Ildiko Gyory

Direct contact details:Ildiko Gyory webimage

Tel: +44 (0)116 229 7011






Personal details

MD, PhD, Postdoctoral Fellow

I joined the Department of Biochemistry at the University of Leicester as a Lecturer in 2013. I have passion for a variety of key areas and specialise in Transcriptional, epigenetic and cell cycle regulation in B-lymphoid cancer.


1. Transcription factor EBF1 is essential for the maintenance of B cell identity and prevention of alternative fates in committed cells.
Nechanitzky R, Akbas D, Scherer S, Györy I, Hoyler T, Ramamoorthy S, Diefenbach A, Grosschedl R.
Nature Immunology. 2013 Jun 30. doi: 10.1038/ni.2641. [Epub ahead of print]

2.  Fejer G, Wegner MD, Györy I, Cohen I, Engelhard P, Voronov E, Manke T, Ruzsics Z, Dölken L, Prazeres da Costa O, Branzk N, Huber M, Prasse A, Schneider R, Apte RN, Galanos C, Freudenberg MA
Nontransformed, GM-CSF-dependent macrophage lines are a unique model to study tissue macrophage functions
Proc Natl Acad Sci U S A. 2013 Jun 11;110(24):E2191-8. doi: 10.1073/pnas.1302877110.  Epub 2013 May 24.

3. Zee T, Boller S, Györy I, Makinistoglu MP, Tuckermann JP, Grosschedl R, Karsenty G.
The transcription factor early B-cell factor 1 regulates bone formation in an osteoblast-nonautonomous manner.
FEBS Lett. 2013 Feb 5. doi:pii: S0014-5793(13)00094-X. 10.1016/j.febslet.2013.01.049. [Epub ahead of print]

4. Marcinowski L, Lidschreiber M, Windhager L, Rieder M, Bosse JB, Rädle B, Bonfert T, Györy I, de Graaf M, Prazeres da Costa O, Rosenstiel P, Friedel CC, Zimmer R, Ruzsics Z, Dölken L.
Real-time transcriptional profiling of cellular and viral gene expression during lytic cytomegalovirus infection.
PLoS Pathogens 2012 Sep;8(9):e1002908. doi: 10.1371/journal.ppat.1002908. Epub 2012 Sep 6.

5.  Györy I, Boller S, Nechanitzky R, Mandel E, Pott S, Liu E, Grosschedl R.
Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferation, and survival of B cells.
Genes and Development . 2012 Apr 1;26(7):668-82.

6.  Treiber T*, Mandel EM*, Pott S*, Gyory I*, Firner S, Liu ET, Grosschedl R. 
Ebf1 regulates B cell gene networks by activation, repression and transcription independent poising of chromatin
Immunity 2010 May 5. [Epub ahead of print] * Equal contribution
7.  Fejer G, Koroknai A, Banati F, Györy I, Salamon D, Wolf H, Niller HH, Minarovits J. 
Latency type-specific distribution of epigenetic marks at the alternative promoters Cp and Qp of Epstein-Barr virus.
Journal of General Virology. 2008 Jun;89(Pt 6):1364-70

8.  Roessler S, Gyory I, Imhof S, Spivakov M, Williams RR, Busslinger M, Fisher AG, Grosschedl R.
Distinct Promoters Mediate the Regulation of Ebf1 Gene Expression by IL-7 and Pax5.             Molecular and Cellular Biology. 2006 Nov 13;

9.  Fejer G, Szalay K, Gyory I, Fejes M, Kusz E, Nedieanu S, Pali T, Schmidt T, Siklodi B, Lazar G Jr, Lazar G Sr, Duda E.
Adenovirus Infection Dramatically Augments Lipopolysaccharide-Induced TNF Production and Sensitizes to Lethal Shock. 
Journal of Immunology.  2005 Aug.1;175(3):1498-506. 

