Erasmus MC

Nitika Taneja is an Associate Professor and Principal Investigator at Erasmus MC, focusing her research on understanding the intricate molecular mechanisms of chromatin remodeling during DNA replication and replication stress to maintain genome stability. During her PhD work under Prof. Christian Lehner at the University of Zurich, Switzerland, she demonstrated the transgenerational propagation of histones/epigenetic marks from fathers to progeny. This research highlighted the essential role of a retained centromere histone variant in male gametes, inherited during the first zygotic DNA replication, crucial for embryonic development.

During her postdoctoral tenure at the National Cancer Institute, NIH, USA, with Dr. Shiv Grewal, Dr. Taneja designed specialized genetic screens to identify factors critical for genome and epigenome stability during DNA replication. In 2018, she established her research program at the Department of Molecular Genetics, Erasmus MC, Netherlands. Her research program explores the role of 3-D chromatin architecture in mediating replication fork stability under replication stress. By uncovering these connections and identifying key factors, her work unveils potential mechanisms and strategies to sensitize cancer cells to chemotherapy. Her team also develops innovative tools and technologies to investigate transient chromatin changes at replication fork sites and genome-wide chromatin spatial reorganization in response to replication stress.

• 2023: ERC starting grant

• 2023: NWO - Aspasia premium award

• 2022: NWO - VIDI Talent award

• 2021: NWO - Women in STEM Incentive grant

• 2021: Convergence Health & Technology: Open Mind Call

• 2020: Erasmus+ grant

• 2018: Daniel den Hoed Stichting Foundation- Young Investigator Award

• 2017: Fellows Award for Research Excellence

• 2012: Sri AsaNanda Young Scientific Talent Award

1. Lo CSY, Taneja N*, Ray Chaudhuri A*. Enhancing quantitative imaging to study DNA damage response: A guide to automated liquid handling and imaging. (DNA repair 2024, DOI: 10.1016/j.dnarep.2024.103769)

2. Uruci, Hoitsma, Solér-Oliva, Bayona-Feliu, Gaggioli, García-Rubio, Lo, Bakker, Marinello, Manolika, Capranico, Luijsterburg, Luger *, Aguilera *, Taneja*. SMARCAD1 Regulates R-Loops at Active Replication Forks Linked to Cancer Mutation Hotspots. (BioRxiv2024.09.13.612941)

3. Davó-Martínez C, Helfricht A, Ribeiro-Silva C, Raams A, Tresini M, Uruci S, van Cappellen WA, Taneja N, Demmers JAA, Pines A, Theil AF, Vermeulen W, Lans W. Different SWI/SNF complexes coordinately promote R-loop- and RAD52-dependent transcription-coupled homologous recombination. (Nucleic Acid Research 2023, DOI: 10.1093/nar/gkad609)

4. Gaggioli V, Lo CSY, Reverón-Gómez N, Jasencakova Z, Domenech H, Nguyen H, Sidoli S, Tvardovskiy A, Uruci S, Slotman JA, Chai Y, Goncalves JG, Manolika EM, Jensen ON, Wheeler D, Sridharan S, Chakraborty S, Demmers J, Kanaar R, Groth A, Taneja N*. Dynamic de novo heterochromatin assembly and disassembly at replication forks ensure fork stability. (Nature Cell Biology 2023, DOI: 10.1038/s41556-023-01167-z)

5. Chakrabarty S, Quiros-Solano, Kuijten M, Haspels B, Mallya S, Lo CSY, Othman A, Gaio N, Odijk H, van de Ven, de Ridder, Weerden W, Jonkers J, Dekker R, Taneja N, Kanaar R, van Gent D. A microfluidic cancer-on-chip platform predicts drug response using organotypic tumor slice culture. (Cancer Research 2022, PMID: 34872965)

6. Uruci S, Lo CSY, Wheeler D, Taneja N*. R-Loops and Its Chro-Mates: The Strange Case of Dr. Jekyll and Mr. Hyde. (IJMS 2021, PMID: 34445553)

