Understanding research · Sharing knowledge
I want to communicate insights from university-based epigenetics research clearly and make them accessible to as many people as possible—helping them better understand their health and opening up new perspectives on a long life with a high quality of life. At the same time, I am working to translate these insights into medical applications that support patients and their clinicians.
About me
My first thanks go to Heinrich Heine University Düsseldorf, my alma mater. It gave me the opportunity to study, conduct research and teach.
Since April 1997, I have conducted research at University Hospital Düsseldorf in the comparatively young field of epigenetics.
I direct the Epigenetics Laboratory for Human Health and Longevity at the Institute of Transplantation Diagnostics and Cell Therapeutics, Faculty of Medicine, Heinrich Heine University Düsseldorf.
More about meHow do our cells use their genes—and what role does our environment play? Eight questions offer an accessible introduction.
Research and knowledge
I want to make insights from epigenetics understandable and accessible to as many people as possible. A deeper understanding of the bridge between our environment and gene regulation can open up new perspectives on health and a long life with a high quality of life.
Learn moreI study how epigenetic regulation and changes in the genome contribute to human evolution. I want to make these connections accessible, because our evolutionary history helps us understand who we are today.
Learn moreI develop epigenetic biomarkers intended to support patients and clinicians in the early detection and assessment of cancer. This platform technology has the potential to be applied to different cancers and to support ongoing monitoring of individual risk.
Learn moreMy research today
I investigate characteristic methylation patterns at the hTERT gene as an epigenetic signal of malignancy. The aim is a broadly applicable platform technology for early detection, prognosis and follow-up.
Explore the research projectThis website is for everyone who wants to understand epigenetics and its significance for life. I also hope to encourage dialogue with scientists, patients, clinical partners and businesses.
03 / CANCER MEDICINE
I develop epigenetic biomarkers for the early detection, diagnosis, prognosis and monitoring of cancer. This work is based on a platform technology with the potential for use across different cancer types. These include prostate, bladder, breast, pancreatic, thyroid, liver, lung, colorectal and skin cancers, as well as certain brain tumours and malignancies of the blood-forming system. It uses a shared methodological approach that can be adapted to each cancer type. The initial focus is on prostate and bladder cancer.
Modern epigenetics also offers the prospect of monitoring current health and susceptibility to malignant disease through regular testing. The aim is to support patients and their clinicians in prevention, individual risk assessment and medical decision-making.
01 / HEALTHY AGEING
Modern epigenetics offers a new and important perspective on the connection between our living conditions and our health. Diet, exercise, physical and psychological stress, living and working conditions, pollutants and medicines can influence the epigenetic regulation of our genes. Our cells therefore use their genetic information under the continuing influence of the conditions in which we live.
This connection is of fundamental importance to medicine. Extensive scientific findings provide evidence that epigenetic dysregulation is involved in the onset and development of numerous diseases. These include many cancers, type 2 diabetes and other metabolic diseases, cardiovascular diseases, autoimmune diseases and certain neurodevelopmental disorders. Characteristic epigenetic changes that contribute to disease development are also found in neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. Epigenetic changes can increase susceptibility to disease and influence the processes through which diseases arise or progress.
To understand such dysregulation, we first need to know what healthy epigenetic regulation looks like. Modern epigenetic methods offer crucial opportunities here: they allow us to characterise the patterns of healthy cells and tissues in detail and, using suitable techniques, to detect changes sensitively and reliably. The “healthy epigenome” is not a single, uniform pattern throughout the human body. Immune cells, blood-forming cells, liver cells, muscle cells and nerve cells each have their own epigenetic programmes that enable their identity and function.
A first step is to decipher these healthy epigenetic reference patterns as comprehensively as possible across all cell types and body compartments. Building on this knowledge, we can determine with increasing precision which environmental influences cause which epigenetic changes, which of these represent beneficial adaptations and which threaten our health. This creates a foundation for shaping living conditions more deliberately and tracking the effects of such changes at the molecular level.
This is where humans have a particular capacity to act: we can shape our environment and living conditions ourselves to an exceptionally far-reaching extent. The better we understand their effects on gene regulation, the more effectively we can use this ability to create conditions that promote health.
A key property of epigenetic regulation works in our favour: epigenetic changes are reversible in principle. Marks can be established, modified and removed again. Such reversal can occur gradually and take time; its extent and course depend on factors including the cell type, the mechanism involved, and the nature and duration of the influence. If we can identify and influence the causes of dysregulation, we open up the possibility of restoring or preserving healthy regulation.
For me, an important next step lies in connecting our ability to shape living conditions with an increasingly precise understanding of their biological effects. This is why I want to make insights from epigenetics research understandable and accessible to as many people as possible. This knowledge can expand our scope for action and help us shape our health and quality of life more consciously, within our biological, personal and social circumstances. In this way, we can increasingly help determine our own health outcomes and be less powerless in the face of what lies ahead, with greater influence over the conditions that affect us—in the spirit of being “Masters of our fate”.
02 / EVOLUTION
I investigate the role of epigenetic mechanisms in human evolution. I am particularly interested in the new explanatory approaches that epigenetics offers for understanding how our development and existence are shaped through close interaction with the environment. For me, epigenetics opens up a new perspective here: it helps us better understand our epigenetic gene regulation, our environment and our existence as interwoven parts of a connected whole.
Our development can be considered on two interconnected levels: individual development over a lifetime, and evolutionary development across many generations. Naturally, each of us places our own life at the centre of our concerns. Yet a fuller understanding of our existence and its continuing interaction with changing living conditions also requires an understanding of our evolutionary history.
I therefore work to understand how epigenetic regulation, changes in the genome and environmental influences interact over evolutionary timescales, and how they contribute to human development. I also want to make these connections understandable to as many people as possible. We carry this history within us: our present biological form and our developmental potential have been shaped by it—and evolution continues.
Research · Motivation · Academic journey
Modern epigenetics is a comparatively young and rapidly developing branch of biology. Its findings reveal the potential to transform our understanding of biology and the possibilities of medicine. They open up new perspectives on understanding our own health and supporting a long life with a high quality of life.
Yet its molecular mechanisms and research methods often seem abstract and difficult to grasp, making this knowledge less accessible to many people. This is where my purpose lies: I want to communicate the latest findings in epigenetics clearly and openly, so that they can reach and benefit as many people as possible.
I studied biology, specialising in genetics. As my research in epigenetics progressed, several deeper questions came to the fore: How does a complex organism develop from a single fertilised egg? In what form does the zygote already contain the specific information for the eventual form of the intended organism? How is that information used and regulated during development so that different cell types, tissues and organs emerge at the right time and in the right place? And how has the environment shaped these developmental programmes over evolutionary time—and how does it continue to influence both their expression during individual development and their further evolution?
These questions become particularly striking when we compare humans with our closest living relatives, chimpanzees. The evolutionary lineages of humans and chimpanzees are estimated to have diverged around six to eight million years ago. In directly comparable DNA regions, our genome sequences are almost 99 per cent identical. A landmark genome comparison published in 2005 revealed how similar human and chimpanzee proteins are: around 29 per cent of the orthologous proteins studied—corresponding proteins in the two species with a shared evolutionary origin—have identical amino acid sequences. A typical pair differs by just two amino acid substitutions, one arising in each lineage since their divergence from a common ancestor. Nevertheless, we differ markedly in anatomy, development and abilities. How do differences in the genome and its epigenetic regulation contribute to a human developing from a human zygote and a chimpanzee from a chimpanzee zygote?
I am particularly interested in how inherited information, epigenetic regulation and environmental signals work together. How do they enable reliable, species-specific development while allowing adaptation to different living conditions? How did these capabilities emerge during evolution?
These questions have a long history. Aristotle (384–322 BCE) described the gradual formation of a living organism during embryonic development. William Harvey (1578–1657) and Caspar Friedrich Wolff (1734–1794) later investigated how organs emerge successively, rather than simply growing from preformed miniature structures.
Jean-Baptiste Lamarck (1744–1829) emphasised the importance of the environment and proposed that acquired changes could be inherited. Charles Darwin (1809–1882) explained evolutionary adaptation through natural selection acting on heritable differences between organisms. The molecular mechanisms connecting inheritance, environment and development were still unknown.
Conrad Hal Waddington (1905–1975) introduced a pivotal perspective. He focused on the developmental processes that connect an organism’s genome with its observable form: how do genetic factors, under the influence of the environment, give rise to a particular developmental trajectory? His “epigenetic landscape” illustrates this interplay as a system of branching valleys. As shown in the illustration at the end of this section, the ball represents a developing cell; the different paths lead, for example, to nerve, muscle, liver or blood cells. The landscape itself symbolises the interactions between genes and regulatory processes that enable and stabilise particular developmental pathways.
