Molecular Genetics

Background information

The department Molecular Genetics is headed by Roland Kanaar and focuses on how the integrity of DNA is maintained by the DNA damage response, a process central to the present-day problems of cancer and aging-related diseases.

Our department has a long history and world-wide reputation in understanding mechanisms of the DNA damage response from defined molecular level to the complex context of physiological processes. Its fundamental studies of molecular mechanisms provide the basis for the rational design and development of novel targeted therapies and evidence-based sustainment of health.

Our ambitions

• Address the fundamental molecular mechanistic aspects of the DNA damage response by pursuing complementary and interwoven approaches at molecular and cellular levels.
• Provide a rational basis for improving existing approaches and developing novel and innovative precision therapies for cancer and aging-related diseases.
• Bring to the clinic better criteria and tools for individual patient selection for precision therapy concerning cancer.
• Develop reliable prognostic tools for treatment of cancer and aging-related diseases. Educate and train the next generation of multidisciplinary life scientists and healthcare professionals.

Our mission

Our mission is to generate fundamental mechanistic knowledge on the DNA damage response through multi-disciplinary and innovative research. As we collaborate with our colleagues in the clinic, we aim at clinical translation by developing novel targeted therapies to improve outcomes and increase the quality of life of cancer patients and to extend the healthy lifespan of the ageing population.

The central research focus of the Department of Molecular Genetics at the Erasmus University Medical Center Rotterdam is the DNA damage response. We analyze this using an integrated approach from the molecular level to the physiological processes in the body, in the context of cancer, aging and aging-related diseases.

The four research lines underlying the central theme are:

1. DNA Recombination and Replication in Cancer
2. Transcription Stress in Ageing and Age-Related Pathologies
3. Genome Maintenance Mechanisms: From Rare Disease to General Population
4. DNA Damage-Based Cancer Therapy Development and Response Prediction

The Department of Molecular houses 17 Principal Investigators contributing to the four research lines. The listed distribution of Principal Investigators over the research lines is fluid, due to intradepartmental collaborations and the fact that projects often span different research lines.

Research Line 1 DNA Recombination and Replication in Cancer

This research line investigates the fundamental molecular mechanisms of the DNA damage response, with a focus on homologous recombination, DNA replication-associated mismatch repair, and the DNA replication stress response. We employ and develop cutting-edge methodologies, including single-molecule biochemistry and biophysics, alongside advanced genomics, proteomics, and microscopy techniques. Our microscopy approaches span high-content and super-resolution imaging, as well as structural techniques such as AFM/SFM and EM, enabling precise analysis of chromatin organisation and genome maintenance dynamics.

By integrating these technologies, we aim to elucidate the complex molecular interactions that safeguard genome integrity, dissect chromatin composition, and resolve three-dimensional genome architecture in the context of DNA repair. The overarching goal is to define the molecular circuits that orchestrate DNA damage response processes and their crosstalk with broader cellular pathways. This mechanistic insight is crucial for identifying novel molecular targets and biomarkers, driving the development of mechanism-based interventions. Ultimately, this knowledge underpins the refinement of existing strategies and the innovation of next-generation precision therapies for cancer. 

• Nitika Taneja
• Roland Kanaar
• Joyce Lebbink
• Arnab Ray Chaudhuri

Research Line 2 Transcription Stress in Aging and Age-Related Pathologies

DNA damage constitutes a major cause of cellular dysfunction, cell death and cellular senescence which are all key drivers of the ageing process. Several rare DNA repair disorders exhibit premature ageing and age-related diseases. Our department pioneered the connection between DNA damage and ageing by generating unique DNA-repair-deficient mouse models that closely mimic human premature ageing syndromes. We also developed advanced imaging and multi-omics approaches, leading to the discovery of DNA damage-driven transcription stress as a fundamental contributor to ageing. Our research investigates transcription-coupled repair pathways, including TC-NER and the recently in our department identified transcription-coupled DNA-protein crosslink repair pathway. 

To study the consequences of transcription-blocking DNA damage, we use both genetically engineered C. elegans and mouse models, each offering unique advantages. Our C. elegans strains enable whole animal live imaging, cell type-specific survival assays, rapid genetic screening, and omics studies to investigate DNA damage-induced transcription stress in differentiated cell types. Our mouse models closely replicate different aspects of DNA repair-deficient progeroid syndromes, providing key insights into the complex mechanisms and pathology of age-related diseases and therefore provide us a distinct advantage to study drivers of ageing. 

