Alison Lloyd Research Group

1985 - BSc Biochemistry - UCL
1989 - PhD - University of London (Chester Beatty Labs, Institute of Cancer Research)
Alison Lloyd
Tel: 020 7679 2240
Fax: 020 7679 7805
1984 Biochemistry Prize (University College London)
1989 EMBO Long Term Fellowship
1990 EEC Cancer Training Fellowship
1993 National Neurofibromatosis Foundation Young Investigator Award; Jaffa Fellowship
1998 Cancer Research UK Senior Cancer Research Fellowship
2004 Renewal of Cancer Research UK Senior Cancer Research Fellowship
2006 Readership in the Dept. of Biochemistry, UCL
2009 Professor of Cell Biology, FLS, UCL
2015 EMBO Member
Previous Posts: 
1989 - Postdoctoral Fellow - Institut de Chimie Biologique, Strasbourg, France
1993 - Postdoctoral Fellow - ICRF, London
1998 - CRUK Senior Cancer Research Fellow/Group Leader – LMCB, UCL
2009 - Professor of Cell Biology - UCL

Cell growth and tissue regeneration

Schwann cells are the main glial cells of the peripheral nervous system. Properties of these cells make them a powerful model system for studying two fundamental biological processes: (1) Cell growth (2) Tissue regeneration. Using a combination of primary in vitro culture systems and in vivo mouse models we aim to study the molecular and cellular mechanisms underlying the homeostatic regulation of these processes and how they become deregulated in diseases such as cancer. These studies should identify novel pathways important in these processes and new targets for regenerative medicine and cancer therapeutics.


Cell growth

Homeostasis in the adult requires a balance of positive and negative regulatory stimuli to control cell size and cell number. Whether a cell divides, grows or dies depends both on the levels of extracellular signals and the intrinsic ability of a cell to respond to these signals. Cell growth (addition of volume/mass), as cell proliferation and survival, requires an instructive signal but the signalling pathways and cell biology underlying cell growth are relatively understudied. Moreover, the additional mass required for tumour formation, requires deregulated growth pathways as well as a loss of proliferative controls but how oncogenic changes effect cell growth control is poorly understood.
Growth is often thought of as a uniform process however, specific cells contain different amounts of protein, membranes and organelles and these can change in response to specific stimuli. How cell set their size, count their organelles and adapt these to changing environments remain key unanswered questions in cell biology.


Enormous variation in cell size and organelle proportionality dependent on instructive extracellular signals.

Projects in the lab include the following

  • Identification of novel cell growth pathways
  • Regulation of organelle biogenesis
  • Cellular mechanisms underlying cell growth
  • Oncogenic regulation of cell growth

Tissue regeneration

The peripheral nervous system is one of the few tissues in the mammalian adult, which is capable of extensive regeneration. This process is all the more remarkable, in that repair can reconnect andre-establish fully transected nerves – requiring both the production of new tissue to bridge the gap between the nerve stumps and the accurate direction of regrowing axons back to their targets. Schwann cells are known to play a pivotal role in this process. In the adult, these highly specialised cells are normally in a quiescent state, myelinating larger axons or bundling together groups of smaller axons. Upon injury however, they dedifferentiate en masse to a progenitor/stem-like state and the proliferation and organisation of these cells is known to be critical for the repair process. Schwann cell number and state is strictly controlled by the axon both during development and following repair. Imbalances in this tightly regulated system would be predicted to result in either degenerative disorders or hyperproliferative disorders such as cancer. Consistent with this view, Schwann cell tumours, especially neurofibromas, resemble an unrepaired wounded nerve, in that Schwann cells within the tumours are dedifferentiated and proliferate in the absence of axonal contact in a mixture of fibroblasts and inflammatory cells.