Waddington called the stability of such developmental pathways “canalisation”: despite some genetic variation or changing environmental conditions, development can reach a consistent outcome. At the same time, the developmental system remains responsive to external influences. Modern molecular epigenetics reveals important mechanisms underlying this connection: DNA methylation and other epigenetic mechanisms help determine which genes a cell can use and how it maintains its identity. Environmental influences can act on this regulation and thereby alter developmental trajectories.
The landscape initially describes development within an organism. Waddington also asked how the shape of the landscape itself could change across generations. He investigated how a trait initially induced by the environment could become evolutionarily established. In experiments with fruit flies, a heat shock induced changes in wing venation. Through selective breeding over successive generations, he established lines in which these changes eventually appeared even without the original heat shock. He called this process “genetic assimilation”: selection makes a developmental response that initially depends on an environmental stimulus increasingly independent of that stimulus.
This provides an important conceptual bridge between Lamarck’s emphasis on environmental influences and Darwin’s explanation of evolutionary change through selection. Epigenetic developmental regulation helps us understand how environmental conditions can influence the expression of traits; selection explains how heritable differences in these developmental responses can be favoured across generations. Waddington’s approach thus brings environment, development and inheritance together within a shared evolutionary framework. My own research builds on this perspective: how can epigenetic regulation and long-term changes in its genetic foundations jointly contribute to evolution?
Modern epigenetics allows us to investigate important aspects of these connections at the molecular level. I am particularly interested in how DNA sequence defines the possibilities for epigenetic regulation, and how patterns are established during development, maintained through cell division and altered over a lifetime.
For us as humans, this offers a particular opportunity: we can substantially shape our environment and living conditions. Understanding which influences change gene regulation, how quickly they act and how long their effects persist could provide a scientific basis for influencing gene activity through deliberate changes in the way we live. Modern epigenetic methods help us measure these changes and follow them over time.
This is the heart of my scientific motivation: to understand this connection more deeply, communicate insights clearly and help translate them into medical applications that support patients and their clinicians. My overarching aim is to preserve health and support a long life with a high quality of life.
Further reading: The history of epigenetics
Further reading: Comparing the human and chimpanzee genomes · Nature, 2005
Historical source: C. H. Waddington: The Strategy of the Genes (1957) – excerpt from the original as a PDF
My educational and academic journey took me from Quirinus-Gymnasium in Neuss to Heinrich Heine University Düsseldorf, where I studied biology, majoring in genetics and minoring in molecular parasitology. I have worked at University Hospital Düsseldorf since April 1997.
In May 1985, I completed my Abitur at Quirinus-Gymnasium . The school has a humanist tradition and a long history: its roots extend to the municipal Latin school first recorded in 1302 and the Jesuit school founded in 1616. It is one of the oldest schools in the German-speaking world.
In April 1988, I began studying biology at Heinrich Heine University Düsseldorf. During the advanced stage of my studies, I focused on genetics and molecular parasitology.
After completing my Diplom in 1996, I turned to epigenetics.
Since April 1997, I have conducted research at University Hospital Düsseldorf in this field. My doctoral work investigated changes in DNA methylation in urological tumour cells and the role of the enzyme DNA methyltransferase 1 (DNMT1).
In June 2000, I completed my doctorate with the distinction magna cum laude. I then worked at the Institute of Transplantation Diagnostics and Cell Therapeutics, studying the epigenetic regulation of the human immune system.
My doctoral thesis: An investigation of DNA methylation changes in urological tumour cells and the role of the enzyme DNMT1.
View the dissertation at the publisher · Shaker, 2000Since January 2008, I have led the Epigenetics Laboratory for Human Health and Longevity at the Faculty of Medicine, Heinrich Heine University Düsseldorf.
In July 2012, I completed my habilitation in Molecular Medicine and was awarded the qualification to teach at university level.
View the habilitation thesis · Epigenetic regulation of KIR receptorsIn July 2019, I was appointed an außerplanmäßiger Professor, a German professorial title awarded outside the regular chair system.
On 15 June 2022, my 25 years of service at Heinrich Heine University Düsseldorf were recognised with a certificate of honour. I am delighted by this long-standing connection to my alma mater and grateful for the opportunity to conduct research and teach here.
My work connects the investigation of fundamental epigenetic mechanisms with the development of medical applications. Heinrich Heine University Düsseldorf is my alma mater and has been my academic home since my student years.
Supporting young people on their scientific journey is particularly important to me. During my time at Heinrich Heine University Düsseldorf, I have supervised doctoral, master’s and bachelor’s theses. The following overview comprises a total of 25 supervised theses.
I also want school students to experience research first-hand and take their first practical steps in the laboratory. My laboratory supported three young school-leavers as they began experimental work on their project “Isolation of Mussel Adhesive” as part of Jugend forscht Bremen, a German youth science competition. During their four-week stay, they were able to advance their project through hands-on research. I also welcomed two students in their tenth and eleventh school years for laboratory work-experience placements.
| Degree | Number of theses |
|---|---|
| Doctoral theses leading to the Dr. rer. nat. | 3 |
| Doctoral theses leading to the Dr. med. | 5 |
| Master’s theses | 5 |
| Bachelor’s theses | 12 |
| Total | 25 |
I have had the pleasure of supporting some students through several stages of their academic development – from a bachelor’s or master’s thesis through to a doctorate.
Six themes provide an overview of my scientific contributions. Open a topic to explore the research and related publications.
In my early postdoctoral years, I was the first to discover and experimentally demonstrate the fundamental epigenetic mechanism controlling cell-specific patterns of KIR gene activity: regulation through DNA methylation. These genes encode important receptors on natural killer cells, a central pillar of human innate immunity. These immune cells play a major role in recognising and combating virus-infected cells and tumour cells.
Our paper published in 2002 showed that DNA methylation plays a decisive role in determining which KIR genes remain silent in an individual natural killer cell and which can become active. This provided the first insight into a central epigenetic basis of the distinct KIR receptor patterns found in these cells. The discovery also offers avenues for harnessing this regulation to advance immunotherapies against viral infections and cancer.
Publication · Journal of Immunology, 2002Another milestone was the development of idiolocal normalisation, published in 2016 as IDLN-MSP: Idiolocal Normalization of Real-Time Methylation-Specific PCR. This approach enables reliable measurement of DNA methylation changes using methylation-specific PCR, even in the presence of genetic abnormalities such as those found in tumours.
In cancer, changes in the copy number of particular DNA regions can distort measurements. Idiolocal normalisation uses a reference sequence close to the region being examined. When the target and reference sequences are affected by the same copy-number change, this approach can prevent such distortions and improve comparisons of epigenetic changes in tumour samples.
Publication · BioTechniques, 2016A further advance was the development of the EpihTERT concept, with far-reaching prospects for modern cancer diagnosis, prognosis and follow-up across numerous cancer types.
Changes in DNA methylation in regulatory regions of the hTERT gene have been described in prostate, bladder, breast, pancreatic, thyroid, liver, lung, colorectal and skin cancers, as well as in certain brain tumours and malignancies of the blood-forming system. These include papillary thyroid carcinoma, hepatocellular carcinoma, pancreatic ductal adenocarcinoma, paediatric high-grade gliomas and ependymomas, and leukaemias. These findings provide the scientific basis for exploring EpihTERT across different cancers.
The focus is the hTERT gene, which encodes the catalytic subunit of the enzyme telomerase. While hTERT is largely silenced in most mature somatic cells, it is reactivated in many tumour cells. Telomerase activity can be detected in approximately 85–90 per cent of human cancers. It enables tumour cells to maintain their chromosome ends—the telomeres—sufficiently to sustain continued cell division.
Certain regulatory regions of hTERT show characteristic DNA methylation patterns associated with aggressive cancer that differ from those in the healthy comparison tissues studied. This offers the potential for a highly specific epigenetic signal of malignancy.
A particular advantage lies in the chemistry of these marks: methyl groups are attached directly to DNA through strong chemical bonds known as covalent bonds. They are therefore stable components of the DNA molecule and can remain on DNA fragments released by tumour cells. This chemical stability makes characteristic methylation patterns particularly well suited as molecular detection signals, both in tissue samples and in cell-free DNA from body fluids such as blood or urine.
With EpihTERT, I aim to make these methylation patterns useful for detecting and assessing cancer. An initial focus is distinguishing less threatening from aggressive forms of prostate and bladder cancer. For targeted, sensitive and rapid detection, we use idiolocally normalised real-time methylation-specific PCR. This normalisation accounts for potential distortions caused by altered DNA copy numbers, providing an important methodological basis for reliable quantitative analysis.
Publication · Cancers, 2025 Background: hTERT, telomerase and sustained cancer-cell division · 2018Another aim of my research is to use epigenetic insights to advance cancer treatment. Together with my colleagues, I investigate how characteristic changes in gene regulation could reveal new targets on cancer cells and support medical decision-making.
Our studies of recurrent DNA hypomethylation in prostate cancer provide a foundation for this work. In genes silenced through methylation, loss of DNA methylation can be sufficient to permit activation. If the gene encodes a cell-surface protein, that protein may then be produced and displayed on the cell surface. Such findings can point to surface features that may serve as targets for precision immunotherapy.