7. Lo CSY, van Toorn M, Gaggioli V, Dias MP, Zhu Y, Manolika EM, Zhao W, van der Does M, Goncalves JG, van Royen M, French P, Demmers J, Smal I, Lans H, Wheeler D, Jonkers J, Ray Chaudhuri A, Marteijn JA, Taneja N*. SMARCAD1 Mediated Active Replication Fork Stability Maintains Genome Integrity. (Science Advances 2021, PMID: 33952518)

   * corresponding author

I am a pathologist by training with a strong background in clinical hematopathology and basic research. In my MD thesis (RWTH Aachen, Germany), I focused on cellular plasticity and tissue engineering of skin and continued independent research projects in parallel to my residency/fellowship in Pathology with focus on the role of the microenvironment in myeloid malignancies but also chronic kidney disease (2008-2012). I performed my post-doc (after MD qualification) in Ben Ebert‘s lab at Harvard Medical School from 2012-2015. After my postdoctoral fellowship, I returned to Aachen to finish my fellowship in Pathology, and started my own independent research laboratory at Erasmus MC. In parallel to running my laboratory at Erasmus MC, I finalized my PhD (conducted at Harvard Medical School, Boston, USA and Erasmus MC, Rotterdam).

My primary focus is disease-oriented laboratory investigation of clonal myeloid neoplasms, employing a range of genomic technologies as well as classical cellular and molecular biology experimental approaches. My central goal is to translate my research directly into development of novel targeted therapeutics for the vast and growing patient population suffering from fibrosis and organ failure due to chronic blood cancer or even cancer more broadly. I made significant discoveries for improved diagnosis and treatments for blood cancers. In summary, the major achievements of my lab have been the identification of fibrosis-driving cells in primary myelofibrosis (PMF) and the identification of their activating mechanisms. This work has led to the initiation of a clinical trial for which we just received funding for and which will be started in 2023. I have filed a priority patent (application # 20187323.9; date of filing: 23/07/2020) to protect the new use of Tasquinimod for MPN after preclinical proof-of-concept was demonstrated. I have received an ERC proof-of-concept grant beginning of 2021 to translate our preclinical findings into a clinical trial. Active Biotech (NASDAQ STOCKHOLM: ACTI) has entered into an exclusive license agreement with us (Oncode Institute) for the global rights to patents relating to the use of tasquinimod and other inhibitors of S100 for use in treatment of myelofibrosis (MF).

As a post-doctoral research fellow, I was the first to discover recurrent mutations in a blood cancer called del(5q) MDS. Importantly, we identified a mechanism in the mutated, disease-causing cells that is an “Achilles Heel” and can be used to specifically eliminate the disease-causing cells without affecting normal blood formation – one of the main challenges in cancer research. In my laboratory at Erasmus MC, we now thrive to identify novel therapeutic strategies to eradicate disease-initiating in myeloid blood cancers. Additionally, I identified that inflammation and activation of the innate immune system are central mechanisms in the development of not of myeloid malignancies. Using CRISPR/Cas9-gene editing, I showed that targeting activated mechanisms can restore the normal function of diseased hematopoietic cells. In my lab, we now focus on understanding the underlying mechanisms for the inflammation in the bone marrow (protein synthesis, aging etc) and are searching for novel therapeutic targets to block inflammation and inhibit disease progression.

In the next 5-10 years I want to focus on identifying novel druggable targets in myeloid malignancies by using the multitude of cellular and molecular assays established in my group. I furthermore intend to bring together scientists, societies and companies working in the abovementioned areas of research, in order to intensify their interaction, and to thereby foster the translation of several innovative treatment concepts into the clinic.