Projects in the lab include the following

  • Understanding the plasticity of the Schwann cell differentiation state
  • Novel mouse models for studying tumour development in NF1
  • Role of the microenvironment in the repair process and cancer


Lab Members: 
Rosalba Camicia
Postdoctoral Fellow
Anne-Laure Cattin
Xavier Garcia Fontana
Ilaria Napoli
Erica Torchiaro
PhD Student
Lucie Van Emmenis
Highlighted publication = Selected Publication

  • 2015
  • Highlighted publication
    Cattin, A. L., Burden, J. J., Van Emmenis, L., Mackenzie, F. E., Hoving, J. J., Garcia Calavia, N., . . . Lloyd, A. C. (2015). Macrophage-Induced Blood Vessels Guide Schwann Cell-Mediated Regeneration of Peripheral Nerves. Cell, 162 (5), 1127-1139. doi:10.1016/j.cell.2015.07.021
  • Jessen, K. R., Mirsky, R., & Lloyd, A. C. (2015). Schwann Cells: Development and Role in Nerve Repair. COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY, 7 (7), ARTN a020487. doi:10.1101/cshperspect.a020487
  • 2014
  • Plotkin, S. R., Albers, A. C., Babovic-Vuksanovic, D., Blakeley, J. O., Breakefield, X. O., Dunn, C. M., . . . Lloyd, A. C. (2014). Update from the 2013 international neurofibromatosis conference. American Journal of Medical Genetics, Part A, 164 (12), 2969-2978. doi:10.1002/ajmg.a.36754
  • 2013
  • Highlighted publication
    Ribeiro, S., Napoli, I., White, I. J., Parrinello, S., Flanagan, A. M., Suter, U., . . . Lloyd, A. C. (2013). Injury signals cooperate with Nf1 loss to relieve the tumor-suppressive environment of adult peripheral nerve. Cell Rep, 5 (1), 126-136. doi:10.1016/j.celrep.2013.08.033
  • Highlighted publication
    Lloyd, A. C. (2013). The regulation of cell size. Cell, 154 (6), 1194-1205. doi:10.1016/j.cell.2013.08.053
  • 2012
  • Highlighted publication
    NAPOLI, I., NOON, L. A., RIBEIRO, S., KERAI, A. P., PARRINELLO, S., ROSENBERG, L. H., . . . LLOYD, A. C. (2012). A central role for the ERK-signaling pathway in controlling Schwann cell plasticity and peripheral nerve regeneration in vivo. NEURON, 73 (4), 729-742.
  • Roberts, S. A., & Lloyd, A. C. (2012). Aspects of cell growth control illustrated by the Schwann cell. Curr Opin Cell Biol, 24 (6), 852-857. doi:10.1016/
  • Highlighted publication
    Collins, M. J., Napoli I, Ribeiro, S., Roberts, S., & Lloyd, A. C. (2012). Loss of Rb Cooperates with Ras to Drive Oncogenic Growth in Mammalian Cells. Current Biology, 22 (19), 1765-1773.
  • Kalamarides, M., Acosta, M. T., Babovic-Vuksanovic, D., Carpen, O., Cichowski, K., Evans, D. G., . . . Ratner, N. (2012). Neurofibromatosis 2011: a report of the Children's Tumor Foundation annual meeting. Acta Neuropathol, 123 (3), 369-380. doi:10.1007/s00401-011-0905-0
  • 2011
  • Feber, A., Wilson, G. A., Zhang, L., Presneau, N., Idowu, B., Down, T. A., . . . Beck, S. (2011). Comparative methylome analysis of benign and malignant peripheral nerve sheath tumors. Genome Res, 21 (4), 515-524. doi:10.1101/gr.109678.110
  • 2010
  • Danovi, D., Cremona, C. A., Machado-da-Silva, G., Basu, S., Noon, L. A., Parrinello, P., & Lloyd, A. C. (2010). A genetic screen for anchorage-independent proliferation in mammalian cells identifies a membrane-bound neuregulin. PLoSONE, 5 (7), e11774-?.
  • Highlighted publication