We have explored this approach in the context of CAR T-cell therapy, in which immune cells are modified to recognise selected features of cancer cells and attack them. Our work describes the prospect of using epigenetic analyses to identify suitable targets in solid tumours, initially focusing on prostate cancer.
In parallel, we investigate how epigenetic markers might inform treatment selection and monitoring. Our work on hTERT epigenetics and the EpihTERT concept connects cancer detection with assessment of biological aggressiveness. In prostate cancer, it is particularly important to identify tumours that require treatment more reliably while avoiding unnecessary treatment of less threatening disease. We also explore prospects for prognosis, follow-up and more informed selection of chemotherapy in the future.
In another paper, we brought together findings on the epigenetic regulation of malignant melanoma and discussed how evidence from other cancers could open new research avenues for its diagnosis and treatment.
My goal is cancer medicine that takes greater account of a tumour’s molecular characteristics, enabling more targeted therapies, clearer treatment decisions and better support for patients.
Selected publications:
Across my three publications on phylo-epigenetics, I have developed a research approach addressing a fundamental question in our evolution: how might environmental conditions, acting through epigenetic regulation, contribute over time to changes in our genome and developmental programmes? The focus is on CpG sites—positions in DNA at which methyl groups can be attached as epigenetic marks. Their conservation or alteration also affects the possibilities for epigenetic regulation available to subsequent generations.
Building on my papers from 2022 and 2024, in 2025 I examined corresponding regions of OCT4, SOX2 and hTERT—genes active early in embryonic development—in ten living primate species, including humans, as well as in Neanderthals and Denisovans. Characteristic patterns of strongly conserved and altered CpG sites allowed major evolutionary relationships to be traced. Frequent changes followed known mutational pathways of methylated CpG sites.
These findings underpin a further hypothesis: environmental conditions, such as nutrition, could influence the likelihood of particular genetic changes through their effects on DNA methylation. If inherited through the germline, such changes can alter the foundations of gene regulation across generations and become subject to natural selection. The distinctive contribution of this approach is to identify a molecularly grounded connection between environment, epigenetic regulation and evolutionary change, opening new avenues for understanding the emergence and continued evolution of developmental programmes.
Publication · Genes, 2025Another focus of my research is how changes in cellular metabolism influence epigenetic regulation and the stability of our genome.
In 2018, my colleagues and I described striking DNA methylation changes at ODC1, AHCY and MTHFR, even in early stages of bladder cancer. These genes encode key enzymes in methyl-group and polyamine metabolism. The changes were accompanied by widespread loss of methylation marks across the genome. We therefore proposed that disrupted regulation of these metabolic pathways could promote and amplify further epigenetic changes.
In our follow-up study in 2020, we investigated this connection experimentally using ODC1. Targeted reduction of its activity in cultured urothelial cells led to loss of methylation marks at LINE-1 elements, increased LINE-1 activity and DNA double-strand breaks. DNA damage and programmed cell death also occurred in the bladder cancer cells studied.
Together, these studies suggest a potentially self-reinforcing relationship between disrupted metabolic regulation, epigenetic changes and genomic instability. They provide an experimental approach to understanding early events in bladder cancer development.
Our 2022 review, “Methyl Group Metabolism in Differentiation, Aging, and Cancer”, broadened this perspective. Methyl-group metabolism provides a fundamental biochemical connection between nutrition, environment and epigenetic gene regulation. Among other functions, it supplies the methyl groups that cells need to establish and maintain DNA methylation patterns. We brought together evidence linking the regulation of these pathways with specialised cell development, ageing and cancer. The review highlights the importance of a well-regulated methyl-group supply for cellular epigenetic stability and opens research avenues into the interplay of living conditions, metabolism and health.
Another area of my research asks how stem cells maintain their distinctive properties and give rise to different specialised cell types. Together with my colleagues, I have investigated the roles of epigenetic mechanisms and the regulation of key genes.
In certain stem cells from human umbilical cord blood, we described an epigenetically poised state of important developmental regulators, including OCT4, SOX2 and NANOG. Although these genes showed little activity, they were not completely epigenetically silenced. This provided clues to how such cells remain receptive to different differentiation and reprogramming signals.
In a collaborative study, we also succeeded in reprogramming these cells into induced pluripotent stem cells. By introducing selected reprogramming factors, we brought them into a state with broad developmental potential.
We pursued a different approach by treating the cells with epigenetically active compounds. This produced a stably altered stem-cell type entirely without transgenic intervention—that is, without introducing additional genes. In the cell line studied, these cells, termed “SpheUSSC”, showed expanded developmental potential: they retained the ability to form bone cells and gained the ability to develop into fat cells.
Together, these studies help explain the regulation, developmental potential and functional identity of stem cells. They provide foundations for selecting and characterising suitable cells, developing disease models and advancing regenerative medicine.
Selected publications:
Scientific publications and developments
Eighteen selected papers exploring my research interests, with accessible English summaries. The complete PubMed publication list, with search and filters, follows below.
Balancing Early Detection and Overtreatment in Prostate Cancer: The Emerging Role of EpihTERT.
Early detection of prostate cancer presents an urgent challenge: overdiagnosis and overtreatment. Screening also identifies tumours that would never cause symptoms during a man’s lifetime. Treating them can lead to lasting consequences, including incontinence and sexual dysfunction, without a corresponding benefit. The challenge is therefore to identify threatening tumours early while avoiding unnecessary treatment.
This is where the EpihTERT concept comes in. Characteristic DNA methylation patterns at hTERT are associated with tumour aggressiveness, disease progression and recurrence risk. Studying these patterns offers the prospect of assessing a tumour’s biological threat more precisely and better informing the choice between active surveillance and treatment. The approach could also help select patients for minimally invasive treatment, such as high-intensity focused ultrasound (HIFU). The aim is timely treatment when needed, while preserving quality of life when treatment is unlikely to offer a benefit.
Santourlidis S, Araúzo-Bravo MJ, Hassan M, Bendhack ML.
Cancers (Basel). 2025 Nov 27;17(23):3799.
DOI: 10.3390/cancers17233799
PMID: 41375001 · PMCID: PMC12691199
hTERT Epigenetics Provides New Perspectives for Diagnosis and Evidence-Based Guidance of Chemotherapy in Cancer.
Our paper combines our own findings in urothelial cancer with evidence from the literature. It describes characteristic methylation patterns in a larger regulatory region of hTERT that we named “Acheron”. Selected patterns can be distinguished using specifically designed PCR assays, providing a foundation for developing cancer markers. This opens perspectives for diagnosis, prognosis and follow-up, as well as more informed selection of chemotherapy in the future.
Santourlidis S, Araúzo-Bravo MJ, Brodell RT, Hassan M, Bendhack ML.
Int J Mol Sci. 2024 Jul 4;25(13):7331.
DOI: 10.3390/ijms25137331
PMID: 39000438 · PMCID: PMC11242863
Epigenetics Meets CAR-T-Cell Therapy to Fight Cancer.
CAR T cells are engineered immune cells that can recognise and attack particular surface features of cancer cells. Our paper describes a research approach that uses recurrent losses of DNA methylation to identify genes with increased activity in tumour cells that may produce suitable surface features. This opens a route towards new CAR T-cell targets in solid tumours, initially focusing on prostate cancer.
Santourlidis S, Araúzo-Bravo MJ, Erichsen L, Bendhack ML.
Cancers (Basel). 2024 May 20;16(10):1941.
DOI: 10.3390/cancers16101941
PMID: 38792020 · PMCID: PMC11119853
Consistent DNA Hypomethylations in Prostate Cancer.
In this study, we examined prostate cancer samples from three patient cohorts for characteristic losses of DNA methylation. Targeted analysis of short, CpG-rich DNA regions revealed recurrent changes that we termed tumour-cell-specific methylation signatures, or TUMS. These findings provide a foundation for developing biomarkers that could improve the detection and molecular classification of prostate tumours.
Araúzo-Bravo MJ, Erichsen L, Ott P, Beermann A, Sheikh J, Gerovska D, Thimm C, Bendhack ML, Santourlidis S.
Int J Mol Sci. 2022 Dec 26;24(1):386.
DOI: 10.3390/ijms24010386
PMID: 36613831 · PMCID: PMC9820221
Differential DNA Methylation of THOR and hTAPAS in the Regulation of hTERT and the Diagnosis of Cancer.
We investigated DNA methylation in the TERT Hypermethylated Oncological Region (THOR) in urothelial cancers, identifying the sites that differed most clearly from healthy comparison tissue. Our findings support a mechanism in which methylation reduces production of the regulatory RNA hTAPAS, thereby releasing a brake on hTERT activity. Precise mapping of these changes enables targeted development of methylation-specific PCR assays and provides an experimental foundation for diagnostic and prognostic applications.