• 2022: Gerhard Domagk Award for Excellence in Cancer Research (Gerhard Domagk Foundation, Münster, Germany)

• 2022 Vidi

• 2021 ERC Proof-of-Concept Grant

• 2019: Swammerdam Award Nederlandse Vereniging voor Hematologie (Dutch Hematology Association)

• 2017: ERC Starting Grant; deFIBER; Dissecting the cellular and molecular dynamics of bone marrow fibrosis for improved diagnostics and treatment

• 2017: EMC fellowship; Functional and molecular dissection of the clonal selection in myeloproliferative neoplasms

• 2017: International MPN foundation; Dissecting the cellular and molecular dynamics of bone marrow fibrosis for improved diagnostics and treatment

• 2018: KWF Bas Mulder Award; Dissecting the mechanisms of malignant transformation in del(5q) myelodysplastic syndrome to selectively target the disease-initiating hematopoietic stem cells

• 2017: European Hematology Association (EHA), John Goldman Clinical Research grant; Functional dissection of abnormal protein translation in the erythroid differentiation defect in del(5q) MDS

• 2017: Johann Georg Zimmermann Award for Excellence in Cancer Research

• 2016 Innovation Award German Academic Medicine (Innovationspreis Deutsche Hochschulmedizin)

• 2016: Artur Pappenheim Award, Deutsche Gesellschaft für Hämatologie und Onkologie (DGHO; German Society for Hematology and Oncology)

1.  Leimkühler NB, Gleitz HFE, Ronghui L, Snoeren IAM , Fuchs SNR, Nagai JS, Banjanin B, Lam KH, Vogl T, Kuppe C, Stalmann USA, Buesche G, Kreipe H, Gütgemann I, Krebs P, Banz Y, Boor P, Wing-Ying E, Brümmendorf TH, Koschmieder S, Crysandt M, Bindels E, Kramann R, Costa IG and Schneider RK. Heterogeneous bone marrow stromal progenitors drive myelofibrosis via a druggable alarmin axis; Cell Stem Cell 2021 Apr 1;28(4):637-652.e8. doi: 10.1016/j.stem.2020.11.004

2. Jansen J, Reimer KC, Nagai JS, Varghese FS, Overheul GJ, de Beer M, Roverts R, Daviran D, Fermin LAS, Willemsen B, Beukenboom M, Djudjaj S, von Stillfried und Rattonitz S, van Eijk LE, Mastik M, Bulthuis M, den Dunnen W, van Goor H , Hillebrands JL, Triana SH, Alexandrov T, Timm MC, Tideman van den Berge T, van den Broek M, Nlandu Q, Heijnert J, Mooren F, Kuppe C, Miesen P, Grünberg K, Ijzermans J, Steenbergen T, Czogalla J…and Costa IG#, Schneider RK#, Smeets B# and Kramann R#. SARS-CoV-2 infects kidney cells and causes kidney fibrosis. Cell Stem Cell 2022 Feb 3;29(2):217-231. #equal contribution.

3. Stalmann USA, Banjanin B, Snoeren IAM, Nagai JS, Leimkühler NB, Li R, Benabid A, Pritchard JE, Malyaran H, Neuss S, Bindels EM, Costa IG, Schneider RK. Single-cell analysis of cultured bone marrow stromal cells reveals high similarity to fibroblasts in situ. Exp Hematol 2022 Mar; epub ahead of print

4. Stalmann USA, Ticconi F, Snoeren IAM, Li R, Gleitz HFE, Cowley GS, McConkey ME, Wong AB, Schmitz S, Fuchs SNR, Sood S, Leimkühler NB, Martinez-Høyer S, Banjanin B, Root D, Brümmendorf TH, Pearce JE, Schuppert A, Bindels EMJ, Essers MA, Heckl D, Stiehl T, Costa IG, Ebert BL, Schneider RK. Genetic barcoding systematically compares genes in del(5q) MDS and reveals a central role for CSNK1A1 in clonal expansion. Blood Adv. 2022 Mar 22;6(6):1780-1796.

