiosensitivity of rectal cancer. Cells., 9 (12):2693. doi: 10.3390/cells9122693.

    3.      Hughes, J.R., and Parsons, J.L. (2020) The E3 ubiquitin ligase NEDD4L targets OGG1 for ubiquitylation and modulates the cellular DNA damage response. Front. Cell Dev. Biol., 8:607060. doi: 10.3389/fcell.2020.607060.

    4.      Vitti, E-T., Kacperek, A., and Parsons, J.L. (2020) Targeting DNA double-strand break repair enhances radiosensitivity of HPV-positive and HPV-negative head and neck squamous cell carcinoma to photons and protons. Cancers., 12 (6):1490, doi: 10.3390/cancers12061490.

    5.      Hussain, R., Coupland, S.E., Khzouz, J., Kalirai, H., and Parsons, J.L. (2020) Inhibition of ATM increases radiosensitivity of uveal melanoma cells to photons and protons. Cancers., 12 (6):1388, doi: 10.3390/cancers12061388.

    6.      Richardson, A., Powell, A.K., Sexton, D.W., Parsons, J.L., Reynolds, N.J., and Ross, K. (2020) microRNA-184 is induced by store-operated calcium entry and regulates early keratinocyte differentiation. J. Cell Physiol., doi: 10.1002/jcp.29579.

    7.      Bennett, L., Madders, E.C.E.T, and Parsons, J.L. (2020) HECTD1 promotes base excision repair in nucleosomes through chromatin remodelling. Nucleic Acids Res., 48 (3), 1301-1313, doi: 10.1093/nar/gkz1129.

    8.      Singh, A.N., Oehler, J., Torrecilla, I., Kilgas, S., Li, S., Vaz, B., Guerillon, C., Fielden, J., Hernandez-Carralero, E., Cabrera, E., Tullis, I.D., Meerang, M., Barber, P.R., Freire, R., Parsons, J., Vojnovic, B., Kiltie, A.E., Mailand, N., and Ramadan, K. (2019) The p97-Ataxin 3 complex regulates homeostasis of the DNA damage response E3-ubiquitin ligase RNF8. EMBO J., 38 (21), doi: 10.15252/embj.2019102361.

    9.      Albelazi, M.S, Martin, P.R., Mohammed, S., Mutti, L., Parsons, J.L., and Elder, R.H. (2019) The biochemical role of the human NEIL1 and NEIL3 DNA glycosylases on model DNA replication forks. Genes, 10 (4):315, doi: 10.3390/genes10040315.

    10.   Carter, R.J., Nickson, C.M., Thompson, J.M., Kacperek, A., Hill, M.A., and Parsons, J.L. (2019) Characterisation of deubiquitylating enzymes involved in the cellular response to high-LET ionising radiation and complex DNA damage Int. J. Radiat. Oncol. Biol. Phys., 104 (3), 656-665, doi: 10.1016/j.ijrobp.2019.02.053.

    11.   Williams, S.C., and Parsons, J.L. (2018) NTH1 is a new target for ubiquitylation-dependent regulation by TRIM26 required for the cellular response to oxidative stress. Mol Cell Biol., 38 (12), e00616-17. doi: 10.1128/MCB.00616-17.

    12.   Bowden, D.L, Sutton, P.A., Wall, M.A., Jithesh, P.V., Jenkins, R.E., Palmer, D.H., Goldring, C.E., Parsons, J.L., Kitteringham, N.R., Park, B.K., and Vimalchandran, D. (2018) Proteomic profiling of rectal cancer reveals acid ceramidase is implicated in radiation response. J. Proteomics, 179, 53-60, doi: 10.1016/j.jprot.2018.02.030.

    13.   Carter, R.J, Nickson, C.M., Kacperek, A., Thompson, J., Hill, M.A., and Parsons, J.L. (2018) Complex DNA damage induced by high-LET α-particles and protons triggers a specific cellular DNA damage response. Int. J. Radiat. Oncol. Biol. Phys., 100 (3), 776-784, doi: 10.1016/j.ijrobp.2017.11.012.

    14.   Martin, P.R, Couvé, S., Zutterling, C., Albelazi, M.S., Groisman, R., Matkarimov, B.T., Parsons, J.L., Elder, R.H., and Saparbaev, M.K. (2017) The human DNA glycosylases NEIL1 and NEIL3 excise psoralen-induced DNA-DNA cross-links in a four-stranded DNA structure. Scientific reports, 7 (1), 17438, doi: 10.1038/s41598-017-17693-4.