Ott P, Araúzo-Bravo MJ, Hoffmann MJ, Poyet C, Bendhack ML, Santourlidis S, Erichsen L.
Cancers (Basel). 2022 Sep 8;14(18):4384.
DOI: 10.3390/cancers14184384
PMID: 36139544 · PMCID: PMC9497117
Lineage-specific transition of histone signatures in the killer cell Ig-like receptor locus from hematopoietic progenitor to NK cells.
How are KIR genes prepared for later activation during the development of blood-forming progenitor cells? We compared DNA methylation, chromatin accessibility and histone marks at the KIR locus in early progenitor cells and different immune-cell types. Histones are proteins around which DNA is wrapped; their chemical modifications influence the regulatory state of chromatin.
Early progenitor cells showed features of epigenetic silencing. Natural killer cells, by contrast, carried histone marks that favour activity—even at individual KIR genes that remained silenced by DNA methylation. The findings support a two-step model: first, a chromatin state appropriate to the cell lineage is established; demethylation of individual KIR genes then permits their activation.
Santourlidis S; Graffmann N; Christ J; Uhrberg M
J Immunol. 2008;180(1):418. · PMID: 18097043
Crucial role of DNA methylation in determination of clonally distributed killer cell Ig-like receptor expression patterns in NK cells.
Natural killer cells form part of innate immunity. Each cell carries a particular selection of KIR receptors involved in recognising target cells. We investigated the molecular mechanism—then unresolved—by which these distinct receptor patterns arise and remain stable.
We showed that active KIR genes are largely unmethylated within a small regulatory CpG island, whereas silent genes carry methylation marks there. Experimentally removing DNA methylation activated previously silent KIR genes and led to the appearance of the corresponding receptors on the cell surface. Conversely, targeted methylation suppressed the activity of the KIR regulatory regions examined. This experimentally established a fundamental epigenetic mechanism underlying cell-specific KIR receptor patterns.
Santourlidis S; Trompeter HI; Weinhold S; Eisermann B; Meyer KL; Wernet P; Uhrberg M
J Immunol. 2002;169(8):4253. · PMID: 12370356
Unrestricted somatic stem cells (USSC) from human umbilical cord blood display uncommitted epigenetic signatures of the major stem cell pluripotency genes.
Certain somatic stem cells from human umbilical cord blood have broad developmental potential, even though key pluripotency factors such as OCT4, SOX2 and NANOG are barely expressed. We investigated whether the epigenetic state of these genes could help explain this potential.
The gene regions examined were not completely epigenetically silenced. We found partially demethylated regions at OCT4 and hTERT, and unmethylated regulatory regions at SOX2 and NANOG. At SOX2, histone marks with opposing effects coexisted, a feature characteristic of a poised state. Experimental introduction of OCT4 rapidly activated SOX2. These results suggest that incomplete epigenetic commitment favours responsiveness to differentiation and reprogramming signals.
Santourlidis S; Wernet P; Ghanjati F; Graffmann N; Springer J; Kriegs C; Zhao X; Brands J; Araúzo-Bravo MJ; Neves R; Koegler G; Uhrberg M
Stem Cell Res. 2011;6(1):60. · PMID: 20933485
Effect on Multipotency and Phenotypic Transition of Unrestricted Somatic Stem Cells from Human Umbilical Cord Blood after Treatment with Epigenetic Agents.
Can targeted epigenetic treatment expand the developmental potential of stem cells without introducing additional genes? We treated somatic stem cells from human umbilical cord blood with 5-aza-2′-deoxycytidine and trichostatin A, compounds that act on DNA methylation and histone modifications, respectively.
In one of the four cord-blood stem cell lines studied, a stable cell type emerged that formed spherical cell clusters. We named these cells “SpheUSSC”. They could be propagated for at least 150 cell divisions and expressed OCT4. They retained their ability to form bone cells and acquired the ability to develop into fat cells. This expanded developmental potential was achieved entirely without transgenic intervention. The study demonstrates how epigenetically active compounds can alter the properties and differentiation potential of a stem cell population, providing a model for studying cellular identity and plasticity.
Ghanjati F; Santourlidis S
Stem Cells Int. 2016;2016:7643218. · Published online 14 December 2015 · PMID: 26788071
Protective vaccination and blood-stage malaria modify DNA methylation of gene promoters in the liver of Balb/c mice.
This study used a mouse model to examine how protective vaccination and subsequent infection with the malaria parasite Plasmodium chabaudi relate to DNA methylation in the liver. The liver plays important roles in defending against the blood stages of this infection.
Following vaccination and during infection, we found altered methylation patterns in the promoters of numerous genes. Affected processes included immune defence, liver regeneration and blood formation. These findings suggest that epigenetic changes may contribute to improved defence after vaccination. The study used an experimental mouse malaria model; it does not establish an equivalent effect in humans.
Al-Quraishy S; Dkhil MA; Abdel-Baki AS; Ghanjati F; Erichsen L; Santourlidis S; Wunderlich F; Araúzo-Bravo MJ
Parasitol Res. 2017;116(5):1463. · PMID: 28315013
Genome-wide screening identifies Plasmodium chabaudi-induced modifications of DNA methylation status of Tlr1 and Tlr6 gene promoters in liver, but not spleen, of female C57BL/6 mice.
How does malaria infection alter epigenetic regulation in its host? We examined gene-promoter DNA methylation in female C57BL/6 mice during blood-stage infection with Plasmodium chabaudi. The changes differed markedly between the liver and spleen.
In the liver, the promoter region examined at Tlr6 lost methylation marks, while a region further upstream of Tlr1 became more methylated. Both genes increased their activity. Their receptors help the innate immune system recognise components of pathogens. These specific changes were found in the liver, not the spleen. The results suggest organ-specific epigenetic fine-tuning of immune defence in this mouse model.
Al-Quraishy S; Dkhil MA; Abdel-Baki AS; Delic D; Santourlidis S; Wunderlich F
Parasitol Res. 2013;112(11):3757–3770. · Published online 16 August 2013 · PMID: 23949311
Phylo-Epigenetic Conservation and CpG Erosion in OCT4, SOX2, and hTERT Intragenic CpG Islands: A Waddingtonian Perspective on Mammalian Developmental Evolution.
I compared epigenetically important DNA regions in OCT4, SOX2 and hTERT—genes active early in embryonic development—across ten living primate species, including humans, as well as Neanderthals and Denisovans. The analysis revealed both strongly conserved CpG sites and characteristic changes consistent with known methylation-dependent mutational mechanisms. The findings suggest an interplay between epigenetic regulation and genetic change over evolutionary time and support further hypotheses about how environment and nutrition might influence these processes.
Santourlidis S.
Genes (Basel). 2025 Sep 18;16(9):1102.
DOI: 10.3390/genes16091102
PMID: 41010047 · PMCID: PMC12470082
Phylo-Epigenetics in Phylogeny Analyses and Evolution.
I compared CpG sites—positions at which methyl groups can be attached to DNA as epigenetic marks—in selected gene regions of modern humans, Neanderthals, Denisovans and other great apes. Conserved and altered CpG sites alone enabled reconstruction of a phylogenetic tree that recapitulates major known relationships and divergence times. The results suggest that changes at these methylatable DNA sites both reflect our evolutionary history and can alter the foundations of epigenetic regulation in subsequent generations.
Santourlidis S.
Genes (Basel). 2024 Sep 12;15(9):1198.
DOI: 10.3390/genes15091198
PMID: 39336789 · PMCID: PMC11430929
Phyloepigenetics.
This paper develops an approach that uses epigenetically important CpG sites to investigate evolutionary relationships. Their distinctive roles in gene regulation and characteristic mutability offer an additional perspective on evolution. The publication provides the conceptual foundation for my later phylo-epigenetic studies.
Santourlidis S.
Biology (Basel). 2022 May 15;11(5):754.
DOI: 10.3390/biology11050754
PMID: 35625482 · PMCID: PMC9138650
Methyl Group Metabolism in Differentiation, Aging, and Cancer.
How do components of our food enter the molecular processes that regulate our genes? This review describes methyl-group metabolism as an important biochemical link between nutrition, cell function and epigenetics. Interconnected metabolic pathways supply methyl groups needed for processes including DNA methylation.
We bring together evidence connecting this supply with cell differentiation, ageing and cancer development. Metabolic disruption can be accompanied by changes in epigenetic patterns. The paper develops research questions about methylome stability and the significance of nutrition and environment. It provides a scientific foundation for my aim of making the connections between living conditions, gene regulation and health accessible to a wider audience.
Erichsen L; Thimm C; Santourlidis S
Int J Mol Sci. 2022;23(15). · PMID: 35955511
Genome-wide hypomethylation of LINE-1 and Alu retroelements in cell-free DNA of blood is an epigenetic biomarker of human aging.
