Dr Maarten Hoogenkamp PhD

Dr Maarten Hoogenkamp

Institute of Cancer and Genomic Sciences
Leukaemia & Lymphoma Research Bennett Fellow

Contact details

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

Maarten Hoogenkamp is a Leukaemia & Lymphoma Research Bennett Fellow. He joined the Institute of Cancer and Genomic Sciences in summer 2012 to establish his own independent research group.

His research focuses on the dynamic interplay between transcription factor complexes and the chromatin, how this regulates cellular identity during differentiation, and how these interactions change during cancerogenesis. This is in particular studied within the context of the haematopoietic system.

Qualifications

  • PhD in Medicine, University of Amsterdam, The Netherlands, 2007
  • MSc in Biology, Utrecht University, The Netherlands, 1999

Biography

From 1994 to 1999 Maarten Hoogenkamp studied biology at Utrecht University (NL). He performed his PhD in Medicine from 1999 to 2004 at the University of Amsterdam (NL) by studying the transcriptional regulation underlying the zonal expression of proteins in the liver.

Maarten then moved to the University of Leeds (UK) as a postdoc with Professor Constanze Bonifer, where he studied the regulation of transcription factor genes in relation to the cellular identity within the haematopoietic system.

After being awarded a Leukaemia & Lymphoma Research Bennett Fellowship he moved to the University of Birmingham in the summer of 2012 to start up his independent line of research. His research focusses on the molecular mechanisms driving differentiation and cell fate decisions in healthy cells and how these processes are perturbed in disease and in particular during cancerogenesis. This is studied at the level of transcription factor binding to the DNA and the resulting changes to the chromatin structure and gene expression within the haematopoietic system.

Teaching

Dr. Hoogenkamp currently has no undergraduate teaching responsibilities

Postgraduate supervision

Maarten supervises / has supervised Masters students and PhD students. He is interested in supervising MRes and PhD students in the following areas:

  • The involvement of the LMO proteins in leukaemia
  • The interaction between co-expressed LMO proteins
  • The role of LMO1 in neuroblastoma

Research

The LIM-domain only (LMO) family of transcription factors consists of four proteins, which are all implicated in cancerogenesis. LMO1, 2, 3 and 4 are closely related proteins which are involved in DNA binding complexes, but do not bind the DNA themselves.

My lab is particular interested in the function of LMO2 in haematopoiesis. Genomic translocations of the LMO2 gene are causal to the development of T-cell acute lymphoblastic leukaemia (T-ALL). For leukaemia to develop secondary mutations are required. We want to understand what the mechanisms are that underly the initial steps in T-ALL leukaemogenesis. Furthermore, LMO2 is also overexpressed in leukaemia of other haematopoietic lineages, however, its involvement in these leukaemia is not clear.
Besides the function of LMO2 in diseased cells, LMO2 is of vital importance to early haematopoietic development. Cells lacking LMO2 cannot form haematopoietic stem cells due to a developmental block at an earlier stage. We are investigating the exact cause of this block, using an embryonic stem (ES) cell differentiation protocol, with the aim to determine which LMO2 functions are vital in normal haematopoietic development.

In addition, we have found that also LMO1 and LMO4 are expressed at particular stages of haematopoietic development. LMO1 is well known for its leukaemic function after genomic translocation and LMO4 is an established oncogene in breast cancer. Recently LMO4 was shown to be overexpressed in particular T-ALL cases with an immature phenotype (leukaemia consisting of immature T-cells), which are associated with poor outcome. We have therefore started to investigate these factors in our model systems.