    15.   Nickson, C.M., Moori, P., Carter, R.J., Rubbi, C.P., and Parsons, J.L. (2017) Misregulation of DNA damage repair pathways in HPV-positive head and neck squamous cell carcinoma contributes to cellular radiosensitivity. Oncotarget, 8 (18), 29963-29975, doi: 10.18632/oncotarget.16265.

    16.   Edmonds, M.J., Carter. R.J., Nickson, C.M., Williams, S.C., and Parsons, J.L. (2017) Ubiquitylation-dependent regulation of NEIL1 by Mule and TRIM26 is required for the cellular DNA damage response. Nucleic. Acids Res., 45 (2), 726-738, doi: 10.1093/nar/gkw959.

    17.   Orlando, G., Khoronenkova, S.V., Dianova, I.I., Parsons, J.L., and Dianov, G.L. (2014) ARF induction in response to DNA strand breaks is regulated by PARP1. Nucleic Acids Res., 42 (4), 2320-2329.

    18.   Parsons, J.L., Khoronenkova, S.V., Dianova, I.I., Ternette, N., Kessler, B.M., Datta, P.K., and Dianov, G.L. (2012) Phosphorylation of PNKP by ATM prevents its proteasomal degradation and enhances resistance to oxidative stress. Nucleic Acids Res., 40 (22), 11404-11415.

    19.   Khoronenkova, S.K., Dianova, I.I., Ternette, N., Kessler, B.M., Parsons, J.L., and Dianov, G.L. (2012) ATM-dependent down-regulation of USP7/HAUSP by PPM1G activates p53 response to DNA damage. Mol Cell., 45 (6), 801-813.

    20.   Markkanen, E., van Loon, B., Ferrari, E., Parsons, J.L., Dianov, G.L., and Hubscher, U. (2012) Regulation of oxidative DNA damage repair by DNA polymerase  and MutYH by cross-talk of phosphorylation and ubiquitination. PNAS., 109 (2), 437-442.

    21.   Meisenberg, C., Tait, P.S., Dianova, I.I., Wright, K., Edelmann, M.J., Ternette, N., Tasaki, T., Kessler, B.M., Parsons, J.L., Kwon, Y.T., and Dianov, G.L. (2012) Ubiquitin ligase UBR3 regulates cellular levels of the essential DNA repair protein APE1 and is required for genome stability. Nucleic Acids Res., 40 (2), 701-711.

    22.   Altun, A., Kramer, H.B., Willems, L.I., McDermott, J.L., Leach, C.A., Goldenberg, S.J., Suresh Kumar, K.G., Konietzny, R., Fischer, R., Kogan, E., Mackeen, M.M., McGouran, J., Khoronenkova, S.V., Parsons, J.L., Dianov, G.L., Nicholson, B., and Kessler, B.M. (2011) Activity-based chemical proteomics accelerates inhibitor development for deubiquitylating enzymes. Chemistry and Biology, 18 (11), 1401-1412.

    23.   Strom, C.E., Mortusewicz, O., Finch, D., Parsons, J.L., Lagerqvist, A., Johansson, F., Schultz., Erixon, K., Dianov, G.L., and Helleday, T. (2011) CK2 phosphorylation of XRCC1 facilitates dissociation from DNA and single-strand break formation during base excision repair. DNA repair, 10 (9), 961-969.

    24.   Parsons, J.L., Dianova, I.I., Khoronenkova, S.V., Edelmann, M.J., Kessler, B.M., and Dianov, G.L. (2011) USP47 is a deubiquitylating enzyme that regulates base excision repair by controlling steady-state levels of DNA polymerase β. Mol. Cell., 41 (5), 609-615.

    25.   Khoronenkova, S.V., Dianova, I.I., Parsons, J.L., and Dianov, G.L. (2011) USP7/HAUSP stimulates repair of oxidative DNA lesions. Nucleic Acids Res., 39 (7), 2604-2609.

    26.   Parsons, J.L., Dianova, I.I., Finch, D., Tait, P.S., Strom, C.E., Helleday, T., Dianov, G.L. (2010) XRCC1 phosphorylation by CK2 is required for its stability and efficient DNA repair. DNA repair, 9 (7), 835-841.