LINE-1 elements are repetitive DNA sequences scattered throughout our genome in several hundred thousand copies. Most copies are permanently inactive, but a small fraction can replicate and insert at new locations in the genome. If inadequately controlled, these elements can cause DNA damage, mutations and disruption of gene regulation. Their activation is associated with ageing, genomic instability and numerous diseases. LINE-1-mediated genomic changes have been demonstrated in various cancers; some can contribute directly to cancer development.
DNA methylation is an essential component of the epigenetic defence mechanisms that silence LINE-1 elements and keep their potentially harmful activity in check. It therefore contributes to genome stability and cellular health. Loss of this control can promote genetic damage and inflammatory processes that affect the whole organism.
We examined DNA methylation of LINE-1 and Alu elements in cellular and cell-free DNA from blood. We found an age-dependent loss of these methylation marks in cell-free DNA, while blood-cell DNA showed no corresponding significant association. Methylation loss in cell-free DNA was more pronounced in smokers.
Our biomarker thus makes a biologically meaningful aspect of epigenetic stability measurable. Idiolocally normalised real-time methylation-specific PCR (IDLN-MSP) allows targeted, quantitative analysis of these methylation patterns. The method offers a molecular tool for detecting age- and environment-related changes in the epigenetic control of repetitive DNA from a blood sample, and for following their course in further studies.
Erichsen L, Beermann A, Arauzo-Bravo MJ, Hassan M, Dkhil MA, Al-Quraishy S, Hafiz TA, Fischer JC, Santourlidis S.
Saudi J Biol Sci. 2018 Sep;25(6):1220-1226. Epub 2018 Feb 13.
DOI: 10.1016/j.sjbs.2018.02.005
PMID: 30174526 · PMCID: PMC6117241
IDLN-MSP: Idiolocal normalization of real-time methylation-specific PCR for genetic imbalanced DNA specimens.
Quantitative DNA methylation analysis compares a target region with a reference. Tumour cells, in particular, may have gained or lost copies of certain DNA regions. If the target and reference regions differ in copy number, conventional normalisation can distort the result.
We developed idiolocal normalisation, or IDLN, as a methodological refinement of real-time methylation-specific PCR. The methylation-independent reference measurement is made close to the target region. As a result, target and reference generally have the same copy number. This reduces an important source of error and enables more reliable quantitative comparisons. The method provides a key foundation for my subsequent research on epigenetic biomarkers.
Santourlidis S; Ghanjati F; Beermann A; Hermanns T; Poyet C
Biotechniques. 2016;60(2):84. · PMID: 26842353
An interdisciplinary methods paper on methylation analysis in genetically imbalanced DNA samples; classified here under cancer research.
Unreserved application of epigenetic methods to define differences of DNA methylation between urinary cellular and cell-free DNA.
Urine contains DNA from shed cells as well as free DNA fragments. We investigated whether this cell-free DNA could be used for detailed epigenetic analyses and how its methylation patterns differ from those of cellular DNA.
Using bisulphite sequencing, real-time methylation-specific PCR and array analyses, we examined individual LINE-1 methylation patterns as well as broader differences in DNA methylation. We found differences between the two DNA fractions and between samples from bladder cancer patients and healthy controls. The study establishes cell-free urinary DNA as material for developing non-invasive epigenetic biomarkers—from discovering suitable marks to detecting them with targeted assays.
Ghanjati F; Beermann A; Hermanns T; Poyet C; Araúzo-Bravo MJ; Seifert HH; Schmidtpeter M; Goering W; Sorg R; Wernet P; Santourlidis S
Cancer Biomark. 2014;14(5):295–302. · PMID: 25171471
66 publications from my PubMed author list. Correction and retraction notices, and retracted articles, are not included in this overview. Updated: 14 October 2026. Each paper appears once, under its primary or closest research area. Interdisciplinary basic and methods papers, and studies on related topics, are identified accordingly. Within each category, publications are ordered by year, newest first.
View the current author list on PubMed
66 of 66 entries
Hassan SY; Santourlidis S; Flanagan TW; Hassan SL; Zhou H; Schmidt MF; Cacchi C; Lammert MF; Megahed M; Yazdi AS; Jonigk DD; Araúzo-Bravo MJ; Brodell RT; Facca S; Haikel Y; Hassan M
Cells. 2026;15(8). · PMID: 42041590
Santourlidis S; Araúzo-Bravo MJ; Hassan M; Bendhack ML
Cancers (Basel). 2025;17(23). · PMID: 41375001
Eshaq AM; Flanagan TW; Hassan SY; Al Asheikh SA; Al-Amoudi WA; Santourlidis S; Hassan SL; Alamodi MO; Bendhack ML; Alamodi MO; Haikel Y; Megahed M; Hassan M
Cancers (Basel). 2024;16(15). · PMID: 39123481
Santourlidis S; Araúzo-Bravo MJ; Brodell RT; Hassan M; Bendhack ML
Int J Mol Sci. 2024;25(13). · PMID: 39000438
Santourlidis S; Araúzo-Bravo MJ; Erichsen L; Bendhack ML
Cancers (Basel). 2024;16(10). · PMID: 38792020
Kharouf N; Flanagan TW; Alamodi AA; Al Hmada Y; Hassan SY; Shalaby H; Santourlidis S; Hassan SL; Haikel Y; Megahed M; Brodell RT; Hassan M
Cells. 2024;13(3). · PMID: 38334632
Al Hmada Y; Brodell RT; Kharouf N; Flanagan TW; Alamodi AA; Hassan SY; Shalaby H; Hassan SL; Haikel Y; Megahed M; Santourlidis S; Hassan M
Cancers (Basel). 2024;16(2). · PMID: 38275910
Kharouf N; Flanagan TW; Hassan SY; Shalaby H; Khabaz M; Hassan SL; Megahed M; Haikel Y; Santourlidis S; Hassan M
Cancers (Basel). 2023;15(12). · PMID: 37370757
Araúzo-Bravo MJ; Erichsen L; Ott P; Beermann A; Sheikh J; Gerovska D; Thimm C; Bendhack ML; Santourlidis S
Int J Mol Sci. 2022;24(1). · PMID: 36613831
Ott P; Araúzo-Bravo MJ; Hoffmann MJ; Poyet C; Bendhack ML; Santourlidis S; Erichsen L
Cancers (Basel). 2022;14(18). · PMID: 36139544
Santourlidis S; Schulz WA; Araúzo-Bravo MJ; Gerovska D; Ott P; Bendhack ML; Hassan M; Erichsen L
Int J Mol Sci. 2022;23(3). · PMID: 35163453
Jamal SME; Alamodi A; Wahl RU; Grada Z; Shareef MA; Hassan SY; Murad F; Hassan SL; Santourlidis S; Gomez CR; Haikel Y; Megahed M; Hassan M
Oncogene. 2020;39(32):5468. · PMID: 32616888
Erichsen L; Seifert HH; Schulz WA; Hoffmann MJ; Niegisch G; Araúzo-Bravo MJ; Bendhack ML; Poyet C; Hermanns T; Beermann A; Hassan M; Theis L; Mahmood W; Santourlidis S
Sci Rep. 2020;10(1):3808. · PMID: 32123240
Selimovic D; Wahl RU; Ruiz E; Aslam R; Flanagan TW; Hassan SY; Santourlidis S; Haikel Y; Friedlander P; Megahed M; Kandil E; Hassan M
Int J Oncol. 2019;55(6):1324. · PMID: 31638203
Erichsen L; Ghanjati F; Beermann A; Poyet C; Hermanns T; Schulz WA; Seifert HH; Wild PJ; Buser L; Kröning A; Braunstein S; Anlauf M; Jankowiak S; Hassan M; Bendhack ML; Araúzo-Bravo MJ; Santourlidis S
Sci Rep. 2018;8(1):3477. · PMID: 29472622
El Jamal SM; Taylor EB; Abd Elmageed ZY; Alamodi AA; Selimovic D; Alkhateeb A; Hannig M; Hassan SY; Santourlidis S; Friedlander PL; Haikel Y; Vijaykumar S; Kandil E; Hassan M
Cell Div. 2016;11:11. · PMID: 27486476
Santourlidis S; Ghanjati F; Beermann A; Hermanns T; Poyet C
Biotechniques. 2016;60(2):84. · PMID: 26842353
An interdisciplinary methods paper on methylation analysis in genetically imbalanced DNA samples; classified here under cancer research.
Ghanjati F; Beermann A; Hermanns T; Poyet C; Araúzo-Bravo MJ; Seifert HH; Schmidtpeter M; Goering W; Sorg R; Wernet P; Santourlidis S
Cancer Biomark. 2014;14(5):295. · PMID: 25171471
An interdisciplinary methods paper on cellular and cell-free urinary DNA; classified here under cancer research.
