About the lab

In cancer, the genome is transformed in such a manner that the uncontrolled cell division and growth of the cancer is destroying the organism itself.

The activity of the genome is controlled by distinct mechanisms on the chromatin level by determining the boundaries of active and inactive regions.

Components of these regulatory processes are the super-enhancers, or clustered enhancers with their transcription factors and the protein complexes that determine the boundaries of chromatin domains.

The changes in cell identity can be identified both on genotype and phenotype levels and their initial phase is initiated by changes on the chromatin level. We plan to characterize these chromatin level changes of tumour evolution.

Featured projects (1)

Project
We aim to characterize on chromatin level the components of cell identity and non-genetic cell variability encoded on the chromatin level.

Featured research (3)

Biobanks operating at ambient temperatures would dramatically reduce the costs associated with standard cryogenic storage. In the present study, we used lyophilization to stabilize unfractionated human cells in a dried state at room temperature and tested the yield and integrity of the isolated RNA by microfluidic electrophoresis, RT-qPCR and RNA sequencing. RNA yields and integrity measures were not reduced for lyophilized cells (unstored, stored for two weeks or stored for two months) compared to their paired controls. The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. RNA sequencing data of three lyophilized samples stored for two weeks at room temperature revealed a high degree of similarity with their paired controls in terms of the RNA biotype distribution, cumulative gene diversity, gene body read coverage and per base mismatch rate. Among the 28 differentially expressed genes transcriptional regulators, as well as certain transcript properties suggestive of a residual active decay mechanism were enriched. Our study suggests that freeze-drying of human cells is a suitable alternative for the long-term stabilization of total RNA in whole human cells for routine diagnostics and high-throughput biomedical research.
Nuclear Receptors are ligand-activated transcription factors that translate information about the lipid environment into specific genetic programs, a property that renders them good candidates to be mediators of rapid adaptation changes of a species. Lipid-based morphogens, endocrine hormones, fatty acids and xenobiotics might act through this class of transcription factors making them regulators able to fine-tune physiological processes. Here we review the basic concepts and current knowledge on the process whereby small molecules act through nuclear receptors and contribute to transgenerational changes. Several molecules shown to cause transgenerational changes like phthalates, BPA, nicotine, tributylin bind and activate nuclear receptors like ERs, androgen receptors, glucocorticoid receptors or PPARγ. A specific subset of observations involving nuclear receptors has focused on the effects of environmental stress or maternal behaviour on the development of transgenerational traits. While these effects do not involve environmental ligands, they change the expression levels of Estrogen and glucocorticoid receptors of the second generation and consequently initiate an altered genetic program in the second generation. In this review we summarize the available literature about the role of nuclear receptors in transgenerational inheritance. Copyright © 2015. Published by Elsevier Ltd.
Evidence is accumulating for the existence of a STAT2/IRF9-dependent, STAT1-independent IFNα signaling pathway. However, no detailed insight exists in the genome-wide transcriptional regulation and the biological implications of STAT2/IRF9 dependent IFNα signaling as compared to ISGF3. In hST2-U3C and mST2-MS1KO cells we observed that the IFNα-induced expression of OAS2 and Ifit1 correlated with the kinetics of STAT2 phosphorylation, and the presence of a STAT2/IRF9 complex requiring STAT2 phosphorylation and the STAT2 transactivation domain. Subsequent microarray analysis of IFNα treated WT and STAT1 KO cells over-expressing STAT2 extended our observations and identified around 120 known antiviral ISRE-containing ISGs commonly up-regulated by STAT2/IRF9 and ISGF3. The STAT2/IRF9 directed expression profile of these ISGs was prolonged as compared to the early and transient response mediated by ISGF3. In addition, we identified a group of "STAT2/IRF9-specific" ISGs, whose response to IFNα was ISGF3-independent. Finally, STAT2/IRF9 was able to trigger an antiviral response upon EMCV and VSV. Our results further prove that IFNα-activated STAT2/IRF9 induces a prolonged ISGF3-like transcriptome and generates an antiviral response in the absence of STAT1.Moreover, the existence of "STAT2/IRF9-specific" target genes predicts a novel role of STAT2 in IFNα signaling.

Lab head

Balint L Balint
Department
  • Department of Biochemistry and Molecular Biology
About Balint L Balint
  • I am an MD, PhD with strong interest in translational medicine. I am specialist in Laboratory Medicine. My goal is to translate the large amount of scientific knowledge and data into usable clinical tools. We use bioinformatic and laboratory tools to identify and test novel biomarkers with clinical importance. Our laboratory has strong expertise in chromatin studies, mainly in ChIP-Seq and related technologies from sample processing to data analysis and data visualization. We are looking for partners and students interested in diving in data and science!

Members (3)

Miklos Laczik
  • Diagenode
Péter Gargya
  • University of Debrecen
Máté Szűcs
  • University of Debrecen

Alumni (7)

Katarzyna Błaszczyk
  • Adam Mickiewicz University
Dora Bojcsuk
  • University of Debrecen
Edina Erdős
  • University of Debrecen
Lilla Ozgyin
  • University of Debrecen