5. Gleitz H, Dugourd AJF, Leimkühler NB, Snoeren IAM, Fuchs SNR, Menzel S, Ziegler S, Kroeger N, Triviai I, Büsche G, Kreipe H, Banjanin B, Pritchard J, Hoogenboezem R, Bindels E, Schumacher N, Rose-John S, Elf S, Saez-Rodriguez J, Kramann R, Schneider RK. Increased CXCL4 expression in hematopoietic cells links inflammation and progression of bone marrow fibrosis in MPN. Blood. 2020 Jul 29:blood.2019004095. doi: 10.1182/blood.2019004095.

6. Ribezzo F*, Snoeren IAM*, Ziegler S, Stoelben J, Olofsen PA, Henic A, Ventura Ferreira M, Chen S, Stalmann USA, Buesche G, Hoogenboezem RM, Kramann R, Platzbecker U, Raaijmakers MHGP, Ebert BL and Schneider RK. Rps14, Csnk1a1 and miRNA145/miRNA146a deficiency cooperate in the clinical phenotype and activation of the innate immune system in the 5q- syndrome. Leukemia, volume 33, pages1759–1772(2019)

7. Kuppe C, Ibrahim MM, …Schneider RK,.. Henderson NC and Kramann R. Decoding myofibroblast origins in human kidney fibrosis. Nature 2021 589(7841):281-286

8. Schneider R. K.#, Mullally A., Dugourd A., Peisker F., Hoogenboezem R., van Strien P. M., Bindels E. M., Heckl D., Büsche G., Fleck D., Müller-Newen G., Wongboonsin J., Ventura Ferreira M., Puelles V. G., Saez-Rodriguez J., Ebert B. L., Humphreys B. D., Kramann R.#. (2017): Gli1+ mesenchymal stromal cells are a key driver of bone marrow fibrosis and an important cellular therapeutic target. Cell Stem Cell, 2018 Aug 2;23(2):308-309. #corresponding author

9. Schneider RK, Schenone M, Ventura Ferreira M, Kramann R, Joyce CE, Hartigan C Beier F, Brümmendorf TH, Germing U, Platzbecker U, Büsche G, Knüchel R, Chen MC, Waters CS, Chen E, Chu LP, Novina CD, Lindsley RC, Carr SA, Ebert BL. Rps14 haploinsufficiency causes a block in erythroid differentiation mediated by S100A8/S100A9. Nature Medicine 2016 Mar;22(3):288-97.

10. Schneider RK, Ademà V, Heckl D, Järås M, Mallo M, Lord AM, Chu LP, McConkey ME, Kramann R, Mullally A, Bejar R, Solé F, Ebert BL. Role of casein kinase 1A1 in the biology and targeted therapy of del(5q) MDS. Cancer Cell. 2014 Oct 13;26(4):509-20.

Jurgen Marteijn started his career as a PhD student in the Central Hematology Laboratory at the Radboud University Medical Center, Nijmegen where he studied the role of the ubiquitin proteasome pathway during haematopoiesis. In 2006 he became a postdoc in the department of Genetics, were he subsequently started his independent research line to study the role of the post-translation modification ubiquitin during DNA-repair and DNA damage-associated signaling (Marteijn, JCB,2009 and van Cuijk, Nat.Com,2015). Using a quantitative proteomics approach to identify DNA damage induced ubiquitylation events, his research group identified UVSSA. This novel identified Transcription-Coupled Repair factor (TCR) is mutated in the UV-sensitive syndrome (Schwertman, Nat.Gen, 2012).

This finding enabled his lab to further dissect the regulation and molecular mechanism of TCR and to understand the severe clinical consequences associated with inherited TCR-defects. Using a combination of live-cell imaging and quantitative proteomics, his research group showed that chromatin remodeling is an essential process during the restart of transcription upon removal of transcription blocking lesions by TCR (Dinant, Mol.Cel, 2013). Furhtermore, his team revealed that the spliceosome is a key target of the DDR and defines a R-loop-dependent, non-canonical ATM activation by transcription-blocking lesions as an important event in the DNA damage response upon transcriptional stress (Tresini, Nature,2015).