Selimovic D; Badura HE; El-Khattouti A; Soell M; Porzig BB; Spernger A; Ghanjati F; Santourlidis S; Haikel Y; Hassan M
Apoptosis. 2013;18(8):980. · PMID: 23564313
Selimovic D; Porzig BB; El-Khattouti A; Badura HE; Ahmad M; Ghanjati F; Santourlidis S; Haikel Y; Hassan M
Cell Signal. 2013;25(1):308. · PMID: 23079083
Neves R; Scheel C; Weinhold S; Honisch E; Iwaniuk KM; Trompeter HI; Niederacher D; Wernet P; Santourlidis S; Uhrberg M
BMC Res Notes. 2010;3:219. · PMID: 20682048
Cetindere T; Nambiar S; Santourlidis S; Essmann F; Hassan M
Cell Signal. 2010;22(2):197. · PMID: 19799997
Santourlidis S; Kimura F; Fischer J; Schulz WA
Biochem Cell Biol. 2004;82(5):589. · PMID: 15499388
An interdisciplinary basic research paper on DNMT1, PCNA and clonogenic cell growth; classified here under cancer research.
Stallmach A; Wittig BM; Kremp K; Goebel R; Santourlidis S; Zeitz M; Menges M; Raedle J; Zeuzem S; Schulz WA
Exp Mol Pathol. 2003;74(3):262. · PMID: 12782013
Kimura F; Seifert HH; Florl AR; Santourlidis S; Steinhoff C; Swiatkowski S; Mahotka C; Gerharz CD; Schulz WA
Int J Cancer. 2003;104(5):568. · PMID: 12594811
Schulz WA; Elo JP; Florl AR; Pennanen S; Santourlidis S; Engers R; Buchardt M; Seifert HH; Visakorpi T
Genes Chromosomes Cancer. 2002;35(1):58. · PMID: 12203790
Leube B; Drechsler M; Mühlmann K; Schäfer R; Schulz WA; Santourlidis S; Anastasiadis A; Ackermann R; Visakorpi T; Müller W; Royer-Pokora B
Prostate. 2002;50(3):135. · PMID: 11813205
Santourlidis S; Warskulat U; Florl AR; Maas S; Pulte T; Fischer J; Müller W; Schulz WA
Mol Carcinog. 2001;32(1):36. · PMID: 11568974
Santourlidis S; Florl A; Ackermann R; Wirtz HC; Schulz WA
Prostate. 1999;39(3):166. · PMID: 10334105
Marey AM; Dkhil MA; Abdel Moneim AA; Santourlidis S; Abdel-Gaber R; Alquraishi MI; Abdalla MS
Microsc Res Tech. 2025;88(1):127. · PMID: 39210696
Marey AM; Dkhil MA; Abdel-Moneim AE; Santourlidis S; Abdel-Gaber R; Abdalla MS
Microsc Res Tech. 2024;87(9):2034. · PMID: 38634191
Selimovic D; Kharouf N; Carrouel F; Hassan SY; Flanagan TW; Hassan SL; Megahed M; Haikel Y; Santourlidis S; Hassan M
Int J Mol Sci. 2023;24(6). · PMID: 36982421
Santourlidis S; Graffmann N; Christ J; Uhrberg M
J Immunol. 2008;180(1):418. · PMID: 18097043
Graffmann N; Santourlidis S; Christ J; Wernet P; Uhrberg M
Anal Biochem. 2006;354(2):308. · PMID: 16750813
An interdisciplinary methods paper on chromatin accessibility; classified here within its immunological research context.
Trundley AE; Hiby SE; Chang C; Sharkey AM; Santourlidis S; Uhrberg M; Trowsdale J; Moffett A
Immunogenetics. 2006;57(12):904. · PMID: 16391939
Trompeter HI; Gómez-Lozano N; Santourlidis S; Eisermann B; Wernet P; Vilches C; Uhrberg M
J Immunol. 2005;174(7):4135. · PMID: 15778373
Santourlidis S; Trompeter HI; Weinhold S; Eisermann B; Meyer KL; Wernet P; Uhrberg M
J Immunol. 2002;169(8):4253. · PMID: 12370356
Ghanjati F; Santourlidis S
Stem Cells Int. 2016;2016:7643218. · PMID: 26788071
Dorn I; Klich K; Arauzo-Bravo MJ; Radstaak M; Santourlidis S; Ghanjati F; Radke TF; Psathaki OE; Hargus G; Kramer J; Einhaus M; Kim JB; Kögler G; Wernet P; Schöler HR; Schlenke P; Zaehres H
Haematologica. 2015;100(1):32. · PMID: 25326431
Hargus G; Ehrlich M; Araúzo-Bravo MJ; Hemmer K; Hallmann AL; Reinhardt P; Kim KP; Adachi K; Santourlidis S; Ghanjati F; Fauser M; Ossig C; Storch A; Kim JB; Schwamborn JC; Sterneckert J; Schöler HR; Kuhlmann T; Zaehres H
Cell Rep. 2014;8(6):1697. · PMID: 25220454
Santourlidis S; Wernet P; Ghanjati F; Graffmann N; Springer J; Kriegs C; Zhao X; Brands J; Araúzo-Bravo MJ; Neves R; Koegler G; Uhrberg M
Stem Cell Res. 2011;6(1):60. · PMID: 20933485
Zaehres H; Kögler G; Arauzo-Bravo MJ; Bleidissel M; Santourlidis S; Weinhold S; Greber B; Kim JB; Buchheiser A; Liedtke S; Eilken HM; Graffmann N; Zhao X; Meyer J; Reinhardt P; Burr B; Waclawczyk S; Ortmeier C; Uhrberg M; Schöler HR; Cantz T; Wernet P
Exp Hematol. 2010;38(9):809. · PMID: 20541586
Liedtke S; Buchheiser A; Bosch J; Bosse F; Kruse F; Zhao X; Santourlidis S; Kögler G
Stem Cell Res. 2010;5(1):40. · PMID: 20434420
Grinstein E; Santourlidis S; Fischer J; Uhrberg M; Wernet P
J Stem Cells Regen Med. 2007;2(1):18. · PMID: 24692882
Grinstein E; Du Y; Santourlidis S; Christ J; Uhrberg M; Wernet P
J Biol Chem. 2007;282(17):12439. · PMID: 17255095
Aguiar J; Santurlidis S; Nowok J; Alexander C; Rudnicki D; Gispert S; Schulz W; Auburger G
Biochem Biophys Res Commun. 1999;254(2):315. · PMID: 9918835
An interdisciplinary basic research paper on regulation of a CpG-island promoter at the SCA2 gene; included here as background to epigenetic gene regulation.
Alharbi HM; Al-Shaebi EM; Al-Quraishy S; Almohawis N; Virk P; Albeshr M; Santourlidis S; Abdel-Gaber R
Curr Microbiol. 2026;83(11). · PMID: 42732010
Al-Shaebi EM; Elabed S; Santourlidis S; Alharbi HM; Dkhil MA; Abdel-Gaber R
Biomed Chromatogr. 2026;40(7):e70501. · PMID: 42206425
Alharbi HM; Dkhil M; Santourlidis S; Albeshr M; Al-Shaebi EM; Abdel-Gaber R
Helminthologia. 2026;63(1):48. · PMID: 42305886
Abdel-Gaber R; Alotaibi M; Albeshr M; Dkhil MA; Santourlidis S; Elghamdy AO; Al-Quraishy S; Al-Shaebi EM
J Helminthol. 2026;100:e64. · PMID: 42290263
Al-Shaebi EM; Dkhil MA; Albeshr M; Elabed S; Santourlidis S; Alharbi HM; Abdel-Gaber R
Biomed Chromatogr. 2026;40(6):e70450. · PMID: 42050801
Abdel-Gaber R; Dkhil MA; Elabed S; Santourlidis S; Alharbi HM; Al-Quraishy S; Al-Shaebi EM
Biomed Chromatogr. 2026;40(4):e70387. · PMID: 41705653
Alotaibi M; Al Quraishy S; Almohawis N; Santourlidis S; Al-Shaebi E; Abdel-Gaber R
Front Cell Infect Microbiol. 2026;16:1774323. · PMID: 41859466
Alotaibi M; Abdel-Gaber R; Al Quraishy S; Santourlidis S; Alharbi HM; Al-Shaebi E
Helminthologia. 2025;62(4):340. · PMID: 41777286
Abdel-Gaber R; Albasyouni S; Santourlidis S; Al Quraishy S; Al-Shaebi E
Front Immunol. 2025;16:1714313. · PMID: 41479898
Abdel-Gaber R; Albasyouni S; Santourlidis S; Al Quraishy S; Al-Shaebi E
Front Cell Infect Microbiol. 2025;15:1724123. · PMID: 41278479
Dkhil MA; Khalil MF; Diab MSM; Bauomy AA; Santourlidis S; Al-Shaebi EM; Al-Quraishy S
Saudi J Biol Sci. 2019;26(7):1468. · PMID: 31762611
Al-Quraishy S; Dkhil MA; Abdel-Baki AS; Ghanjati F; Erichsen L; Santourlidis S; Wunderlich F; Araúzo-Bravo MJ
Parasitol Res. 2017;116(5):1463. · PMID: 28315013
Al-Quraishy S; Dkhil MA; Abdel-Baki AA; Delic D; Santourlidis S; Wunderlich F
Parasitol Res. 2013;112(11):3757. · PMID: 23949311
Rizk S; Abdel Moneim AE; Abdel-Gaber RA; Alquraishi MI; Santourlidis S; Dkhil MA
ACS Omega. 2023;8(44):41865. · PMID: 37969968
A related study on organ injury and protection. It examines acute kidney injury rather than ageing or life extension directly.