Notably, our work revealed that DNA damage response activation during chemotherapy, surgery, and organ transplantation can have detrimental effects, which can be mitigated by nutritional interventions. This research, originally focused on rare DNA repair disorders, has now evolved into the development of novel interventions for age-related diseases.

• Jurgen Marteijn
• Jan Hoeijmakers
• Hannes Lans
• Joris Pothof
• Ingrid van der Pluijm
• Wim Vermeulen

Research Line 3 Genome Maintenance Mechanisms: From Rare Disease to General Population

This research investigates the molecular mechanisms governing the DNA damage response and the pathological consequences of their disruption, from hereditary DNA repair syndromes to broader public health implications. Elucidating these pathways is critical for identifying molecular targets to modulate genome stability, refine therapeutic strategies, and advance next-generation interventions for cancer and age-related diseases.

Our research focuses on nucleotide excision repair, interstrand and intrastrand crosslink repair pathways. Using advanced interaction proteomics and genome-wide genetic screens in cellular and model organisms, we have identified several novel repair factors and their mechanisms of action. We employ state-of-the-art live-cell and single-molecule imaging, integrated with CRISPR/Cas9-mediated gene editing, to investigate DNA repair dynamics in real time. Coupled with biochemical analysis of repair complexes, this multifaceted approach elucidates the molecular mechanisms governing DNA repair, reveals pathway crosstalk within cellular physiology, and deciphers the dynamic interactions driving repair complex assembly and disassembly.

We established functional DNA repair assays that are the international standard for stratification of clinical patients with DNA repair disorders. We employ these assays as a member of the Erasmus MC Expertise Centre for DNA Repair Disorders. This allows genotype-phenotype correlations for mutations in DNA repair genes, yielding not only critical mechanistic insights but also informing patient prognosis. We are currently extending DNA damage response genotype-phenotype correlations by studying the molecular consequences on genome instability of polymorphisms obtained by large GWAS studies from cohorts of the general population, whose general health status has been followed for decades. 

• Wim Vermeulen
• Ines Chaves
• Jeroen Essers
• Jan Hoeijmakers
• Hannes Lans
• Jurgen Marteijn
• Joris Pothof
• Ingrid van der Pluijm

Research Line 4 DNA Damaged Based Cancer Therapy Development and Response Prediction

Many anticancer strategies exploit the cytotoxicity of DNA-damaging agents, with treatment efficacy critically dependent on tumour-specific DNA damage response alterations. Since tumours typically exhibit compromised DNA damage response pathways, these deficiencies provide opportunities for refined patient stratification, targeted treatment selection, and the development of precision oncology interventions.

We have established a robust clinic-to-lab pipeline for obtaining tumour resection specimens and biopsies, enabling the development of functional ex vivo assays using viable, organotypic tumour slices from individual patients. Several assays have been validated by correlating ex vivo responses with clinical outcomes. The goal is now to refine this approach for individualized therapy response predictions to support clinical decision-making. This strategy is further extended to Cancer-on-Chip models, which allow real-time monitoring of treatment responses.

In parallel, we have developed imaging-based single-cell omics platforms that integrate high-throughput screening microscopy with detailed genomic, proteomic, and transcriptomic analyses. This approach enables us to characterize distinct cancer cell subpopulations exhibiting clinically relevant phenotypes, thereby identifying targetable pathways and predictive biomarkers.

Our research also examines tumour responses to radiotherapy, including conventional photon irradiation, and proton therapy at the Holland Proton Therapy Centre. Furthermore, we study the cellular mechanisms of targeted radionuclide therapies in preclinical models and clinical contexts. The overarching aim is to identify biomarkers that enable individualized therapy selection (radiation dose, radionuclide characteristics) and optimize radiation-induced DNA damage to expand therapeutic windows.