    27.   Parsons, J.L., Tait, P.S., Finch, D., Dianova, I.I., Edelmann, M.J., Khoronenkova, S.V., Kessler, B.M., Sharma, R.A., McKenna, W.G., and Dianov, G.L. (2009) Ubiquitin ligase ARF-BP1/Mule modulates base excision repair. EMBO J., 28 (20), 3207-3215.

    28.   Yang, J., Parsons, J.L., Caporali, S., Finch, D., D’Atri, S., Harrington, C., Nicolay, N., Singh, R., Farmer, P.B., Johnston, P.G., McKenna, W.G., Dianov, G.L., and Sharma, R.A (2009) Cells deficient in the base excision repair protein, DNA polymerase beta, are hypersensitive to oxaliplatin chemotherapy. Oncogene., 29 (3), 463-468.

    29.   Woodhouse, B.C., Dianova, I.I., Parsons, J.L., and Dianov, G.L. (2008) Poly(ADP-ribose) polymerase-1 modulates DNA repair capacity and prevents formation of DNA double strand breaks. DNA repair, 7 (6), 932-940.

    30.   Parsons, J.L., Tait, P.S., Finch, D., Dianova, I.I., Allinson, S.L., and Dianov, G.L. (2008) CHIP-mediated degradation and DNA damage-dependent stabilization regulate base excision repair proteins. Mol. Cell, 29 (4), 477-487.

    31.   Parsons, J.L., Kavli, B, Slupphaug, G., and Dianov, G.L. (2007) NEIL1 is the major DNA glycosylase that processes 5´-hydroxyuracil in close proximity to a DNA single strand break. Biochemistry, 46 (13), 4158-4163.

    32.   Parsons, J.L., Preston, B.D., O’Connor, T.R., and Dianov, G.L. (2007) DNA polymerase δ dependent repair of DNA single strand breaks containing 3′-end proximal lesions. Nucleic Acids Res., 35 (4), 1054-1063.

    33.   Schwerdtle, T., Hamann, I., Jahnke, G., Walter, I., Richter, C., Parsons, J.L., Dianov, G.L., and Hartwig, A. (2007) Impact of copper on the induction and repair of oxidative DNA damage, poly(ADP-ribosyl)ation and PARP-1 activity. Mol Nutr Food Res., 51(2), 201-10.

    34.   Walter I., Schwerdtle, T., Thuy, C., Parsons, J.L., Dianov, G.L. and Hartwig, A. (2007) Impact of arsenite and its methylated metabolites on PARP-1 activity, PARP-1 gene expression and poly(ADP-ribosyl)ation in cultured human cells. DNA Repair, 6 (1), 61-70.

    35.   Chipman, J.K., Parsons, J.L., and Beddowes, E.J. (2006) The multiple influences of glutathione on bromate genotoxicity: Implications for the dose-response relationship. Toxicology, 221 (2-3), 187-189.

    36.   Parsons, J.L., Dianova, I.I., Boswell, E., Weinfeld, M., and Dianov, G.L. (2005) End-damage specific proteins facilitate recruitment or stability of XRCC1 at the sites of DNA single-strand break repair. FEBS J., 272 (22), 5753-5763.

    37.   Parsons, J.L., Zharkov, D.O., and Dianov, G.L. (2005) NEIL1 excises 3'-end proximal oxidative DNA lesions resistant to cleavage by NTH1 and OGG1. Nucleic Acids Res., 33 (15), 4849-4856.

    38.   Madhusudan, S., Smart, F., Shrimpton, P., Parsons, J.L., Houlbrook, S., Talbot, D.C., Hammonds, T., Freemont, P.A., Dianov, G.L., and Hickson, I.D. (2005) Isolation of a small molecule inhibitor of DNA base excision repair: implications for cancer therapy. Nucleic Acids Res., 33 (15), 4711-4724.

    39.   Parsons, J.L., Dianova, I.I., Allinson, S.L., and Dianov, G.L. (2005) DNA polymerase β promotes recruitment of DNA ligase III-XRCC1 to sites of base excision repair. Biochemistry, 44 (31), 10613-10619.

    40.   Parsons, J.L., Dianova, I.I., and Dianov, G.L. (2005) APE1-dependent repair of DNA single strand breaks containing 3’-end 8-oxoguanine. Nucleic Acids Res., 33 (7), 2204-2209.