Erichsen L; Thimm C; Santourlidis S
Int J Mol Sci. 2022;23(15). · PMID: 35955511
Erichsen L; Beermann A; Arauzo-Bravo MJ; Hassan M; Dkhil MA; Al-Quraishy S; Hafiz TA; Fischer JC; Santourlidis S
Saudi J Biol Sci. 2018;25(6):1220. · PMID: 30174526
Graffmann N; Brands J; Görgens A; Vitoriano da Conceição Castro S; Santourlidis S; Reckert A; Michele I; Ritz-Timme S; Fischer JC; Adjaye J; Kögler G; Giebel B; Uhrberg M
Stem Cells Dev. 2015;24(17):2018. · PMID: 25961873
Santourlidis S
Genes (Basel). 2025;16(9). · PMID: 41010047
A comparative basic research study of the epigenetically relevant CpG architecture of developmental genes and its changes during primate evolution.
Santourlidis S
Genes (Basel). 2024;15(9). · PMID: 39336789
A basic research study reconstructing evolutionary relationships from epigenetically relevant CpG sites.
Santourlidis S
Biology (Basel). 2022;11(5). · PMID: 35625482
A conceptual paper on phyloepigenetics and the evolutionary significance of epigenetically relevant CpG sites.
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Four inventions arising from my scientific work, documented in the following patent publications.
A method for normalised determination of DNA methylation with reference to transposable elements in the genome.
Determination of the degree of DNA methylation
View patent · WO2010084154A2A method for determining normalised DNA methylation levels, with applications to biomarkers for prostate and bladder cancer.
Method for determining the degree of DNA methylation
View patent · EP3981885B1An epigenetic approach to assessing stem cell quality.
Quality determination of stem cells
View patent · WO2012049154A1A method for the epigenetic reprogramming of foetal stem cells.
Epigenetic reprogramming of foetal stem cells
View patent · EP2952578A1My ambition extends beyond scientific discovery: research should lead to applications that help people. Building on my work at Heinrich Heine University Düsseldorf, I therefore co-founded the German biotechnology and healthcare spin-off EpiproCare with my partner, Prof. Marcelo Bendhack. Prof. Bendhack is President of the Uro Oncology Latin American Association (UROLA) and works at Universidade Positivo in Curitiba, Brazil. He completed his specialist training at the renowned Department of Urology at University Hospital Düsseldorf under the leadership of Prof. Rolf Ackermann. During this period, I was also working on my doctoral dissertation there.
I received decisive support in establishing EpiproCare from my late mentor Prof. Rolf Ackermann, former Chair of Urology and Medical Director of the Medical Institutions of Heinrich Heine University Düsseldorf. Equally important were my friends Prof. Marcelo Bendhack, my clinical partner, Dr. Lars Erichsen, my former doctoral student (dissertation), and Prof. Marcos J. Araúzo-Bravo, my long-standing research collaborator in bioinformatics (Max Planck profile · Ikerbasque profile · Publications). Their support and our close, partly interdisciplinary collaboration shaped and enabled this important journey. Together, we brought epigenetic research, clinical experience and bioinformatics into a productive scientific partnership.
Through EpiproCare, I aim to further develop insights and methods from epigenetics for medical applications and make them available to patients and doctors worldwide. The spin-off connects my university research with practical implementation.
Heinrich Heine University is also an entrepreneurial university and supports the translation of scientific discoveries into new businesses.
My special thanks go to my academic teachers: Prof. Dr. Wolfgang Schulz, Prof. Dr. Rolf Ackermann, Prof. Dr. Frank Wunderlich and Dr. Hans-Peter Schmitt-Wrede. They have shaped my scientific journey and offered valuable insights that continue to inform my work.
Additional thanks go to Prof. James Adjaye. A word of thanks to Prof. Peter Wernet.
Knowledge for everyone · No prior knowledge needed
Our genes provide the foundation. How our cells use this information, and the role our environment plays, are central to our lives. Here I answer eight common questions about epigenetics, with examples from development, environment, cancer medicine and ageing.
Epigenetics studies mechanisms that influence how cells use their genetic information. These mechanisms help determine which genes are active, when and where they are active, and how strongly they are expressed, without changing the sequence of DNA bases. Certain epigenetic states can be passed on during cell division.
A useful starting image is to think of DNA as an extensive library. A single human chromosome set contains around three billion base pairs—the paired “letters” of our genetic information. It provides the foundations for the development of around 200 broad cell types and their countless developmental and maturation states. Epigenetic mechanisms influence which parts of this library a cell uses at a particular time, helping shape its development and function.
Genetics studies the genome, its variation and inheritance. Epigenetics examines an additional layer: how the use of genetic information is regulated and stabilised. The two fields are closely connected. Genes and their regulation work together in development and cellular function.
A distinctive feature of epigenetic mechanisms is that they can be influenced by many environmental factors. Nutrition, exercise, pollutants and other living conditions affect biological processes that can also alter gene regulation. Epigenetics therefore forms an important bridge between our environment and the genetic foundations of our lives.
We are gaining a clearer understanding of how this connection works. Epigenetic regulation can help cells adapt to changing conditions and maintain their functions. Harmful environmental influences can also disrupt this regulation and promote changes associated with disease.
This opens new horizons for health and the way we live. People can substantially shape their living conditions and reduce some harmful exposures. The better we understand epigenetic mechanisms and the timescales over which they change, the more precisely we can investigate which changes in our lives support health-promoting gene regulation.
Modern epigenetic methods allow us to measure these changes and follow them over time. This creates new opportunities to study environmental influences and develop evidence-based approaches to prevention, health and quality of life.
Most cells in the body have largely the same genetic information in their nuclei, but they use different parts of it. A skin cell needs a different set of active genes from a nerve cell. Epigenetic mechanisms help establish these distinct programmes and maintain them through cell division.
Many specialised cell types can thus emerge from a common starting cell. The developmental paths towards a skin cell or nerve cell pass through numerous intermediate stages, which are also epigenetically regulated. Epigenetics therefore shapes both a cell’s development and the maintenance of its specialised function.
DNA methylation involves attaching small chemical groups, called methyl groups, to particular DNA building blocks. In humans, this occurs mainly at CpG sites, where the DNA bases cytosine and guanine follow one another directly.
These marks form characteristic, cell-type-specific patterns across a cell’s entire genome. The complete set of these methylation patterns is called the methylome . DNA methylation is one of the best-studied epigenetic mechanisms through which additional information is placed on the genome and its use is regulated.
Its effects depend on where the marks are located and on their biological context. More methylation does not therefore always mean less gene activity. What matters is the appropriate pattern.
A human somatic cell with a double set of chromosomes may carry roughly 80 million methyl groups on its DNA. The actual number varies with cell type and state.
Cells have powerful molecular mechanisms to preserve this extensive pattern during division. As DNA is copied, specialised proteins recognise existing marks and add methylation to the newly formed strands. This restores the patterns in daughter cells with high accuracy, helping them retain the characteristic properties and functions of their parent cell. At the same time, methylation patterns can change during development, in response to environmental influences or in disease.
In my view, this holds an important key to preserving health and quality of life as we age: cellular mechanisms should be maintained and supported so that methylation patterns important to cell identity are restored as accurately as possible in daughter cells. Reliable transmission helps newly generated cells retain their specialised roles. Understanding how this epigenetic stability can be preserved over the long term is therefore an important avenue in healthy-ageing research.
Cells supply the necessary methyl groups through a tightly coordinated metabolic network known as one-carbon metabolism. Nutrients in our food—including methionine, folate and choline—play important roles. The immediate donor of methyl groups for DNA methylation is the body’s own molecule S-adenosylmethionine, or SAM.
This reveals a tangible biochemical bridge between nutrition, environment and gene regulation. Our bodies contain trillions of nucleated cells. A comprehensive study estimated around seven trillion in its adult reference model, which represents an adult man. Some cell populations renew within days; others turn over very slowly, and some specialised cells rarely divide. Cell division and other metabolic processes therefore require a continuously available, carefully regulated supply of methyl groups.
This offers an important approach to understanding a long life in good health and with a high quality of life: how can nutrition and living conditions help preserve epigenetic regulation? A well-balanced biological equilibrium is central. A continuous, sufficient supply of the required methyl groups is an important prerequisite for dividing cells to restore their methylation patterns reliably and pass their characteristic properties and functions to daughter cells. A better understanding of this supply and its regulation offers prospects for supporting health and quality of life and favourably influencing ageing processes.