More information can be found at:

• Julie Nonnekens
• Miao Ping Chien
• Jeroen Essers
• Dik van Gent
• Roland Kanaar

Breakthrough discoveries

• First molecular cloning of a chromosome translocation break point in cancer, providing insight in the molecular basis of cancer and enabling development of the first cancer type specific drug (Imatanib/Gleevec)
• Molecular cloning of the first mammalian DNA repair gene and discovery of the very strong evolutionary conservation of DNA repair
• Discovery of the connection between transcription and DNA repair and identification of human transcription syndromes
• Discovery of the role of mammalian photolyase paralogs in the circadian/biological clock
• Discovery of the connection between the DNA damage response
• Identification of nutritional interventions for the treatment of human DNA repair syndromes exhibiting accelerated aging
• Discovery of the pathways of random DNA integration in mammalian genomes

Please visit Pure for all our Research output

Our key papers:

M. Tresini, D.O.  Warmerdam, P. Kolovos, L. Snijder, M.G. Vrouwe, J.A. Demmers, W.F. van IJcken, F.G. Grosveld, R.H. Medema, J.H. Hoeijmakers, L.H. Mullenders, W. Vermeulen and J.A. Marteijn.
The core spliceosome as target and effector of non-canonical ATM signaling.
Nature, 523: 53-58 (2015) 
doi: 10.1038/nature14512. PMID: 26106861

C. Dinant, G. Ampatziadis-Michailidis, H. Lans, M. Tresini, A.F. Theil, W.A. van Cappellen, H. Kimura, J. Bartek, M. Fousteri, A.B. Houtsmuller, W. Vermeulen and Marteijn, J.A.
Enhanced chromatin dynamics by FACT promotes transcriptional restart after DNA damage.
Molecular Cell 51: 469-79 (2013).
doi: 10.1016/j.molcel.2013.08.007. PMID: 23973375

P. Schwertman, A. Lagarou, D.H. Dekkers, J. Raams, A.C. van der Hoek, C. Laffeber, J.H.  Hoeijmakers, J.A. Demmers, M. Fousteri, W. Vermeulen and J.A. Marteijn.
UV-sensitive syndrome protein KIAA1530 recruits USP7 to regulate transcription coupled repair.
Nature Genetics 44: 598-602 (2012).
doi: 10.1038/ng.2230. PMID: 22466611

P.M. Krawczyk, B. Eppink, J. Essers, J. Stap, H. Rodermond, H. Odijk, A. Zelensky, C. van Bree, L.J. Stalpers, M.R. Buist, T. Soullié, J. Rens, H.J. Verhagen, M.J. O'Connor, N.A. Franken, T.L. ten Hagen, R. Kanaar and J.A. Aten.
Mild hyperthermia inhibits homologous recombination, induces BRCA2 degradation, and sensitizes cancer cells to poly (ADP-ribose) polymerase-1 inhibition.
Proc. Natl. Acad. Sci. USA 108, 9851-9856 (2011).
doi: 10.1073/pnas.1101053108. PMID: 21555554

M. Modesti, M. Budzowska, C. Baldeyron, J.A. Demmers, R. Ghirlando and R. Kanaar.  RAD51AP1 is a structure-specific DNA binding protein that stimulates joint molecule formation during RAD51-mediated homologous recombination. 
Molecular Cell 28, 468-481 (2007).
PMID: 17996710

K. Hanada, M. Budzowska, S.L. Davies, E. van Drunen, B.H. Beverloo, A. Maas, J. Essers, I.D. Hickson and R. Kanaar.
The structure-specific endonuclease Mus81-Eme1 contributes to replication restart by generating double-strand DNA breaks.
Nat. Struct. Mol. Biol. 14, 1096-1104 (2007).
PMID: 17934473

L.J. Niedernhofer, G.A. Garinis, A. Raams, S.A. Lalai, R.A. Robinson, E. Appeldoorn, H. Odijk, R. Oostendorp, A. Ahmad, W. van Leeuwen, A. Theil, W. Vermeulen, G.T. van der Horst, P. Meinecke, W. Kleijer, J. Vijg, N.G.J. Jaspers, J.H.J. Hoeijmakers.
A new progeriod syndrome reveals that genotoxic stress suppresses the somatotroph axis.
Nature 444: 1038-1043 (2006).
PMID: 17183314