    Parrinello, S., Napoli, I., Ribeiro, S., Wingfield Digby, P., Fedrova, M., Parkinson, D. B., . . . Lloyd, A. C. (2010). EphB signalling directs peripheral nerve regeneration through Sox2-dependent Schwann cell sorting. Cell, 143, 145-155.
  • 2009
  • Echave, P., Machado-da-Silva, G., Arkell, R. S., Duchen, M. R., Jacobson, J., Mitter, R., & Lloyd, A. C. (2009). Extracellular growth factors and mitogens cooperate to drive mitochondrial biogenesis. Journal of Cell Science, 122 (24), 4516-4525.
  • Cremona, C. A., & Lloyd, A. C. (2009). Loss of anchorage in checkpoint-deficient cells increases genomic instability and promotes oncogenic transformation. J Cell Sci, 122 (Pt 18), 3272-3281. doi:10.1242/jcs.047126
  • Parrinello, Lloyd, S. A., & A, C. (2009). Neurofibroma development in NF1--insights into tumour initiation. Trends in Cell Biology, 19 (8), 395-403.
  • 2008
  • Parkinson, D. B., Bhaskaran, A., Arthur-Farraj, P., Noon, L. A., Woodhoo, A., Lloyd, A. C., . . . Jessen, K. R. (2008). c-Jun is a negative regulator of myelination. The Journal of Cell Biology, 181 (4), 625-637. doi:10.1083/jcb.200803013
  • Rubio, D., Garcia, S., Paz, M. F., De, L. C. T., Lopez-Fernandez, L. A., Lloyd, A. C., . . . Bernad, A. (2008). Molecular characterization of spontaneous mesenchymal stem cell transformation. PLoS ONE, 3 (1), e1398-?.
  • Highlighted publication
    Parrinello, S., Noon, L. A., Harrisingh, M. C., Wingfield Digby, P., Echave, P., Cremona, C. A., . . . Lloyd, A. C. (2008). NF1 loss disrupts Schwann cell-axonal interactions: a novel role for semaphorin 4F. Genes and Development, 22 (23), 3335-3348.
  • 2007
  • Highlighted publication
    Echave, P., Conlon, I. J., & Lloyd, A. C. (2007). Cell size regulation in mammalian cells. Cell Cycle, 6 (2), 218-224.
  • Rubio, D., Garcia, S., De, L. C. T., Paz, M. F., Lloyd, A. C., Bernad, A., & Garcia-Castro, J. (2007). Human mesenchymal stem cell transformation is associated with a mesenchymal-epithelial transition. Experimental Cell Research, 314 (4), 691-698.
  • Noon, L. A., & Lloyd, A. C. (2007). Treating Leprosy: an Erb-al remedy?. Trends in Pharmacological Sciences, 28 (3), 103-105.
  • 2006
  • Lloyd, A. C. (2006). Distinct functions for ERKs?. Journal of Biology, 5, 13-?.
  • 2005
  • Rubio, D., Garcia-Castro, J., Martin, M. C., de, L. F. R., Cigudosa, J. C., & Lloyd, A. C. A. B. A. (2005). Spontaneous human adult stem cell transformation. cancer research, 65 (8), 3035-3039.
  • 2004
  • Conlon, I., Lloyd, A. C., & Raff, M. C. (2004). Co-ordination of cell growth and cell-cycle progression in proliferating mammalian cells. In M. N. Hall, M. Raff, G. Thomas (Eds.), Cell Growth: Control of Cell Size (pp. 85-101). Cold Spring Harbour Laboratory Press.
  • Perez-Nadales, E., & Lloyd, A. C. (2004). Essential function for ErbB3 in breast cancer proliferation. Breast Cancer Research, 6, 137-139.
  • Harrisingh, M. C., & Lloyd, A. C. (2004). Ras/Raf/ERK signalling and NF1. Cell Cycle, 3 (10), 1255-1258.
  • Highlighted publication
    Harrisingh, M. C., Perez-Nadales, E., Parkinson, D. B., Malcolm, D. S., Mudge, A. W., & Lloyd, A. C. (2004). The Ras/Raf/ERK signalling pathway drives Schwann cell dedifferentiation. The EMBO Journal, 23 (15), 3061-3071. doi:10.1038/sj.emboj.7600309
  • 2003
  • Mitchell, P. J., Perez-Nadales, E., Malcolm, D. S., & Lloyd, A. C. (2003). Dissecting the Contribution of p16 INK4A and the Rb Family to the Ras Transformed Phenotype. Molecular and Cellular Biology, 23 (7), 2530-2542. doi:10.1128/MCB.23.7.2530-2542.2003