10.  Gyory I., Minarovits J. 
Epigenetic regulation of lymphoid specific gene sets.      
Biochemistry and Cell Biology. 2005 Jun;83(3):286-95. Review.

11. Gyory I, Wu J, Fejer G, Seto E, Wright KL.
PRDI-BF1 Recruits the Histone H3 Methyltransferase G9a in Transcriptional Silencing.
Nature Immunology 2004 Mar;5(3):299-308. Epub 2004 Feb 22.

12.  Gyory I, Fejér G, Ghosh N,  Seto E, Wright KL.
Myeloma Cells Express a Truncated PRDM1 Protein with Impaired Transcriptional Repression Function. 
Journal of Immunology.  2003, 170:3125-3133

13.  Rezai-Zadeh N, Namour F, Fejer G, Wen Y-D, Yao Y-L, Gyory I, Wright KL, Seto E.  
Targeted Recruitment of Histone H4-specific Methyltransferase by the Transcription Factor YY1
Genes and Development . 2003 Apr 15;17(8):1019-29

14. Ghosh N, Gyory I, Wright G, Wood J and Wright KL. 
Positive regulatory domain I binding factor 1 silences Class II Transactivator Expression in Multiple Myeloma Cells.
Journal of  Biological Chemistry.  2001 276:15264-8

15. Fejér G, Gyory I, Tufariello J and Horwitz MS.
Characterization of Transgenic Mice Containing Adenovirus Early Region 3 
Genomic DNA.
Journal of  Virology.  1994  68: 5871-5881


Transcriptional, epigenetic and cell cycle regulation in B-lymphoid cancer.

Carcinogenesis is caused by mutations in the genetic material of normal cells
Cancerous cells may:
-Acquire self-sufficiency in growth, leading to independence of external growth signals
Lose sensitivity to anti-growth signals that leads to unchecked growth
-Lose their capacity for programmed cell death in response to genetic errors
-Lose their capacity to repair genetic errors, leading to an increased mutation rate (genomic instability)

Normal cells respond to DNA damage by halting cell-cycle progression to allow the repair of the errors. If the damage is too extensive to repair, cells chose to undergo programmed cell death.  It is still not clearly understood how the processes of cell-cycle arrest or apoptosis are coordinated with DNA repair and the cell-type specific extrinsic and intrinsic growth signals to optimize the outcome for the cell or the organism.
Lymphocytic cells also break their DNA on purpose to generate diversity in antibodies, T-cell receptors and other highly variable immune system proteins. These physiologic DNA-breaks are repaired by a large complex of enzymes, some of which are lymphocyte specific, and some are expressed in multiple cell types. The cell cycle arrest during recombination events is tightly coordinated with the cell specific developmental regulatory programs of signal transduction and gene expression, and if the recombination does not yield a functional in frame antibody or T-cell receptor, lymphocytes undergo apoptosis.

Typically, lymphocytic malignancies arise when the coordination of the recombination events and the developmental program is impaired and the resulting mutant cells are either not recognized or not eliminated. Our laboratory investigates the intersection of the lymphocyte specific pathways with the basic cellular regulation of cell cycling and cell death.

Transformation of lymphoid progenitor cells leads to the development of acute lymphoblastic leukaemia (ALL). The majority of ALL cases involve transformation of B lineage cells, with only a small percentage of cases resulting from T cell transformation.
By regulating important components of transcription factor and signaling networks, Ebf1 functions as a molecular node that helps to coordinate proliferation, survival, and differentiation of normal B-lineage cells. Mutations in the EBF1 gene have been found in ~25% of adult and ~5% of childhood B-progenitor acute lymphoblastic leukaemia. These mutations seem to co-operate with deregulated signal transduction of STAT5 or the leukemic fusion protein Etv6-Runx1 in cellular transformation. Our laboratory is interested in finding the molecular basis of these interactions and in finding novel possibilities for targeted therapy in ALL patients.

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