Apostolos Mourtzinos

My background

Research interests

During my academic career I have been exposed to multiple research topics in biology and the biomedical sciences, ranging from the mechanisms of plant immunity to macromolecular interactions in human disease. My current research interests concern the role of human LINE-1 retrotransposons in healthy aging and disease. To improve our understanding of how LINE-1 activation contributes to disease, we employ affinity capture and mass spectrometry along with other biochemical approaches. These help us identify the interactions responsible for disease progression and dissect their mechanisms of action. Despite my focus on LINE-1 biology, I have been involved in several other projects. One of them was the characterization of the affinity-captured DNAJB1-PRKACA protein interactome in fibrolamellar hepatocellular carcinoma, a pediatric liver cancer whose oncogenesis is driven by a fusion between the DNAJB1 and PRKACA genes.

• RNA biology
• Proteomics
• Interactomics
• LINE-1 retrotransposons

Research project

The role of LINE-1-derived pathogen-associated molecular patterns in senescence and inflammaging

Transposable elements (TEs), also known as “jumping genes”, are mobile DNA elements that can replicate and integrate themselves into different locations within the host genome. We aim to characterize the composition of LINE-1 ribonucleoprotein complexes in cell senescence and dissect the immune pathways associated with the nucleic acids they carry, in particular cDNAs, dsRNAs and DNA-RNA hybrids generated by aberrant cytoplasmic LINE-1 activity.

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Transposable elements (TEs), also known as “jumping genes”, are defined as mobile DNA elements that can replicate and integrate themselves into different locations within the host genome¹. TEs have been identified in all organisms and often occupy a large proportion of their host genome². TEs are divided into two classes based upon their mechanism of transposition. Class I TEs (also known as retrotransposable elements, or RTEs) mobilize via a ‘copy-and-paste’ mechanism, where an RNA intermediate is reverse-transcribed into cDNA that is subsequently inserted in a different location within the host genome³. Class II TEs (also known as DNA transposons) proliferate through a DNA intermediate in a more direct way, through a ‘cut-and-paste’ mechanism^4,5. The most abundant RTEs in the human genome are LINE-1 (L1) and Alu elements, accounting for ~30% of the genome⁶. Unlike Alu, L1s encode their own proteins and are therefore capable of autonomous retrotransposition. In more detail, L1 consists of a 5’ UTR with an internal promoter, two open reading frames (ORFs, namely ORF1 and ORF2) and a 3’ UTR with a weak cleavage and polyadenylation signal^7-9. ORF1 encodes ORF1p (~40 kDa), which forms a homotrimer and is a putative nucleic acid chaperone^10,11, whereas ORF2 encodes ORF2p (~150 kDa), a multidomain enzyme with both endonuclease (EN) and reverse transcriptase (RT) activities^12,13. L1 ORF1p and ORF2p preferentially assemble with their own encoding RNA (cis preference), forming ribonucleoprotein complexes (RNPs), presumably near or at the site of translation^14,15. Notably, at all stages of the L1 retrotransposition process (i.e., L1’s ‘life cycle’), L1s engage various host-encoded proteins, some facilitating and others impeding its action^16-23.

L1 retrotransposition proceeds through DNA/RNA/protein-containing intermediates across cellular compartments, predominantly in the nucleus and cytoplasm (Fig. 1). L1 enters the nucleus and gains access to chromatin as the cell starts to divide and the nuclear membrane breaks down²⁴. According to the most recent model for L1 proliferation, termed target-primed reverse transcription (TPRT)^25,26, cDNA production by ORF2p takes place in the nucleus and is primed by a free 3’ hydroxyl group, generated by ORF2p EN cleavage of host DNA. In healthy cells, L1 transcription is suppressed both epigenetically and by p53 and other transcription factors^27-33. However, in cell senescence L1s become activated and trigger a type I interferon (IFN-I) response, causing inflammation³⁴. Additionally, cell senescence is characterized by cell proliferation arrest, as well as by abnormal ORF2p-driven production of cytoplasmic cDNAs and DNA-RNA hybrids. Consequently, L1 RNPs become trapped and accumulate in the cytoplasm, while the hybrids produced act as pathogen-associated molecular patterns (PAMPs) that activate host cytoplasmic pattern recognition receptors (PRRs), including the cGAS/STING DNA sensing pathway^35-37. As a result, this induces an IFN-I response, leading to increased secretion of proinflammatory cytokines, known as the senescence-associated secretory phenotype (SASP)³⁴.