Giglia-Mari, G., Coin, F., Ranish, J.A., Hoogstraten, D., Theil, A., Wijgers, N., Jaspers, N.G., Raams, A., Argentini, M., van der Spek, P.J., Botta, E., Stefanini, M., Egly, J.M., Aebersold, R., Hoeijmakers, J.H., and Vermeulen, W.
A new, tenth subunit of TFIIH is responsible for the DNA repair syndrome trichothiodystrophy group A.
Nature Genetics 36: 714-719 (2004).
PMID: 15220921

J.A. Aten, J. Stap, P.M. Krawczyk, C.H. van Oven, R.A. Hoebe, J. Essers and R. Kanaar.
Dynamics of DNA double-strand breaks revealed by clustering of damaged chromosome domains. 
Science 303, 92-95 (2004).
PMID: 14704429

Hoogstraten, D., Nigg, A.L., Heath, H., Mullenders, L.H., van Driel, R., Hoeijmakers, J.H., Vermeulen, W. and Houtsmuller, A.B.
Rapid switching of TFIIH between RNA polymerase I and II transcription and DNA repair in vivo.
Molecular Cell 10: 1163-1174 (2002)
PMID: 12453423

J. de Boer, J.O. Andressoo, J. de Wit, J. Huijmans, R.B. Beems, H. van Steeg, G. Weeda, G.T.J. van der Horst, W. van Leeuwen, A.P.N. Themmen, M. Meradji and J.H.J. Hoeijmakers.
Premature aging in mice deficient in DNA repair and transcription.
Science (research article), 296: 1276-1279 (2002).
PMID: 11950998

W. Vermeulen, S. Rademakers, N.G.J. Jaspers, E. Appeldoorn, A. Raams, B. Klein, W. Kleijer, L. Kjærsgård and J.H.J. Hoeijmakers.
A temperature-sensitive disorder in basal transcription and DNA repair in man.
Nature Genetics 27: 299-303 (2001).
PMID: 11242112

M. de Jager, J. van Noort, D.C. van Gent, C. Dekker, R. Kanaar and C. Wyman.
Human Rad50/Mre11 is a flexible complex that can tether DNA ends.
Molecular Cell 8: 1129-1135 (2001).
PMID: 11741547

Vermeulen, W., Bergmann, E., Auriol, J., Rademakers, S., Frit, P., Appeldoorn, E., Hoeijmakers, J.H., and Egly, J.M.
Sublimiting concentration of TFIIH transcription/DNA repair factor causes TTD-A trichothiodystrophy disorder.
Nature Genetics 26: 307-313 (2000).
PMID: 11062469

A.B. Houtsmuller, S. Rademakers, A.L. Nigg, D. Hoogstraten, J.H.J. Hoeijmakers, W. Vermeulen.
Action of DNA repair endonuclease ERCC1/XPF in living cells.
Science 284: 958-961 (1999).
PMID: 10320375

H. Okamura, S. Miyake, Y. Sumi, S. Yamaguchi, A. Yasui, M. Muijtjens, J.H.J. Hoeijmakers and G.T.J. van der Horst.
Photic induction of mPer1 and mPer2 in Cry-deficient mice lacking a biological clock.
Science 286: 2531-2534 (1999).
PMID: 10617474

G.T.J. van der Horst, M. Muijtjens, K. Kobayashi, R. Takano, S-I. Kanno, M. Takao, J. de Wit, A. Verkerk, A.P.M. Eker, D. van Leenen, R. Buijs, D. Bootsma, J.H.J. Hoeijmakers, A. Yasui.
Mammalian blue-light receptor homologs CRY1 and CRY2 are essential for maintenance of the biological clock.
Nature 398: 627-630 (1999).
PMID: 10217146

K. Sugasawa, J.M.Y. Ng, C. Masutani, P.J. van der Spek, A.P.M. Eker, F. Hanaoka, D. Bootsma and J.H.J. Hoeijmakers.
Xeroderma pigmentosum group C complex is the initiator of global genome repair.
Molecular Cell 2: 223-232 (1998).
PMID: 9734359

G.T.J. van der Horst, H. van Steeg, R.J.W. Berg, A.J. van Gool, J. de Wit, G. Weeda, H. Morreau, R.B. Beems, C.F. van Kreijl, F.R. de Gruijl, D. Bootsma and J.H.J. Hoeijmakers.
Defective transcription-coupled repair in Cockayne syndrome B mice is associated with skin cancer predisposition.
Cell 89: 425-435 (1997).
PMID: 9150142