Other activities

Occasional involvement in charity fundraising events

Publications

Zhang, H., Ye, M., Alberich-Jorda, M., Amabile, G., Yang, H., Staber, P.B., DiRuscio, A., Welner, R., Ebralidze, A., Zhang, J., Levantni, E., Lefebvre, V., Valk., P.J.M., Delwel, R., Hoogenkamp, M., Nerlov, C., Cammenga, J., Saez, B., Scadden, D.T., Bonifer, C., Tenen, D.G. (2013) Sox4 is a key oncogenic target in C/EBPα mutant acute myeloid leukemia. Cancer Cell in press in press

Ladopoulos, V., Hofemeister, H., Hoogenkamp, M., Riggs, A.D., Stewart, A.F., Bonifer, C. (2013) The histone methyltransferase KMT2B is required for RNA polymerase II association and protection from DNA-methylation at the MagohB CpG island promoter. Mol. Cell. Biol. 33, 1383-139333, 1383-1393

Ptasinska, A., Assi, S.A., Mannari, D., James, S.R., Williamson, D., Dunne, J., Hoogenkamp, M., Wu, M., Care, M., McNeill, H., Cauchy, P., Cullen, M., Tooze, R.M., Tenen, D.G., Young, B.D., Cockerill, P.N., Westhead, D.R., Heidenreich, O., Bonifer, C.(2012) Depletion of RUNX1/ETO in t(8;21) AML cells leads to genome-wide changes in chromatin structure and transcription factor binding. Leukemia 26, 1829-1841

Leddin, M.*, Perrod, C.*, Hoogenkamp, M.*, Ghani, S.*, Assi, S., Heinz, S., Wilson, N.K., Follows, G.A., Schönheit, J., Vockentanz, L., Mosamam, A., Chen, W., Tenen, D.G., Westhead, D.R., Göttgens, B., Bonifer, C., Rosenbauer, F. (2011) Two distinct auto-regulatory loops operate at the Pu.1 locus in B cells and myeloid cells. Blood 117, 2827-2838hani, S.*, Assi, S., Heinz, S., Wilson, N.K., Follows, G.A., Schönheit, J., Vockentanz, L., Mosamam, A., Chen, W., Tenen, D.G., Westhead, D.R., Göttgens, B., Bonifer, C., Rosenbauer, F. (2011) Two distinct auto-regulatory loops operate at the Pu.1 locus in B cells and myeloid cells. 117, 2827-2838

Bruno, L., Mazzarella, L., Hoogenkamp, M., Hertweck, A., Cobb, B.S., Sauer, S., Hadjur, S., Leleu, M., Naoe, Y., Telfer, J., Bonifer, C., Taniuchi, I., Fisher, A.G., Merkenschlager, M. (2009) Runx proteins regulate FoxP3 expression. J. Exp. Med. 206, 2329-2337206, 2329-2337

Hoogenkamp, M.*, Lichtinger, M.*, Krysinska, H.*, Lancrin, C.*, Clarke, D., Williamson, A., Mazzarella, L., Ingram, R., Jorgensen, H., Fisher, A., Tenen, D.G., Kouskoff, V., Lacaud, G., Bonifer, C. (2009) Early chromatin unfolding by RUNX1 – a molecular explanation for differential requirements during specification versus maintenance of the hematopoietic gene expression program. Blood 114, 299-309114, 299-309

Ebralidze, A.K., Guibal, F.C., Steidl, U., Zhang, P., Lee, S., Bartholdy, B., Jorda, M.A., Petkova, V., Rosenbauer, F., Huang, G., Dayaram, T., Klupp, J., O’Brien, K., Will, B., Hoogenkamp, M., Borden, K.L., Bonifer, C., Tenen, D.G. (2008) PU.1 expression is modulated by the balance of functional sense and antisense RNAs regulated by a shared cis-regulatory element. Genes Dev. 22, 2085-209222, 2085-2092

Hoogenkamp, M., Krysinska, H., Ingram, R., Huang, G., Barlow, R., Clarke, D., Ebralidze, A., Zhang, P., Tagoh, H., Cockerill, P.N., Tenen, D.G., Bonifer, C. (2007) The Pu.1 locus is differentially regulated at the level of chromatin structure and non-coding transcription by alternate mechanisms at distinct developmental stages of hematopoiesis. Mol. Cell. Biol. 27, 7425-7438 27, 7425-7438

*Joint authorship

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