L1 RNPs are highly heterogeneous in composition and apart from DNA-RNA hybrids they also include other PAMPs. For example, L1 RNAs are enriched in CpG motifs and are therefore PAMPs themselves, but they also assemble with dsRNA-forming Alus^38,39. L1 RNPs can therefore act as sites of aggregation of cytoplasmic hybrids and other PAMPs. Collectively, stimulation of innate immunity in response to RTE nucleic acids (NAs), especially by ORF2p-derived cDNAs and hybrids, constitutes a novel mechanism for understanding senescence-associated diseases. L1 RNPs assemble several pathogenic NAs, but their relative contributions to host innate immune responses remain uncharacterized. We aim to characterize the composition of L1 RNPs in cell senescence and dissect the immune pathways associated with RTE-derived NAs, in particular cDNAs, dsRNAs and DNA-RNA hybrids generated by aberrant cytoplasmic L1 activity.

References

1. Saleh, A., Macia, A. & Muotri, A. R. Transposable elements, inflammation, and neurological disease. Front. Neurol. 10, 894 (2019).
2. Muñoz-López, M. & García-Pérez, J. L. DNA transposons: nature and applications in genomics. Curr. Genomics 11, 115-128 (2010).
3. Boeke, J. D., Garfinkel, D. J., Styles, C. A. & Fink, G. R. Ty elements transpose through an RNA intermediate. Cell 40, 491-500 (1985).
4. Rubin, G. M., Kidwell, M. G. & Bingham, P. M. The molecular basis of P-M hybrid dysgenesis: the nature of induced mutations. Cell 29, 987-994 (1982).
5. Greenblatt, I. M. & Alexander Brink, R. Transpositions of Modulator in Maize into Divided and Undivided Chromosome Segments. Nature 197, 412-413 (1963).
6. Bennett, E. A., Coleman, L. E., Tsui, C., Pittard, W. S. & Devine, S. E. Natural genetic variation caused by transposable elements in humans. Genetics 168, 933-951 (2004).
7. Holmes, S. E., Dombroski, B. A., Krebs, C. M., Boehm, C. D. & Kazazian, H. H. A new retrotransposable human L1 element from the LRE2 locus on chromosome 1q produces a chimaeric insertion. Nat. Genet. 7, 143-148 (1994).
8. Belancio, V. P., Whelton, M. & Deininger, P. Requirements for polyadenylation at the 3’ end of LINE-1 elements. Gene 390, 98-107 (2007).
9. Moran, J. V., DeBerardinis, R. J. & Kazazian, H. H. Exon shuffling by L1 retrotransposition. Science 283, 1530-1534 (1999).
10. Khazina, E. & Weichenrieder, O. Human LINE-1 retrotransposition requires a metastable coiled coil and a positively charged N-terminus in L1ORF1p. eLife 7, e34960 (2018).
11. Martin, S. L., Branciforte, D., Keller, D. & Bain, D. L. Trimeric structure for an essential protein in L1 retrotransposition. Proc Natl Acad Sci USA 100, 13815-13820 (2003).
12. Feng, Q., Moran, J. V., Kazazian, H. H. & Boeke, J. D. Human L1 retrotransposon encodes a conserved endonuclease required for retrotransposition. Cell 87, 905-916 (1996).
13. Mathias, S. L., Scott, A. F., Kazazian, H. H., Boeke, J. D. & Gabriel, A. Reverse transcriptase encoded by a human transposable element. Science 254, 1808-1810 (1991).
14. Wei, W. et al. Human L1 retrotransposition: cis preference versus trans complementation. Mol. Cell. Biol. 21, 1429-1439 (2001).
15. Kulpa, D. A. & Moran, J. V. Cis-preferential LINE-1 reverse transcriptase activity in ribonucleoprotein particles. Nat. Struct. Mol. Biol. 13, 655-660 (2006).
16. Pizarro, J. G. & Cristofari, G. Post-Transcriptional Control of LINE-1 Retrotransposition by Cellular Host Factors in Somatic Cells. Front. Cell Dev. Biol. 4, 14 (2016).
17. Taylor, M. S. et al. Dissection of affinity captured LINE-1 macromolecular complexes. eLife 7, e30094 (2018).
18. Taylor, M. S. et al. Affinity proteomics reveals human host factors implicated in discrete stages of LINE-1 retrotransposition. Cell 155, 1034-1048 (2013).
19. Liu, N. et al. Selective silencing of euchromatic L1s revealed by genome-wide screens for L1 regulators. Nature 553, 228-232 (2018).