J. Essers, R.W. Hendriks, S.M.A. Swagemakers, C. Troelstra, J. de Wit, D. Bootsma, J.H.J. Hoeijmakers and R. Kanaar.
Disruption of mouse RAD54 reduces ionizing radiation resistance and homologous recombination. 
Cell 89: 195-204 (1997).
PMID: 9108475

H. Roest, J. van Klaveren, J. de Wit, C.G. van Gurp, M.H.M. Koken, M. Vermey, J.H. van Roijen, J.T.M. Vreeburg, W.M. Baarends, D. Bootsma, J.A. Grootegoed and J.H.J. Hoeijmakers.
Inactivation of a ubiquitin-conjugating DNA repair enzyme in mice causes a defect in spermatogenesis associated with chromatin modification.
Cell 86: 799-810 (1996).
PMID: 8797826 

Schaeffer, L., Roy, R., Humbert, S., Moncollin, V., Vermeulen, W., Hoeijmakers, J.H., Chambon, P. and Egly, J.M. (1993).
DNA repair helicase: a component of BTF2 (TFIIH) basic transcription factor.
Science 260: 58-63 (1993).
PMID: 8465201

Troelstra, A. van Gool, J. de Wit, W. Vermeulen, D. Bootsma and J.H.J. Hoeijmakers.
ERCC6, a member of a subfamily of putative helicases is involved in Cockayne's syndrome and preferential repair of active genes.
Cell 71: 939-953 (1992).
PMID: 1339317

G. Weeda, R.C.A. van Ham, W. Vermeulen, D. Bootsma, A.J. van der Eb and J.H.J. Hoeijmakers.
A presumed DNA helicase, encoded by the excision repair gene ERCC-3 is involved in the human repair disorders xeroderma pigmentosum and Cockayne's syndrome.
Cell 62: 777-791 (1990).
PMID: 2167179

M. van Duin, J. de Wit, H. Odijk, A. Westerveld, A. Yasui, M. Koken, J.H.J. Hoeijmakers and D. Bootsma.
Molecular characterization of the human excision repair gene ERCC-1: cDNA cloning and aminoacid homology with the yeast DNA repair gene RAD10.
Cell 44: 913-923 (1986).
PMID: 2420469

Westerveld, J.H.J. Hoeijmakers, M. van Duin, J. de Wit, H. Odijk, A. Pastink, R.D. Wood and D. Bootsma.
Molecular cloning of a human repair gene.
Nature 310: 425-429 (1985).
PMID: 6462228

 Research facilities

The department makes use of the following Erasmus MC core facilities:

• Applied Molecular Imaging Erasmus MC (AMIE): AMIE offers multimodal and high resolution in vivo imaging of small animals and tissue. We analyze genetically-engineered mouse models in cancer and aging research.
• Erasmus Center for Animal Research: We generate and house mouse strains.
• Erasmus Optical Imaging Center: An expert center for advanced optical imaging knowledge and equipment. We conduct cell biological analyses of the DNA damage response. 
• ERGO: A prospective cohort study on the risk factors and determinants of chronic diseases in middle-aged and elderly persons. We identify circadian disturbance-related epigenetic risk markers for aging related pathologies.
• Generation R: A population-based prospective cohort study from fetal life until adulthood. We identify pre- and early postnatal circadian disturbance-related epigenetic risk markers for later life disease.
• Genomics: Expertise Center for Genomics Research. We conduct sequence-based experiments on the effect of the DNA damage response in cancer and aging at Erasmus Center for Biomics and and HuGe-F.
• iPS facility: We conduct the derivation and distribution of iPSCs for human disease modelling. We derive iPS cells from patients with a DNA damage response defect. We also use it as a user facility location and to conduct onsite training. 
• Erasmus MC Proteomics Center: Mass spectrometry-based proteomics services for the Erasmus MC community and external researchers. We conduct biochemical analyses of protein complexes involved in the DNA damage response.

Upcoming Speakers 2025

	Coming up soon!
	November 20, 2025 Jessica Downs, The Institute of Cancer Research, London, UK The SWI/SNF chromatin remodeling complex facilitates replication at challenging sites to promote genome stability Live at Ee 822 and hybrid

The talks begin at 4 pm CET, 3 pm GMT, 10 am EST, 7 am PST.