    41.   Parsons, J.L., Dianova, I.I., Allinson, S.L., and Dianov, G.L. (2005) Poly(ADP-ribose) polymerase-1 protects excessive DNA strand breaks from deterioration during repair in human cell extracts. FEBS J., 272 (8), 2012-2021.

    42.   Parsons, J.L., and Dianov, G.L. (2004) Monitoring base excision repair proteins on damaged DNA using human cell extracts. Biochem. Soc. Trans., 32 (6), 962-963.

    43.   Parsons, J.L., Dianova, I.I., and Dianov, G.L. (2004) APE1 is the major 3’-phosphoglycolate activity in human cell extracts. Nucleic Acids Res., 32 (12), 3531-3536.

    44.   Dianova, I.I., Sleeth, K.M., Allinson, S.L., Parsons, J.L., Breslin, C., Caldecott, K.W., and Dianov, G.L. (2004) XRCC1-DNA polymerase  interaction is required for efficient base excision repair. Nucleic Acids Res., 32 (8), 2550-2555.

    45.   Parsons, J.L. and Elder, R.H. (2003) DNA N-glycosylase deficient mice: a tale of redundancy. Mut. Res., 531 (1-2), 165-175.

    46.   Karahalil, B., de Souza-Pinto, N.C., Parsons, J.L., Elder, R.H. and Bohr, V.A. (2003) Compromised incision of oxidized pyrimidines in liver mitochondria of mice deficient in NTH1 and OGG1 glycosylases. J. Biol. Chem., 278 (36), 33701-33707.

    47.   Parsons, J.L. and Chipman, J.K. (2000) The role of glutathione in DNA damage by potassium bromate. Mutagenesis, 15 (4), 311-316.

    48.   Chipman, J.K., Davies, J.E., Parsons, J.L., Nair, J., O’Neill, G. and Fawell, J.K. (1998) DNA oxidation by potassium bromate; a direct mechanism or linked to lipid peroxidation? Toxicology, 126 (2), 93-102.

    Review articles

    1.      Fok, M., Toh, S., Easow, J., Fowler, H., Clifford, R., Parsons J., and Vimalachandran, D. (2021) Proton beam therapy in rectal cancer: A systematic review and meta-analysis. Surg. Oncol., 38:101638,

    2.      Fabbrizi, M.R., and Parsons J.L. (2020) Radiotherapy and the cellular DNA damage response: Current and future perspectives on head and neck cancer treatment. Cancer Drug Resist.,

    3.      Hughes, J.R., and Parsons J.L. (2020) FLASH radiotherapy: Current knowledge and future insights using proton beam therapy. Int. J. Mol. Sci., 21 (18):E6492, doi: 10.3390/ijms21186492.

    4.      Grundy, G.J., and Parsons J.L. (2020) Base excision repair and its implications to cancer therapy. Essays Biochem., EBC20200013, doi: 10.1042/EBC20200013.

    5.      Zhou, C., and Parsons J.L. (2020) The radiobiology of HPV-positive and HPV-negative head and neck squamous cell carcinoma. Expert Rev. Mol. Med., 22:e3, doi: 10.1017/erm2020.4.

    6.      Madders, E.C.E.T., and Parsons, J.L. (2020) Base excision repair in chromatin and the requirement for chromatin remodelling Adv. Exp. Med. Biol., 1241, 59-75, doi: 10.1007/978-3-030-41283-8_5.

    7.      Vitti, E-T., and Parsons, J.L. (2019) The radiobiological effect of proton beam therapy: Impact on DNA damage and repair. Cancers., 11 (7):946, doi: 10.3390/cancers11070946.

    8.      Govindarajah, N., Clifford, R, Bowden, D., Sutton, P.A., Parsons, J.L., and Vimalchandran, D. (2019) Sphingolipids and acid ceramidase as therapeutic targets in cancer therapy. Crit. Rev. Oncol. Hematol., 138, 104-111, doi: 10.1016/j.critrevonc.2019.03.018.

    9.      Clifford, R, Govindarajah, N., Parsons, J.L., Gollins, S., West, N.P., and Vimalchandran, D. (2018) Systematic review of treatment intensification using novel agents for chemoradiotherapy in rectal cancer. Br. J. Surg., 105 (12), 1553-1572.