20. Goodier, J. L., Cheung, L. E. & Kazazian, H. H. MOV10 RNA helicase is a potent inhibitor of retrotransposition in cells. PLoS Genet. 8, e1002941 (2012).
21. Niewiadomska, A. M. et al. Differential inhibition of long interspersed element 1 by APOBEC3 does not correlate with high-molecular-mass-complex formation or P-body association. J. Virol. 81, 9577-9583 (2007).
22. Suzuki, J. et al. Genetic evidence that the non-homologous end-joining repair pathway is involved in LINE retrotransposition. PLoS Genet. 5, e1000461 (2009).
23. Arjan-Odedra, S., Swanson, C. M., Sherer, N. M., Wolinsky, S. M. & Malim, M. H. Endogenous MOV10 inhibits the retrotransposition of endogenous retroelements but not the replication of exogenous retroviruses. Retrovirology 9, 53 (2012).
24. Mita, P. et al. LINE-1 protein localization and functional dynamics during the cell cycle. eLife 7, e30058 (2018).
25. Luan, D. D., Korman, M. H., Jakubczak, J. L. & Eickbush, T. H. Reverse transcription of R2Bm RNA is primed by a nick at the chromosomal target site: a mechanism for non-LTR retrotransposition. Cell 72, 595-605 (1993).
26. Cost, G. J. & Boeke, J. D. Targeting of human retrotransposon integration is directed by the specificity of the L1 endonuclease for regions of unusual DNA structure. Biochemistry 37, 18081-18093 (1998).
27. Hata, K. & Sakaki, Y. Identification of critical CpG sites for repression of L1 transcription by DNA methylation. Gene 189, 227-234 (1997).
28. Kato, Y. et al. Role of the Dnmt3 family in de novo methylation of imprinted and repetitive sequences during male germ cell development in the mouse. Hum. Mol. Genet. 16, 2272-2280 (2007).
29. Walter, M., Teissandier, A., Pérez-Palacios, R. & Bourc’his, D. An epigenetic switch ensures transposon repression upon dynamic loss of DNA methylation in embryonic stem cells. eLife 5, e11418 (2016).
30. Woodcock, D. M., Lawler, C. B., Linsenmeyer, M. E., Doherty, J. P. & Warren, W. D. Asymmetric methylation in the hypermethylated CpG promoter region of the human L1 retrotransposon. J. Biol. Chem. 272, 7810-7816 (1997).
31. Sun, X. et al. Transcription factor profiling reveals molecular choreography and key regulators of human retrotransposon expression. Proc Natl Acad Sci USA 115, E5526-E5535 (2018).
32. Tiwari, B. et al. p53 directly represses human LINE1 transposons. Genes Dev. 34, 1439-1451 (2020).
33. Briggs, E. M. et al. Unbiased proteomic mapping of the LINE-1 promoter using CRISPR Cas9. Mob. DNA 12, 21 (2021).
34. De Cecco, M. et al. L1 drives IFN in senescent cells and promotes age-associated inflammation. Nature 566, 73-78 (2019).
35. Li, D. & Wu, M. Pattern recognition receptors in health and diseases. Signal Transduct. Target. Ther. 6, 291 (2021).
36. Gorbunova, V. et al. The role of retrotransposable elements in ageing and age-associated diseases. Nature 596, 43-53 (2021).
37. Amarante-Mendes, G. P. et al. Pattern recognition receptors and the host cell death molecular machinery. Front. Immunol. 9, 2379 (2018).
38. Barak, M. et al. Purifying selection of long dsRNA is the first line of defense against false activation of innate immunity. Genome Biol. 21, 26 (2020).
39. Šulc, P. et al. Repeats mimic immunostimulatory viral features across a vast evolutionary landscape. bioRxiv (2021).

Research project

Dissecting the molecular features of a rare pediatric cancer, fibrolamellar carcinoma, using a double-barreled interactome mapping approach

Fibrolamellar carcinoma (FLC) is a rare and lethal subtype of liver cancer that primarily affects adolescent and pediatric patients without a history of liver disease. We aim to compare the protein interactions and phosphorylation patterns of wild-type PRKACA, DNAJB1 and the DNAJB1-PRKACA fusion protein in normal liver, liver adenoma, hepatocellular carcinoma and FLC tissues.