For more information contact us!

Past Speakers

	January 27, 2025 Sven Rottenberg, University of Bern, Switzerland Mechanisms of anti-cancer therapy resistance in BRCA1/2-mutated mouse mammary tumors Live at Ee 822 and hybrid
	April 24, 2024 Karlene Cimprich, Stanford University, School of Medicine, USA The causes and consequence of replication stress Live at Ee 822 and hybrid
	December 12, 2023 Karolin Luger, University of Colorado, Dept. of Biochemistry, USA Still surprising after all these years: histones and their post-translational modifications
	October 11, 2023 Andre Nussenzweig, National Cancer Institute, Center for Cancer Research, USA DNA damage in mitotic and post-mitotic cells
	October 4, 2023 Steve Jackson, Cancer Research UK, University of Cambridge, UK Cellular responses to DNA damage – mechanistic insights and implications for cancer therapy
	June 15, 2023 Marcel van Vugt, Cancer Research Center, Groningen University, UMCG, NL Dealing with DNA damage during mitosis Live at EE 822 and hybrid
	June 5, 2023 Bennet van Houten, University of Pittsburgh, Dept. Of Pharmacology &   Chemical Biology, USA    Watching the confluence of base and nucleotide excision repair: from cells to single molecules   Live at EE 822 and hybrid
	Lecture has been rescheduled to April 2024 May 25 Karlene Cimprich, Stanford University, School of Medicine, USA The causes and consequence of replication stress Live at Ee 822 and hybrid
	April 12, 2023 Orlando Scharer, UNIS, IBS Center for Genomic Integrity, Korea Understanding and targeting nucleotide excision repair Live at EE 822 and hybrid
	November 17, 2022 Wolf Dietrich Heyer, University of California, Davis, USA RAD52 and BRCA2 regulate pathway choice in double-stranded DNA break repair
	October 4, 2022 Robert Sobol, University of South Alabama, USA Replication associated base excision repair
	September 13, 2022 Dipanjan Chowdhury, Dana Farber Cancer Institute, USA Expanding the scope of DNA repair factors- novel roles and applications
	July 12, 2022 Wei Yang, NIH, USA The ins-and-outs of V(D)J recombination
	June 28, 2022 Anja Groth, University of Copenhagen, Denmark Chromatin replication in epigenome and genome maintenance
	May 24, 2022 Laura Niedernhofer, University of Minnesota, USA Cell fates in response to endogenous DNA damage
	April 12, 2022 Petr Cejka, Institute for Research in Biomedicine, Switzerland The function of nucleases in homologous recombination and replication stress
	January 11, 2022  Taekjip Ha, John Hopkins School of Medicine, USA Light, CRISPR and DNA repair
	December 7, 2021 Jan Vijg, Albert Einstein College of Medicine, USA Somatic mutations, genome mosaicism, aging and disease
	October 6, 2021 Andrew Jackson, MRC Human Genetics Unit, UK Human disease to molecular mechanism: genome instability, inflammation and mutagenesis
	September 8, 2021 Titia de Lange, The Rockefeller University, USA    Telomeres and cancer: tumor suppression and genome instability
	July 6, 2021 Judy Campisi, Buck Institute, USA Cancer and aging: Rival demons?
	June 2, 2021 Genevieve Almouzni, Institute Curie, France Histone H3 variants and their chaperones and cell fate
	May 11, 2021 Simon Boulton, Crick Institute, UK Mechanism of Chromosome end protection
	April 12, 2021 Johannes Walter, Harvard (HHMI), USA Signals and Mechanisms for Replisome Disassembly
	March 16, 2021 David Pellman, Dana-Farber (HHMI), USA Mechanisms driving the rapid evolution of cancer genome

News

See NTR Wetenschap Instagram for the whole story

Friday, March 7, 2025 was the official opening of the Netherlands Women's Health Research and Innovation Center.

Ingrid van der Pluijm is one of the authors of the Research & Innovation Agenda on which this Center is established.

Read more: Articles on Amazing Erasmus MC

Molecular Genetics PhD defense calendar

2025

August 27 at 10:30 am, Roisin McMorrow: ‘Harnessing the light: Therapy and optical imaging for pancreatic cancer’. Querido Zaal , Erasmus MC

September 9 at 1 pm, Melanie van der Woude: ‘Simple models for a complex mechanism -TFIIH and transcription stress in cells and C. elegans’.