• 2020:Ammodo Science Award for groundbreaking team research in the life sciences

• 2018: VICI Grant of Netherlands Organisation for Scientific Research

• 2014: VIDI Grant of Netherlands Organisation for Scientific Research

• 2011: Erasmus MC Fellowship

• 2008: Veni Grant of Netherlands Organisation for Scientific Research

1. DNA damage-induced transcription stress triggers the genome-wide degradation of promoter-bound Pol II

Barbara Steurer, Roel C Janssens, Marit E Geijer, Fernando Aprile-Garcia, Bart Geverts , Arjan F Theil, Barbara Hummel, Martin E van Royen, Bastiaan Evers, René Bernards, Adriaan B Houtsmuller, Ritwick Sawarkar, Marteijn JA

Nature Communications, 2022 Jun 24

2. Active DNA damage eviction by HLTF stimulates nucleotide excision repair

Marvin van Toorn, Yasemin Turkyilmaz, Sueji Han, Di Zhou, Hyun-Suk Kim, Irene Salas-Armenteros, Mihyun Kim, Masaki Akita, Franziska Wienholz, Anja Raams, Eunjin Ryu, Sukhyun Kang, Arjan F Theil, Karel Bezstarosti, Maria Tresini, Giuseppina Giglia-Mari, Jeroen A Demmers , Orlando D Schärer, Jun-Hyuk Choi, Wim Vermeulen, Marteijn JA

Molecular Cell, 2022 April 7

3. Elongation factor ELOF1 drives transcription-coupled repair and prevents genome instability

Geijer ME, Zhou D, Selvam K, Steurer B, …, Bernards R, Svejstrup JQ, Chaudhuri AR, Wyrick J, Marteijn JA

Nature Cell Biology, 2021 Jun 23

4. The DNA damage response to transcription stress.

Lans H, Hoeijmakers JHJ, Vermeulen W, Marteijn JA

Nature Reviews Molecular & Cellular Biology,2019 Dec 20

5. Live-cell analysis of endogenous GFP-RPB1 uncovers rapid turnover of initiating and promoter-paused RNA Polymerase II

Steurer B, Janssens R, Geverts B, Geijer M, Wienholz F, Theil A, Chang J, Dealy S, Pothof J, van Cappellen W, Houtsmuller A, Marteijn JA.

PNAS March 12, 2018

Highlighted with commentary in PNAS, “Transient pausing by RNA polymerase II” (2018)

6. SUMO and ubiquitin-dependent XPC exchange drives nucleotide excision repair.

van Cuijk L, van Belle GJ, Turkyilmaz Y, Poulsen SL, Janssens RC, Theil AF, Sabatella M, Lans H, Mailand N, Houtsmuller AB, Vermeulen W, Marteijn JA.

Nature Communications. 2015 Jul 7;6:7499.

7. The core spliceosome as target and effector of non-canonical ATM signalling.Tresini M, Warmerdam DO, Kolovos P, Snijder L, Vrouwe MG, Demmers JA, van IJcken WF, Grosveld FG, Medema RH, Hoeijmakers JH, Mullenders LH, Vermeulen W, Marteijn JA.

Nature. 2015 Jul 2;523(7558):53-8.

8. Understanding nucleotide excision repair and its roles in cancer and ageing.

Marteijn JA, Lans H, Vermeulen W, Hoeijmakers JH.

Nature Reviews Molecular Cell Biology. 2014 Jul;15(7):465-81.

9. Enhanced chromatin dynamics by FACT promotes transcriptional restart after UV-induced DNA damage.

Dinant C, Ampatziadis-Michailidis G, Lans H, Tresini M, Lagarou A, Grosbart M, Theil AF, van Cappellen WA, Kimura H, Bartek J, Fousteri M, Houtsmuller AB, Vermeulen W, Marteijn JA.

Molecular Cell. 2013 Aug 22.