    10.   Carter. R.J., and Parsons, J.L. (2016) Base excision repair: A pathway regulated by post-translational modifications. Mol. Cell Biol., 36 (10), 1426-1437.

    11.   Edmonds, M.J., and Parsons, J.L. (2014) Regulation of base excision repair proteins by ubiquitylation. Exp. Cell Res., 329 (1), 132-138.

    12.   Nickson, C.M., and Parsons, J.L. (2014) Monitoring regulation of DNA repair activities of cultured cells in-gel using the comet assay. Front. Genet., 5 (232), 1-11.

    13.   Parsons, J.L., Dianov G.L. (2013) Co-ordination of base excision repair and genome stability. DNA repair, 12 (5), 326-333.

    14.   Parsons, J.L., Nicolay, N.H., and Sharma, R.A. (2013) Biological and therapeutic relevance of non-replicative DNA polymerases to cancer. Antioxidants and Redox Signaling, 18 (8), 851-873.

    15.   Dianov, G.L., Meisenberg, C., and Parsons, J.L. (2011) Regulation of DNA repair by ubiquitylation. Biochemistry (Moscow), 76 (1), 69-79.

    16.   Dianov, G.L., and Parsons, J.L. (2007) Co-ordination of DNA single strand break repair. DNA repair, 6 (4), 454-460.

    Methods articles

    1.        Fabbrizi, M.R., Hughes, J.R., and Parsons, J.L. (2021) The enzyme-modified neutral comet (EMNC) assay for complex DNA damage detection. Methods Protoc., 4 (1):14. doi: 10.3390/mps4010014.

    2.        Parsons, J.L., and Dianov, G.L. (2012) In vitro base excision repair using mammalian cell extracts. Methods Mol Biol., 920, 245-262

    Book Chapters

    1.      Carter. R.J., and Parsons, J.L. (2018) Regulation of the base excision repair pathway by ubiquitination. Ed. Boutou, E., and Stürzbecher, H-W., InTechOpen.

    2.      Parsons, J.L., and Edmonds, M.J. (2015) The base excision repair pathway. In: Encyclopedia of Cell Biology. Ed. Bradshaw, R.A., and Stahl, P.D. Elsevier.

    3.      Dianov, G.L., Orlando, G., and Parsons, J.L. (2012) Tumour suppressor protein-mediated regulation of base excision repair in response to DNA damage. In: The cellular response to the genotoxic insult: The question of threshold for genotoxic carcinogens. Ed. Greim, H., and Albertini, R., The Royal Society.

    4.      Parsons, J.L., Boswell, E., and Dianov, G.L. (2006) Processing of 3′-end modified DNA strand breaks induced by oxidative damage. In: Oxidative Damage to Nucleic Acids. Ed. Evans, M.D., and Cooke, M.S.,

  • Novel insights into the cellular response to complex DNA damage induced by proton beam therapy

    Medical Research Council (MRC) – September 2021-August 2024


    Realizing the radiobiological impact of protons and high-LET particles in head and neck cancer and glioblastoma models

    National Institutes of Health (NIH) – July 2021-April 2026


    Profiling ADP-ribosylation enzymes and PARP inhibition in head and neck squamous cell carcinoma

    North West Cancer Research (NWCR) – November 2019-November 2024

    Advanced technologies for radiobiology and clinical radiotherapy

    Science and Technology Facilities Council (STFC) – October 2019-September 2021

    Improving the biological response of proton beam therapy in head and neck cancer

    North West Cancer Research (NWCR) – June 2019-August 2022

    Isolation and identification of the chromatin remodelling enzymes required for base excision repair

    North West Cancer Research (NWCR) – October 2017-September 2020

    Proton beam therapy in head and neck squamous cell carcinoma and uveal melanoma

    North West Cancer Research (NWCR) – October 2016-September 2020

    The radiobiology of proton therapy

    North West Cancer Research (NWCR) – March 2016-February 2019

    The cellular response to complex DNA damage induced by ionising radiation

    Medical Research Council (MRC) – November 2014-November 2017

    Molecular mechanism of regulation of the cellular protein levels of endonuclease III homologue (NTH1), in response to DNA damage

    North West Cancer Research (NWCR) – October 2014-September 2017

    The cellular response to DNA damage: Ubiquitylation-dependent regulation of 8-oxoguanine DNA glycosylase (OGG1)

    North West Cancer Research (NWCR) – October 2013-September 2016