Our cells respond to signals from within the body and from the environment. Nutrition, tobacco smoke and other influences can also affect epigenetic patterns. Epigenetics thus provides an important connection between living conditions and gene regulation.
Smoking is a well-studied example: large studies show characteristic differences in blood DNA methylation between smokers and non-smokers. Such associations help researchers investigate the biological effects of environmental exposures.
The agouti mouse offers a particularly vivid example. In mice carrying the Aᵛʸ variant, an inserted DNA sequence of retroviral origin can keep the agouti gene continuously active. When this sequence is weakly methylated, mice are often yellow and prone to obesity, disturbances of glucose metabolism including diabetes, and—depending on their genetic background—certain tumours. Greater methylation silences the sequence and more often produces a brown coat and a metabolically healthier phenotype.
In 2003, Waterland and Jirtle showed that maternal nutrition can influence this pattern. Supplementing the maternal diet with folate, vitamin B12, choline and betaine increased methylation at the relevant locus and shifted offspring coat colours towards brown. The study directly demonstrated an effect of maternal nutrition on methylation and gene regulation. It measured methylation and coat colour; the disease susceptibility of the yellow phenotype is established by other studies of this mouse model.
Human studies also suggest lasting effects of early nutritional conditions. During the Dutch Hunger Winter of 1944–45, pregnant women experienced severe undernutrition. Around 60 years later, Heijmans and colleagues found lower DNA methylation in a regulatory region of the growth-factor gene IGF2 in people exposed around conception, compared with their unexposed same-sex siblings.
A further study, published in 2013, examined a total of 360 adults in the grandchildren’s generation, comparing offspring of parents who had been exposed to famine before birth with offspring of unexposed parents. Children of men who had themselves been exposed in the womb were, on average, 4.9 kilograms heavier and had a body mass index 1.6 units higher than children of unexposed fathers. This association was not found in children of similarly exposed mothers. The study found no differences in general health.
These findings illustrate how far the effects of early living conditions may reach. The grandchildren study alone, however, does not prove inheritance of altered DNA methylation: it measured body size and reported health, rather than transmission of specific epigenetic marks. Together with the methylation findings, it provides important leads for investigating the interplay of nutrition, development and later health.
Yes. Epigenetic patterns change during development and can remain responsive to internal and external influences later in life. Some changes are temporary, while others persist. How readily a pattern changes depends on factors including cell type and the mechanism involved. This does not mean we can control our genes at will: research investigates precisely which changes have which consequences.
This offers an important opportunity for health. Many epigenetic changes are, in principle, reversible, although reversal may take time. After smoking cessation, for example, some methylation patterns can gradually move towards those of non-smokers. Depending on the site examined, this may take months or years, while other changes persist much longer. Reversibility depends on the particular pattern, cell type and living conditions. Understanding these timescales helps us interpret long-term changes in our lives and their biological effects.
Cancer cells can show changes in both their DNA sequence and its epigenetic regulation. For example, altered regulation can reduce the activity of genes that restrain cell growth.
Characteristic epigenetic patterns can be measured. Depending on the cancer type and marker studied, they can contribute to diagnosis, prognosis or treatment selection. This is also the starting point for my research on epigenetic biomarkers.
Healthy cells likewise have characteristic methylation patterns. Immune cells, blood-forming progenitor cells, liver cells and cells of other organs each carry epigenetic features associated with their identity and specialised function. These patterns provide important reference points for distinguishing physiological states from disease-associated changes.
This perspective extends beyond detecting disease at a single point in time. Repeated epigenetic analyses offer the possibility of following selected molecular states and revealing changes over time. Cell-free DNA in blood can contain traces of different cell types. With suitable markers validated for the question being asked, it can provide information about cellular origins, cell injury or altered regulation. This is the potential of long-term epigenetic monitoring of health and disease.
Certain DNA methylation patterns change with age. Researchers use such patterns to construct epigenetic clocks: statistical models that estimate age from molecular measurements. These help investigate ageing processes and differences between individuals.
Such a measurement alone does not reveal how healthy a person is or how long they will live. I am interested in how a better understanding of epigenetic regulation can help preserve health and quality of life in later years.
Together with my colleagues, I have developed an epigenetic method that makes an important aspect of epigenetic integrity measurable from a blood sample. Using idiolocally normalised real-time methylation-specific PCR, we analyse methylation patterns of repetitive LINE-1 and Alu elements in cell-free DNA. Our published findings show an age-dependent loss of these marks and a more pronounced loss in smokers.
Cell-free DNA in blood carries molecular information from different cells in the body, including immune cells, blood-forming progenitor cells and liver cells. Our method examines methylation patterns in this DNA, providing an overall view of an important aspect of the epigenetic integrity of the body compartments represented in the sample. My goal is to develop this measurement as a surrogate marker—an indirect molecular indicator—of epigenetic stability, current health, susceptibility to disease and aspects of biological ageing. Repeated measurements offer the prospect of tracking age- and environment-related changes and scientifically investigating the effects of changes in living conditions.
Explore the topics of Cancer medicine, healthy ageing and Evolution or discover my scientific publications.
From scientific discovery to medical application
Cancer cells leave molecular traces. My research focuses on characteristic epigenetic changes at the hTERT gene. This gene encodes a central component of telomerase, an enzyme that enables many cancer cells to sustain continued division.
In certain regions involved in hTERT regulation, striking DNA methylation patterns occur across numerous cancers. These chemical marks form the basis of the EpihTERT concept. I investigate them as an epigenetic signal of malignancy: a molecular trace that may provide information about malignant cells and their biological properties.
Scientific background · hTERT epigenetics, 2024
The scientific literature shows that certain hTERT methylation patterns can distinguish tumour tissue from healthy comparison tissue. In prostate cancer, increased methylation of the TERT Hypermethylated Oncological Region (THOR) has also been associated with higher Gleason scores, invasive growth and an increased risk of recurrence.
This opens perspectives for early detection and prognosis: finding cancer as early as possible and better assessing which disease poses a serious threat. Follow-up is another goal. In future, repeated analyses are intended to help identify residual tumour activity or recurrence at an early stage. Further clinical studies are examining how reliably EpihTERT can fulfil these roles.
For detection, we use idiolocally normalised methylation-specific PCR. In simple terms, a selected DNA region is amplified, with its methylation pattern determining the measurement. Normalisation helps account for distortions caused by altered DNA copy numbers in tumour cells. The method can also be applied to DNA from formalin-fixed, paraffin-embedded tissue, such as biopsy samples.
Body fluids offer another route. When tumour cells die, they release DNA fragments that retain their stable epigenetic marks. Within tumours, these fragments often account for a relatively high proportion of the total cell-free DNA. Such cell-free DNA traces can be analysed specifically for characteristic methylation patterns.
Urine is of particular interest in urothelial carcinoma, including bladder cancer: tumours of the urinary tract can release their DNA directly into urine. The main local sources of non-tumour-derived cell-free DNA include healthy cells of the urinary tract lining, kidney cells and immune cells. Through direct release into urine, tumour DNA can account for a substantial proportion of the cell-free DNA present. This creates favourable conditions for detecting characteristic epigenetic tumour signals.
Early detection is particularly important in bladder cancer. Blood in the urine is often what first prompts a medical consultation. In many cases, this warning sign occurs in the late stages of the disease. This highlights an important potential application of our molecular urine test: detecting tumour signals before noticeable symptoms appear.
Loss of DNA methylation at LINE-1 elements, known as LINE-1 hypomethylation, is a characteristic epigenetic finding already present in the early stages of urothelial carcinoma. Our 2014 study showed that differences in LINE-1 methylation can be detected sensitively in cell-free urinary DNA, including differences between patients with bladder cancer and healthy comparison participants. Together, these findings provide an important foundation for developing non-invasive tests for the early detection of urothelial carcinoma.
The underlying principle resembles forensic DNA analysis: small quantities of genetic material are selectively amplified and examined. Here, we look for stable epigenetic features of cancer cells. These can be detected reliably, with very high sensitivity and reproducibility.
I aim to validate EpihTERT systematically across as many cancer types and clinically important questions as possible. I investigate the marker both on its own and in combination with other cancer-specific markers identified by our group. My goal is a broadly applicable platform technology that supports patients and their clinicians from early detection through assessment of disease course to follow-up.
View selected publicationsDialogue and collaboration
I welcome scientific collaborations and dialogue with clinical institutions and industrial partners. I am particularly interested in joint projects involving the clinical validation of epigenetic biomarkers and the development of epigenetic methods. Together, I hope to help translate scientific insights into reliable medical applications.
Prof. PD Dr. Simeon Santourlidis
Epigenetics Laboratory for Human Health and Longevity
Institute of Transplantation Diagnostics and Cell Therapeutics
University Hospital Düsseldorf
Heinrich Heine University Düsseldorf
Moorenstraße 5 · 40225 Düsseldorf, Germany
Building 14.80 · Floor 3 · Room 2
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