10. UV-sensitive syndrome protein UVSSA recruits USP7 to regulate transcription-coupled repair.

Schwertman P, Lagarou A, Dekkers DH, Raams A, van der Hoek AC, Laffeber C, Hoeijmakers JH, Demmers JA, Fousteri M, Vermeulen W, Marteijn JA.

Nat Genetics 2012 May

Full publication list can be found on: www.researcherid.com/rid/B-5696-2014.

Roland Kanaar studied chemistry at Leiden University. He performed his PhD research (1984-1988) in the lab of Piet van de Putte on the mechanism of site-specific DNA recombination. His post-doctoral work at the University of California, Berkeley, with Nick Cozzarelli and Don Rio aimed at understanding the molecular mechanisms of homologous DNA recombination and RNA splicing, respectively. In 1995 he moved to the Erasmus University Medical Center to become professor of Molecular Genetics in 2000.

His current research addresses the mechanisms and biological relevance of the DNA damage response (DDR). Defects in the DDR lead to the accumulation of DNA lesions and mutations, which causes hereditary diseases, cancer, cell decay and aging. A central theme in the lab concerns the mechanisms of DNA double-strand break metabolism.

A breakthrough discovery was the revelation that homologous recombination in mammalian organisms contributes to repair of ionizing radiation-induced DNA double-strands. This was contrary to the existing dogma, which held that in mammals DNA double strand breaks were repaired almost exclusively by non-homologous DNA end-joining. Importantly, using mouse reverse genetics his team demonstrated that homologous recombination and non-homologous DNA end-joining pathway have overlapping, as well as specialized roles. Furthermore, his team discovered that hyperthermia augments DNA damage based anti-cancer treatments by degrading BRCA2, a mechanistic insight with direct clinical implications.

• 2013: Elected member of the KNAW (Royal Netherlands Academy of Arts and Sciences)

• 2012: Cozzarelli Prize, National Academy of Sciences, USA

• 2002: Elected member of EMBO

1. Modesti, M., Budzowska, M., Baldeyron, C., Demmers, J. A., Ghirlando, R., & Kanaar, R. (2007). RAD51AP1 is a structure-specific DNA binding protein that stimulates joint molecule formation during RAD51-mediated homologous recombination. Molecular cell, 28(3), 468-481.

2. Kanaar, R., & Wyman, C. (2008). DNA repair by the MRN complex: break it to make it. Cell, 135(1), 14-16.

3. Agarwal, S., van Cappellen, W. A., Guénolé, A., Eppink, B., Linsen, S. E., Meijering, E., ... & Essers, J. (2011). ATP-dependent and independent functions of Rad54 in genome maintenance. The Journal of cell biology, 192(5), 735-750.

4. Krawczyk, P. M., Eppink, B., Essers, J., Stap, J., Rodermond, H., Odijk, H., ... & Soullié, T. (2011). Mild hyperthermia inhibits homologous recombination, induces BRCA2 degradation, and sensitizes cancer cells to poly (ADP-ribose) polymerase-1 inhibition. Proceedings of the National Academy of Sciences, 108(24), 9851-9856.

5. Tham, K. C., Hermans, N., Winterwerp, H. H., Cox, M. M., Wyman, C., Kanaar, R., & Lebbink, J. H. (2013). Mismatch repair inhibits homeologous recombination via coordinated directional unwinding of trapped DNA structures. Molecular cell, 51(3), 326-337.

6. Zelensky, A. N., Schimmel, J., Kool, H., Kanaar, R., & Tijsterman, M. (2017). Inactivation of Pol θ and C-NHEJ eliminates off-target integration of exogenous DNA. Nature communications, 8(1), 66.

Ruud Delwel started his career in 1983 in the lab of Bob Lowenberg, studying the in vitro behaviour of human acute myeloid leukemia cells in vitro. He obtained his PhD in 1990 (Cum Laude) and became a post doctoral fellow in the group of Dr. James Ihly, at the St. Jude’s Children’s Research Hospital in Memphis, Tennessee Leiden, and carried out retroviral insertional mutagenesis to discover novel disease genes in AML. He discovered the EVI1 gene to be one of the most severe disease genes in mouse leukemia’s and in human. When back in the Netherlands, ErasmusMC, he moved on studying the biological consequences of altered gene expression in human and murine AML.