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Fibrolamellar carcinoma (FLC) is a rare and lethal subtype of liver cancer with a global incidence of 0.02 per 100,000 per year¹. However, this tumor primarily affects adolescent and pediatric patients without a history of liver disease, making it a devastatingly impactful disease despite its comparative rarity. The mainstay of treatment is complete surgical removal, due to its refractory nature against potential cures such as chemoradiation². FLCs lack obvious symptoms or serum tumor markers. Metastasis at presentation is frequent and often progressive and therefore fatal in nature¹. A specific diagnostic genetic fusion event, DNAJB1-PRKACA, was identified as a candidate driver of FLC³. A deletion of 400 kb in chromosome 19 results in the fusion of fragments of the genes encoding the heat shock protein DNAJ (Hsp40), subfamily B, member 1 (DNAJB1) and the catalytic subunit alpha of protein kinase A (PRKACA)³. The deletion results in a chimeric RNA transcript in which exon 1 of DNAJB1 replaces exon 1 of PRKACA. This produces a fusion protein in which the J-domain of DNAJB1 (also known as HSP40) replaces an amino-terminal segment of the catalytic subunit alpha of the cyclic AMP-dependent protein kinase A (also known as PKA Cα)⁴, referred to as DP hereafter (diagrammed in Fig. 1). Notably, DP retains kinase activity and has been shown to have tumorigenic properties not explainable by simple overexpression of PRKACA⁵.

While the DP gene fusion event was previously thought to be unique to FLC, recent studies have also identified other pancreatobiliary neoplasms that exhibit the same defect (and others)^6,7. This underscores the importance and health relevance of studying the roles of rare kinase fusion events in hepatopancreatobiliary tumors, as well as the role of this specific fusion event in FLC. We aim to conduct a comparative analysis of the protein interactions and phosphorylation patterns exhibited by wild-type PRKACA, DNAJB1 and DP fusion proteins, comparing what is observed in normal liver, liver adenoma, hepatocellular carcinoma and FLC tissues.

References

1. Lalazar, G. & Simon, S. M. Fibrolamellar carcinoma: recent advances and unresolved questions on the molecular mechanisms. Semin. Liver Dis. 38, 51-59 (2018).
2. Mavros, M. N., Mayo, S. C., Hyder, O. & Pawlik, T. M. A systematic review: treatment and prognosis of patients with fibrolamellar hepatocellular carcinoma. J. Am. Coll. Surg. 215, 820-830 (2012).
3. Honeyman, J. N. et al. Detection of a recurrent DNAJB1-PRKACA chimeric transcript in fibrolamellar hepatocellular carcinoma. Science 343, 1010-1014 (2014).
4. Liu, C., Ke, P., Zhang, J., Zhang, X. & Chen, X. Protein kinase inhibitor peptide as a tool to specifically inhibit protein kinase A. Front. Physiol. 11, 574030 (2020).
5. Kastenhuber, E. R. et al. DNAJB1-PRKACA fusion kinase interacts with β-catenin and the liver regenerative response to drive fibrolamellar hepatocellular carcinoma. Proc Natl Acad Sci USA 114, 13076-13084 (2017).
6. Zhu, C. et al. The fusion landscape of hepatocellular carcinoma. Mol. Oncol. 13, 1214-1225 (2019).
7. Vyas, M. et al. DNAJB1-PRKACA fusions occur in oncocytic pancreatic and biliary neoplasms and are not specific for fibrolamellar hepatocellular carcinoma. Mod. Pathol. 33, 648-656 (2020).

Publications

1. Reverse transcriptase inhibitors induce autophagy in a LINE-1 ORF1p-dependent manner

   Damizia M, Baranzini M, Sciamanna I, Altieri L, Rovella P, Rosas Bringa OG, Hozeifi S, Saba LJ, Mourtzinos A, O’Shea A, Ansari MSZ, Andreola F, Cirilli R, Sbardella G, Serafino A, Schumann GG, Trisciuoglio D, LaCava J, Lavia P, Spadafora C

   Communications Biology (2026)

2. Targeted detection of endogenous LINE-1 proteins and ORF2p interactions

   Nielsen MI, Wolters JC, Rosas Bringas OG, Jiang H, Di Stefano LH, Oghbaie M, Hozeifi S, Nitert MJ, van Pijkeren A, Smit M, Ter Morsche L, Mourtzinos A, Deshpande V, Taylor MS, Chait BT, LaCava J

   Mobile DNA 16, 3 (2025)

3. Growth differentiation factor 7 autocrine signaling promotes hepatic progenitor cell expansion in liver fibrosis

   Kong D, Mourtzinos A, Heegsma J, Blokzijl H, de Meijer VE, Faber KN

   Stem Cell Research & Therapy 14, 288 (2023)

See all publications on Google Scholar

Research experience

1. Dec 2022 to present

   Brown University

   Providence, United States

   PhD candidate in the Department of Pathology and Laboratory Medicine (Prof. Dr. Martin S. Taylor), Pathobiology Graduate Program. My project is elucidating the molecular mechanisms of cytoplasmic cDNA synthesis by LINE-1 retrotransposons.