  • 2002
  • Lloyd, A. C. (2002). Limits to Lifespan. Nature Cell Biology, 4, 0.
  • Lloyd, A. C. (2002). Limits to lifespan. Nat Cell Biol, 4 (2), E25-E27. doi:10.1038/ncb0202-e25
  • 2001
  • Mathon, N. F., & Lloyd, A. C. (2001). Cell Senescence and Cancer. Nature Reviews Cancer, 1, 203-213.
  • Tang, D. G., Tokumoto, Y. M., Apperly, J. A., Lloyd, A. C., & Raff, M. C. (2001). Lack of replicative senescence in cultured oligodendrocyte precursor cells. Science, 291 (5505), 868-871. doi:10.1126/science.1056780
  • Highlighted publication
    Mathon, N. F., Malcolm, D. S., Harrisingh, M. C., Cheng, L., & Lloyd, A. C. (2001). Lack of replicative senescence in normal rodent glia. Science, 291, 872-875. doi:10.1126/science.1056782
  • 2000
  • Lloyd, A. (Ed.). (2000). p53: Only ARF the story. Nature Cell Biology, 2, 48-50.
  • 1998
  • Lloyd, A. C. (1998). Ras versus cyclin-dependent kinase inhibitors. Current Opinion in Genetics and Development, 8, 43-48.
  • 1997
  • Lloyd, A. C., Obermuller, F., Staddon, S., Barth, C., McMahon, M., & Land, H. (1997). Co-operating Oncogenes Target Cyclin/Cdk Activity. Genes and Development, 11, 663-677.
  • Sewing, A., Wiseman, B., Lloyd, A. C., & Land, H. (1997). high Intensity Raf Signal Causes Cell-Cycle Arrest Mediated by p21Cip1. Molecular and Cellular Biology, 17, 5588-5597.
  • 1991
  • Lloyd, A. C., Yancheva, N., & Wasylyk, B. (1991). Transformation suppressor Activity of a Jun transcription Factor Lacking its Activation Domain. Nature, 352, 635-638.
  • 1989
  • Flores, P., Gutman, A., Imler, J. L., Lloyd, A. C., Schneikert, J., Wasylyk, C., & Wasylyk, B. (1989). AP1 and PEA3 are Nuclear targets for Transcriptional Activation by Non-nuclear oncogenes. Hormones and Cell Regulation, 198, 57-62.
  • Lloyd, A. C., Davies, S. A., Crossley, I., Whitaker, M., Houslay, M. D., Hall, A., . . . Wakelam, M. J. O. (1989). Bombesin stimulation of inositol 1,4,5-trisphosphate generation and intracellular calcium release is amplified in a cell line overexpressing the N-ras proto-oncogene. Biochemical Journal, 260, 813-819.
  • Lloyd, A. C., Paterson, H. F., Morris, J. D., Hall, A., & Marshall, C. J. (1989). p21H-Ras Induced Morphological Transformation and Increases in c-myc Expression are Independent of functional Protein kinase C. The EMBO Journal, 8, 1099-1104.
  • Morris, J. D. H., Price, B., Lloyd, A. C., Self, A. J., Marshall, C. J., & Hall, A. (1989). Scrape-loading of Swiss 3T3 cells with ras protein rapidly activates protein kinase C in the absence of phosphoinositide hydrolysis. Oncogene, 4, 27-31.
  • Marshall, C. J., Lloyd, A. C., Morris, J. D., Paterson, H., Price, B., & Hall, A. (1989). Signal transduction by p21ras. International Journal of Cancer - Supplement, 4, 29-31.
  • 1988
  • Hall, A., Cales, C., Hancock, J. F., Lloyd, A. C., Self, A., Gardener, S., . . . Marshall, C. J. (1988). Analysis of mammalian Ras effector function. Cold Spring Harbor Symposium on Quantitative Biology, 53, 855-862.
  • 1986
  • Lloyd, A. C., Carpenter, C. A., & Saggerson, E. D. (1986). Intertissue differences in the hysteretic behaviour of carnitine palmitoyltransferase in the presence of malonyl-CoA. Biochemical Journal, 237, 289-291.
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