His two major breakthrough studies are 1) The discovery that human AML can be classified based on unique gene expression signatures and on specific gene methylation profiles. These studies led to the uncover of a subset of unique AML cases with aberrant expression of the EVI1 gene. Further in depth analysis revealed a unique mechanism of enhancer deregulation in a subset of human EVI1-AMLs. Ruud Delwel and his team have been able to combine patient analysis with molecular studies using in vitro and in vivo modelling to improve our insight into molecular aspects of acute myeloid leukemia. These studies and the proposal that followed on these studies have been awarded by the Dutch Cancer Society or "Koningin Wilhelmina Fonds” with the "Koningin Wilhelmina Onderzoek prijs", or KWO Award.

Our research now focusses on the mechanisms of aberrant gene (EVI1) control by hijacked enhancers and how we may interfere with the aberrant expression of those genes. Applying sophisticated in vitro models we screened for compounds, using the drug repurposing library obtained by Oncode, to uncover ways to interfere with oncogene expression. We obtained several interesting hits, which are investigated further in the next five years within Oncode.

• 2017: Jose Carreras Lecture/Price

• 2015: KWO Award

• 1994: Fellowship from the Royal Dutch Academy of Science (KNAW)

1. Smeenk L, Ottema S, Mulet-Lazaro R, Ebert A, Havermans M, Varea AA, Fellner M, Pastoors D, van Herk S, Erpelinck-Verschueren C, Grob T, Hoogenboezem RM, Kavelaars FG, Matson DR, Bresnick EH, Bindels EM, Kentsis A, Zuber J, Ruud Delwel. Selective Requirement of MYB for Oncogenic Hyperactivation of a Translocated Enhancer in Leukemia. Cancer Discov. 2021 Nov;11(11):2868-2883.

2. Ottema S, Mulet-Lazaro R, Erpelinck-Verschueren C, van Herk S, Havermans M, Arricibita Varea A, Vermeulen M, Beverloo HB, Gröschel S, Haferlach T, Haferlach C, J Wouters B, Bindels E, Smeenk L, Ruud Delwel. The leukemic oncogene EVI1 hijacks a MYC super-enhancer by CTCF-facilitated loops. Nat Commun. 2021 Sep 28;12(1):5679.

3. Mulet-Lazaro R, van Herk S, Erpelinck C, Bindels E, Sanders MA, Vermeulen C, Renkens I, Valk P, Melnick AM, de Ridder J, Rehli M, Gebhard C, Ruud Delwel, Wouters BJ. Allele-specific expression of GATA2 due to epigenetic dysregulation in CEBPA double-mutant AML. Blood. 2021 Jul 15;138(2):160-177

4. Sophie Ottema, Roger Mulet-Lazaro, H. Berna Beverloo, Claudia Erpelinc, Stanley van Herk, Marije Havermans, Tim Grob, Peter J. M. Valk, Eric Bindels, Torsten Haferlach, Claudia Haferlach, Leonie Smeenk, Ruud Delwel. Atypical 3q26/MECOM rearrangements genocopy inv(3)/t(3;3) in acute myeloid leukemia. Blood. 2020 Jul 9;136(2):224-234.

5. Gröschel, S., Sanders, M.A., Hoogenboezem, R., De Wit, E., Bouwman, B.A.M., Erpelinck, C., ... & Ruud Delwel. (2014). An oncogenic enhancer-rearrangement causes concomitant deregulation of EVI1 and GATA2 in leukemia. 2014, Cell, 157(2), 369-81.