   Core skills

   • Immunoprecipitation
   • Molecular cloning (site-directed mutagenesis)
   • Cell culture and transfection of suspension cells
   • Generation of stable cell lines
   • In vitro transcription
   • mRNA transfection
   • qPCR
   • Flow cytometry and FACS sorting

2. Dec 2022 to present

   The Rockefeller University

   New York City, United States

   Research assistant (internship) in the Laboratory of Cellular and Structural Biology (Prof. Dr. Michael Rout and Prof. Dr. John LaCava). Investigating the interplay of LINE-1 retrotransposon proteins with mitochondria and their contribution to the production of immune-triggering cytoplasmic RNA-DNA hybrids.

   Core skills

   • Mitochondrial isolation by differential centrifugation and affinity capture
   • Subcellular fractionation by density gradient ultracentrifugation
   • Immunoprecipitation
   • Molecular cloning (site-directed mutagenesis)
   • Cell culture and transfection of suspension cells

3. Dec 2020 to Oct 2022

   European Research Institute for the Biology of Ageing (ERIBA)

   Groningen, The Netherlands

   Research technician in the Laboratory of Macromolecules and Interactomes (Prof. Dr. John LaCava).

   • Gained exposure to a variety of molecular techniques, including CRISPR/Cas9, cell culture, western blot, immunoprecipitation, molecular cloning, transfection, fluorescence microscopy, DNA/protein extraction and bacterial transformation.
   • Designed small-scale experiments, such as the generation of cell lines and vector cloning.
   • Collaborated with labs around the world, including the Rout Lab at The Rockefeller University, the Yilmaz Lab at MIT, the Burns Lab at Dana-Farber Cancer Institute, the lab of Dr. Benjamin Greenbaum at Memorial Sloan Kettering Cancer Center and the lab of Prof. Dr. Tomas Mustelin at the University of Washington.
   • Collaborated with the pharmaceutical industry, namely Ribon Therapeutics and ROME Therapeutics.

   Projects I contributed to

   • Dissection of the DNAJB1-PRKACA protein interactome by affinity purification and mass spectrometry from patient material with fibrolamellar hepatocellular carcinoma (FLHCC)
   • Comparative interactomic analyses of LINE-1 ribonucleoprotein from carcinoma cells
   • The role of LINE-1 retrotransposable elements in neurodegeneration and autoinflammatory diseases
   • Interplay of LINE-1 proteins with mitochondria

4. Nov 2021 to May 2022

   University Medical Center Groningen (UMCG)

   Groningen, The Netherlands

   Internship in the Department of Gastroenterology and Hepatology (Prof. Dr. Klaas Nico Faber). I investigated the role of GDF7 in liver fibrosis and its effect on liver proliferation, work that contributed to our 2023 paper in Stem Cell Research & Therapy.

   Core skills

   • FFPE tissue preparation
   • Immunofluorescence
   • Immunohistochemistry
   • Organoid culture
   • RNA extraction
   • cDNA synthesis
   • qPCR

5. Jun 2019 to Aug 2020

   Biomedical Research Foundation Academy of Athens

   Athens, Greece

   Internship in the Department of Fundamental Research (Dr. Marios Agelopoulos).

   • Performed phylogenetic analysis of sequence data using Ensembl, NCBI, UniProt, Galaxy, Clustal, iTOL and R.
   • Identified potential transcription factor binding sites on DNA sequences.
   • Gained knowledge of laboratory procedures such as ChIP-seq and cell culture.

6. 2019 to 2020

   The University of Sheffield

   Sheffield, United Kingdom

   Final year research project in the Department of Animal and Plant Sciences (Prof. Dr. Jurriaan Ton).

   • Investigated the role of extracellular self-DNA (self-exDNA) in the immunity of Arabidopsis thaliana.
   • Explored the hormone signaling pathways induced in response to self-exDNA.
   • Examined the defense-eliciting activity of synthetic self-exDNA relative to genomic self-exDNA, as well as potential size-dependent effects of exDNA in inducing plant immunity.

