Professor Malcolm Taylor PhD

Professor Malcolm Taylor

Institute of Cancer and Genomic Sciences
Emeritus Professor of Cancer Genetics

Contact details

Address
Institute of Cancer and Genomic Sciences
University of Birmingham
Edgbaston
Birmingham
B15 2TT
UK

Malcolm Taylor is an Emeritus Professor of Cancer Genetics within the Institute of Cancer and Genomic Sciences. Malcolm has published over 120 Research papers and received consistent major support from Cancer Research UK as well as the Leukaemia Research Fund.

He also has a close relationship with the charity, the Ataxia -Telangiectasia Society and his laboratory is NCG designated for the confirmation of the clinical diagnosis of ataxia telangiectasia in the UK.

Qualifications

  • PhD in Cancer Studies 1973
  • MSc 1970 Radiobiology
  • BSc 1969 Biological Sciences

Biography

Professor Taylor gained his BSc in Biological Sciences at the University of London, Queen Elizabeth College, (now part of King’s College) in 1969. In 1970 he obtained an MSc in Radiobiology at the University of Birmingham, Department of Physics, and then moved to the Department of Cancer Studies where in 1973 he obtained his PhD.

While studying for his PhD in the Department of Cancer studies, Professor Taylor developed his lifelong interest in the genetic predisposition to cancer and particularly the role of the predisposition to cancer in patients with the neurodegenerative disorder ataxia telangiectasia

Teaching

  • MBChB
    • Year 2 - ‘Cancer: Causes to Cures'
  • BDS Year 1- Genetics 
  • BMedSc
    • Year 1 Genetics
    • Year 2 Cancer Biology
    • Year 3 option ‘Cancer pathogenesis and treatment’
    • Year 3 option ‘DNA damage pathways in human disease’.‘

Postgraduate supervision

Malcolm is interested in supervising doctoral students in the following areas

  • The role of the ATM gene in cancer development 
  • Identifying new defects in the cellular response to DNA damage

Research

  • Professor Taylor is interested in the cellular response to DNA damage, and particularly where a defective response can lead to cancer development. 
  • Particular interest in the ATM gene and the effects of biallelic mutation of this in the development of ataxia telangiectasia. 
  • Interest in the threshold level of ATM kinase activity required to ameliorate clinical and cellular phenotypes 
  • Range of clinical and cellular phenotypes associated with A-T. 
  • Range of tumour types associated with ataxia telangiectasia. 
  • Effects of loss of the components of the MRN (Mre11, Nbs1, Rad50) complex at both the cellular and clinical levels. 
  • Threshold levels of these proteins required for activity. 
  • Effect of loss of RNF168 protein. 
  • Interest in identifying new genes important in theDNA damage response 
  • Interest in a mouse model for ataxia telangiectasia 
  • Interest in mutations of the ATM gene in sporadic tumours, particularly breast cancer and lymphoid tumours.

Other activities

  • Chairman, Subgroup on Range of Human Radiosensitivity, Advisory Group on Ionizing Radiation, Health Protection Agency.
  • Formerly Member of Committee on Medical Aspects of Radiation in the Environment (COMARE).

Publications

Marston E, Weston V, Jesson J, Maina E, McConville C, Agathanggelou A, Skowronska A, Mapp K, Sameith K, Powell JE, Lawson S, Kearns P, Falciani F, Taylor M, Stankovic T Stratification of paediatric ALL by in vitro cellular responses to DNA double strand breaks provides insight into the molecular mechanisms underlying clinical response. Blood. 2009; 113: 117-126.

Stewart GS, Panier S, Townsend K, Al-Hakim AK, Kolas NK, Miller ES, Nakada S, Ylanko J, Olivarius S, Mendez M, Oldreive C, Wildenhain J, Tagliaferro A, Pelletier L, Taubenheim N, Durandy A, Byrd PJ, Stankovic T, Taylor AM, Durocher D. The RIDDLE syndrome protein mediates a ubiquitin-dependent signaling cascade at sites of DNA damage. Cell. 2009 136:420-34.

Barone G, Groom A, Reiman A, Srinivasan V, Byrd PJ and Taylor AM. Modeling ATM mutant proteins from missense changes confirms retained kinase activity. Human Mutation 2009; 30: 1222-1230

Mijke M.M. Verhagen, Farid W. Abdo, Michèl A.A.P. Willemsen Frans Hogervorst, Dominique F.C.M. Smeets, Johan Hiel, Ewout.R.P. Brunt, M.A. van Rijn, Danielle Majoor Krakauer, Rogier A. Oldenborg, Annegien Broeks, Last JI, L.J. van ’t Veer, Tijssen MA, Dubois AM, Kremer HP, Corry M.R. Weemaes, Taylor A.M.R., Marcel van Deuren. Clinical spectrum of Ataxia-Telangiectasia in adulthood. Neurology 2009, 73: 430-437.

Blackford AN, Patel RN, Forrester NA, Theil K, Groitl P, Stewart G, Taylor AMR, Morgan IM, Dobner T, Grand RJA, Turnell, AS. Adenovirus 12 E4orf6 inhibits ATR activation by promoting TOPBP1 degradation. Proc. Natl. Acad. Sci (USA). 2010 107; 12251-56.

Weston VJ, Oldreive CE, Skowronska A, Oscier DG, Pratt GE, Dyer MJS, Smith G, Powell JE, Rudzki Z, Kearns P, Moss PAH, Taylor AMR, Stankovic T. The PARP inhibitor olaparib induces significant killing of ATM deficient lymphoid tumour cells in vitro and in vivo. Blood 2010, 116: 4578-4587.

Exley AR, Buckenham S, Hodges E, Hallam R, Byrd P, Last J, Trinder C, Harris S, Screaton N, Williams AP, Taylor AM, Shneerson JM. Premature ageing of the immune system underlies immunodeficiency in ataxia telangiectasia. Clin Immunol. 2011 Mar 13. [Epub ahead of print]

View all publications in research portal

Expertise

Rare disease, ataxia telangiectasia