Queridozaal, Erasmus MC

October 28 at 1 pm, Gerarda van de Kamp: ‘DNA Double Strand Break Repair Mechanisms in Response to Proton Radiotherapy: Implications for Cancer Treatment’.

Queridozaal, Erasmus MC

November 12 at 10:30 am, Tim Heemskerk: ‘Advancing Proton Radiotherapy: Mechanistic Studies and Biological Applications of DNA Double Strand Break Repair’.

Queridozaal, Erasmus MC

December 3 at 3:30 pm, Diana Llerena Schiffmacher: ‘Taking the Next steps in Unraveling tC-NER’.

Queridozaal, Erasmus MC

Internships for HLO-BSc and MSc students

The Department of Molecular Genetics has been the driving force behind two novel educational programs at the Erasmus MC:

The Molecular Research Master Molecular Medicine and the Nanobiology Program. Principal Investigators from the department are the educational directors of the programs. In both programs, teachers are Principal Investigators and post-doctoral fellows who are actively involved in the different research lines of the department. They are therefore able to transfer their knowledge, fascination and dedication to research to the students.

Students in the Research Master Molecular Medicine do research internships in the department under the supervision of experienced lab members. The students contribute to research, and some have become authors on publications. A number of them go on to the PhD program in the department or elsewhere. 

The Nanobiology BSc (started in 2012) and MSc (started in 2015) are unique programs in fundamental biology for the future. They combine a strong basis in math, physics and programming to help understand the complexity of biology. They are also joint degree programs with TU Delft. Nanobiology prepares scientists/engineers to take on difficult societal challenges focusing on medicine and health. To date, about half of the MSc graduates have entered PhD programs in biomedical fields, while others are working in the high tech industry, teaching and government agencies.

While the Molecular Medicine program mainly covers the translation of biomedical research to clinical problems and the reverse, Nanobiology concentrates on combining mathematics and physics into biological experimentation. These areas nicely cover the breadth of research in the department, making a natural connection for students and the various research groups.

Please contact dr. Ines Chaves for more information

The Erasmus MC Postdoc Network was initiated in 2011 to advance the careers of Postdocs and final year PhD students. It brings postdocs and final year PhD students within the Erasmus MC together to raise awareness of all relevant aspects important for a successful career in science. The postdoc network organizes network meetings, plenary sessions, workshops and discussions on how to shape a scientific career and to develop academic as well as transferable skills. It provides a platform for postdocs to exchange work experiences, plans, challenges, tips and tricks. Each Postdoc Network meeting will end with an informal reception for networking.

The Biomedical Sciences PhD program

When it comes to PhD education, the department contributes to a ‘Cell and Developmental Biology’ course and organizes and contributes to ‘Special topics in Biochemistry, Biophysics and Cell biology’ such as CRISPR-Cas and Optogenetics courses. The Nanobiology and Medicine educational programs also provide the opportunity for PhD students to gain experience as teaching assistants and as supervisors of Nanobiology BSc and MSc research projects.

Besides doing research, PhD students from 6 departments at Erasmus MC (Cell Biology, Molecular Genetics, Developmental Biology, Genetic Identification, Biochemistry and Neuroscience) also have to follow the Biomedical Sciences PhD program, which is briefly described in the "Teaching Program of Biomedical Sciences". 

Embedded

The Biomedical Sciences PhD program is embedded in the Graduate School Medical Genetics Center South West Netherlands.

The additional requirements, courses, and modules of this program are aimed at further improving education, training and technical expertise of PhD students at Erasmus MC.

In addition, the Biomedical Sciences PhD program incorporates obligatory courses offered by the Erasmus MC. More information on being a PhD student within the Erasmus MC can be found at STiP.

Requirements

Attending (inter)national meeting(s) in your scientific field and presenting your work  is obligatory. Also PhD students of the Medical Genetics Center yearly organize themselves a 3 day scientific retreat at an attractive location in one of the neighbouring countries. We adhere to the Erasmus MC requirement that a total of 30 training credits (ECTS) points are obtained by the student at the end of the PhD. Students can obtain ECTS points for each course and lecture they follow.

Check our career opportunities.