Dr James Last PhD, BSc (Hons)

 

Research Fellow

School of Cancer Sciences

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Contact details

School of Cancer Sciences
University of Birmingham
Vincent Drive
Edgbaston
Birmingham
B15 2TT

About

James Last is a postdoctoral Research Fellow in the School of Cancer Sciences working in the laboratory of Professor Malcolm Taylor.

Qualifications

  • PhD in Cancer Sciences, University of Birmingham 2005 
  • BSc (Hons) in Molecular Cell Biology, University of Nottingham 1998

Biography

James qualified with a BSc (Hons) in Molecular Cell Biology from the University of Nottingham in 1998. Following this, he undertook a technician post in the Department of Cancer Studies in 1999, working in the laboratory of Professor Malcolm Taylor.

In 2000, James went on to study for a PhD in the same laboratory, studying the kinase activity of different mutant ATM proteins. After he graduated in 2005, James took up a postdoctoral position in Professor Taylor’s lab where he continues to study ataxia telangiectasia (A-T) and related disorders to A-T and their impact on DNA repair.

Teaching

  • BMedSci (tutorials)
  • MBChB BMS 2nd year (SGT)

Research

The main emphasis of James’ work is studying the function of the ATM gene, mutated in the autosomal recessive neurodegenerative disease ataxia telangiectasia (A-T). A-T patients show a complex phenotype including neurodegeneration, radiosensitivity, immunodeficiency but also an increased predisposition to the development of tumours, particularly of lymphoid origin.

The severity of the A-T phenotype shows variation and part of James’ work over the last 12 years has been to show a clear relationship between residual ATM kinase activity and a less severe clinical phenotype in A-T patients. Another aspect of his work helped establish that female carriers of ATM mutations are at an increased risk of developing breast cancer and that A-T patients themselves also have a higher risk of developing breast cancer than the normal population.

Several other neurodegenerative disorders share phenotypic similarities with A-T, including ATLD and the more recently discovered AOA1 and AOA2. James’ work over the last 6 years has been to identify UK AOA1 and AOA2 patients.

Part of James’ ongoing work is to help screen for A-T, AOA1 and AOA2 patients, as well as for patients with novel disorders similar to A-T.

Publications

Albertyn, C., Cawley, N., Taylor, A.T., Srinivasan, V., Last, J.I., Murphy, R.P. (2010) POG02 Variant ataxia telangiectasia in siblings with normal {alpha}-fetoprotein levels. J Neurol Neurosurg Psychiatry 81 (11), e48.

Verhagen, M.M.M., Abdo, W.F., Willemsen, M.A.A.P., Hogervorst, F.B.L., Smeets, D.F.C.M., Hiel, J.A.P., Brunt, E.R., van Rijn, M.A., Majoor Krakauer, D., Oldenburg, R.A., Broeks, A., Last, J.I., van’t Veer, L.J., Tijssen, M.A.J., Dubois, A.M.I., Kremer, H.P.H., Weemaes, C.M.R., Taylor, A.M.R., van Deuren, M. (2009) Clinical spectrum of Ataxia-Telangiectasia in adulthood. Neurology 73 (6), 430-437.

Dutton, A., Woodman, C.B., Chukwuma, M.B., Last, J.I.K., Wei, W., Vockerodt, M., Baumforth, K.R.N., Flavell, J.R., Rowe, M., Taylor, A.M.R., Young, L.S., Murray, P.G. (2007) BMI-1 is induced by the Epstein-Barr virus oncogene LMP1, and regulates the expression of viral target genes in Hodgkin’s lymphoma cells. Blood 109 (6), 2597-2603.

Hiel, J.A., van Engelen, B.G., Weemaes, C.M., Broeks, A., Verrips, A., ter Laak, H., Vingerhoets, H.M., van den Heuvel, L.P., Lammens, M., Gabreels, F.J., Last, J.I., Taylor, A.M. (2006) Distal spinal muscular atrophy as a major feature of adult-onset ataxia telangiectasia. Neurology 67 (2), 346-349.

Thompson, D., Duedal, S., Kirner, J., McGuffog, L., Last, J., Reiman, A., Byrd, P., Taylor, A.M.R., Easton, D. (2005) Cancer risks and mortality in heterozygous ATM mutation carriers. J Natl Cancer Inst. 97 (11), 813-822.

Meyer, S., Kingston, H., Taylor, A.M.R., Byrd, P.J., Last, J.I., Brennan, B.M., Trueman, S., Kelsey, A., Taylor, G.M., Eden, O.B. (2004) Rhabdomyosarcoma in Nijmegen Breakage Syndrome: strong association with perianal primary site. Cancer Genet Cytogenet. 154 (2), 169-174.

Sutton, I., Last, J.I.K., Byrd, P.J., Taylor, A.M.R. (2004) Adult-onset ataxia telangiectasia due to ATM 5762ins137 mutation homozygosity. Ann Neurol. 55 (6), 891-895.

Stankovic, T., Stewart, G.S., Moss, P.A.H., Fegan, C., Pettitt, A., Bedenham, T., Last, J.I.K., Byrd, P.J., Taylor, A.M.R. (2002) Ataxia telangiectasia mutated- deficient B-CLL occurs in pre-germinal centre cells and results in defective damage response and unrepaired chromosome damage. Blood 99, 300-309.

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