7. Jun to Jul 2018

   Agios Savvas General Anticancer Oncology Hospital

   Athens, Greece

   Summer internship in the Department of Cancer Cytogenetics.

   • Gained experience in routine procedures of blood analysis for cancer diagnosis and prognosis.
   • Trained in genomic DNA extraction from whole blood, cytogenetic analysis (blood cell culture, chromosome isolation, chromosome staining and G-banding, karyotyping) and fluorescence in situ hybridization (FISH) in lymphocytes from patients with leukemia.

Education

1. 2025 to present

   PhD candidate, Pathobiology Graduate Program

   Brown University, United States of America

2. 2023 to 2025

   PhD student

   University of Groningen, The Netherlands

   Funded by a fellowship from the Graduate School of Medical Sciences. Research in Dr. John LaCava’s Laboratory of Macromolecules and Interactomes on the role of LINE-1 retrotransposons as provocateurs of autoinflammation and inflammaging.

3. 2021 to 2023

   MSc in Molecular Medicine and Innovative Treatment

   University of Groningen, The Netherlands

   Graduated cum laude.

4. 2017 to 2020

   BSc in Biology

   The University of Sheffield, United Kingdom

   First-class honours.

5. 2016 to 2017

   Foundation year in biology

   Network Foundation, Athens, Greece

   Grade 80% (A).

6. 2011 to 2017

   Secondary education

   2nd High School of Vrilissia, Athens, Greece

Awards, scholarships and grants

• Best poster prize

  2024

  Awarded by The EMBO Journal for outstanding poster presentation at the India EMBO Lecture Course in Greater Noida, India.

• PhD fellowship from GSMS Groningen

  2023 to 2027

  Funds a four-year doctoral program at the UMCG. It is granted to just four students of the MMIT master’s program who submit the most outstanding research proposals, after a thorough assessment by a scientific committee.

• Marko Polo Fund from the University of Groningen

  2022/2023

  A grant offered to exceptional students to conduct an internship abroad at a top university outside Europe.

• Groningen University Fund (GUF)

  2022

  The GUF subsidizes activities that benefit studies at the University of Groningen.

• Holland Scholarship

  2022/2023

  Made available by the Dutch Ministry of Education, Culture and Science together with Dutch research universities, for students who want to do research or an internship outside the European Economic Area.

• De Cock-Hadders Stichting

  Financial support for CPE, MMIT and IMIM students doing international internships in medicine, dentistry and movement sciences.

• MMIT GUIDE funding

  Reimbursement from the Groningen University Institute for Drug Exploration (GUIDE) for costs directly related to internships abroad, such as travel, visa fees and rent.

• MMIT Ubbo Emmius funding

  A grant for second-year MMIT students who do not receive a full scholarship from the UMCG, to conduct a research internship abroad.

News

Stay updated on the latest discoveries and progress in my research journey.

1. September 2026

   Paper published in Communications Biology

   Our collaborative study showing that reverse transcriptase inhibitors induce autophagy in a LINE-1 ORF1p-dependent manner is now published in Communications Biology. Read the paper.

2. June 2024

   Poster prize

   I am thrilled to announce that I have won the best poster prize at the India EMBO Lecture Course on post-transcriptional regulation in ageing and age-related diseases, held in Greater Noida, India. The prize is awarded by The EMBO Journal for outstanding poster presentation. The course, with its focus on cutting-edge research in gene expression regulation, provided an incredible platform for sharing my work with leading scientists and experts in the field from all over the world. I am grateful for the opportunity to present my findings and to be recognized by such a distinguished audience. This achievement inspires me to continue pursuing excellence in my scientific endeavors.

   

3. August 2023

   Master’s graduation

   I am happy to announce that I have graduated with distinction cum laude from the MSc in Molecular Medicine and Innovative Treatment at the University of Groningen in the Netherlands. This journey has been a remarkable exploration of cutting-edge research and innovative treatments in the field of molecular medicine. I am grateful for the support of my professors and peers and for the invaluable knowledge I gained during this program. I look forward to applying this expertise to make meaningful contributions to the world of science and healthcare.

   

4. July 2023

   PhD fellowship

   I am delighted to share the wonderful news that I have been awarded a prestigious fellowship from the Graduate School of Medical Sciences (GSMS) of the University of Groningen. It will fund my PhD studies for the next four years. I am excited to embark on this research adventure and contribute to the field.

   

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