Miao-Ping Chien is a multidisciplinary scientist. She obtained her PhD in chemistry and biochemistry at University of California, San Diego, where she successfully invented a nanomaterial that can specifically be targeted to and deposited in tumor tissues for a long period of time, through which the tumor can be detected with conjugated probes (fluorescent or MRI contrast agents) and treated with attached drugs (Doxorubicin). After that, she pursued her postdoctoral training in optical engineering and computational biology with Dr. Adam Cohen at Harvard University, where she developed technologies that are applicable to single cell biology and high-throughput measurements.

In 2017 June, Miao-Ping joined Erasmus MC as a group leader. Her research focuses on developing and applying multidisciplinary technologies (advanced microscopy and imaging, computation, single cell technology and bioinformatics) to investigate the underlying mechanisms of tumorigenesis, particularly of rare cancer-driving cells. Her main research goals are: the creation and application of technology for (early) detection and treatment of tumors, and the creation and application of single cell technology to facilitate the discovery and interpretation of genetic, transcriptomic and proteomic profiles of aberrant (single) cancer cells, with the aim of translating the knowledge gained to clinical applications. She is a founder of UFO Biosciences, which aims to profile rare & cancer-driving cells and identify actionable targets driving clinically relevant tumorigenic phenotypes.

• 2024: ERC Consolidator Grant

• 2024: NWO XL Consortium Grant
• 2023: EMC2 Synergy grant
• 2023: Aspasia award
• 2022: NWO Vidi Award
• 2022: KWF Public-Private-Partnership TKI grant
• 2022: Flagship Consortium Grants
• 2022: Computable Award
• 2022: Inspiring Fifty Deep Tech
• 2020: Ammodo Science Award
• 2020: Josephine Nefkens Foundation Grant
• 2020: Erasmus MC-TU Delft Convergence Grant
• 2018: Erasmus MC Fellowship
• 2017: CancerGenomiCs.nl Junior Fellow
• 2017: NWO Veni Award

1. You, L.*, Su, P.R.*, Betjes, M.*, Ghadiri Rad, R., Chou, T.C., Beerens, C., van Oosten, E., Leufkens, F., Gasecka, P., Muraro^, M., van Tol^, R., van Steenderen, D., Farooq, S., Hardillo, J.A.O., Baatenburg de Jong, R., Brinks, D., Chien, M.P. “Linking the genotypes and phenotypes of cancer cells in heterogenous populations via real-time optical tagging and image analysis”, Nature Biomedical Engineering, 2022 (DOI: 10.1038/s41551-022-00853-x).
2. Chou, T.C.*, You, L.*, Beerens, C., Feller, K.F., Storteboom, J., Chien, M.P. "Instant processing of large-scale image data with FACT, a real-time cell segmentation and tracking algorithm". Cell Reports Methods, 2023 (DOI:https://doi.org/10.1016/j.crmeth.2023.100636)
3. Su, P.R., Chien, M.P. Functional Single-Cell Proteomics: Technology and Biological Applications. In: Callmann, C. (eds) Biomedical Nanotechnology. Methods in Molecular Biology (Springer Nature Protocols), 2025, vol 2902. Humana, New York, NY. https://doi.org/10.1007/978-1-0716-4402-7_9.
4. Brinks, D., Chien, M.P. "Functional single-cell sequencing links dynamic phenotypes to their genotypes". Nature Biomedical Engineering (research briefing), 2022. (https://rdcu.be/cJr8o) (https://doi.org/10.1038/s41551-022-00877-3)
5. Cheng, K.W., Su, P.R., Feller, K.J.A., Chien, M.P.*, Hsu, C.C.* “Investigating the Metabolic Heterogeneity of Cancer Cells Using Functional Single-Cell Selection and nLC Combined with Multinozzle Emitter Mass Spectrometry”. Analytical Chemistry. 2024, 96, 2, 624–629. https://doi.org/10.1021/acs.analchem.3c03688.
6. Chen, T.Y., You, L. Hardillo, J.A.U., Chien, M.P. "Spatial Transcriptomic Technologies." Cells. 2023, 12(16), 2042, DOI: https://doi.org/10.3390/cells12162042.
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