Dr Eva Petermann PhD

Dr Eva Petermann

Institute of Cancer and Genomic Sciences
Reader in Genome Biology

Contact details

Institute of Cancer and Genomic Sciences
Institute for Biomedical Research (West)
College of Medical and Dental Sciences
University of Birmingham
B15 2TT

Dr Petermann’s research focuses on mechanisms of mammalian DNA replication stress, with an emphasis on oncogene-induced replication stress and homologous recombination. She has published more than 35 research papers and review articles in the field of DNA replication and DNA repair. Her lab has received research funding from Cancer Research UK, MRC, BBSRC, Worldwide Cancer Research, the Royal Society and the Wellcome Trust.

Research group page: https://www.evapetermann.org/

The Petermann group is a member of the Birmingham Centre for Genome Biology.


  • PG Cert Learning and Teaching in Higher Education, 2012
  • PhD in Biochemistry, 2004 
  • BSc/MSc in Biochemistry, 2001


I qualified in 2001 with a BSc and MSc in Biochemistry at the Martin Luther University Halle-Wittenberg in Germany and then obtained a PhD in Biochemistry (2004) at the Free University Berlin, where I worked on PARP1 and DNA base excision repair.

I continued with postdoctoral research in the field of DNA repair and replication in the lab of Keith Caldecott at the Sussex Centre for Genome Damage and Stability in Brighton and then moved to the lab of Thomas Helleday at the University of Oxford, where I was also a Junior Research Fellow at Linacre College.

I joined the University of Birmingham as a Lecturer in 2010. I received the European Environmental Mutagen Society Young Scientist Prize in 2010. In 2019, the Petermann lab was awarded £1.6 million in funding from Cancer Research UK and the Medical Research Council.


Postgraduate supervision

Dr Petermann is interested in supervising doctoral researchers in
the following areas:

- Fundamental mechanisms of DNA replication stress and DNA repair
- Oncogene-induced replication stress
- Conflicts between replication and transcription
- Targeted cancer therapies
- Cancer chemotherapy and replication stress


DNA replication is the process by which dividing cells copy their genetic information. Replication is very important but also dangerous for cells, because if obstacles inhibit the movement of the replication apparatus, this can lead to DNA damage, mutations or cell death. This is called replication stress (Jones and Petermann, 2012; Petermann and Helleday, 2010). My group investigates molecular mechanisms of replication stress in cancer development and -treatment.


Transcription-replication conflicts in cancer

Replication stress, or replication-associated DNA damage, occurs frequently in cancer. There is a growing interest in targeting oncogene-induced replication stress for cancer therapy. Effective targeting will require mechanistic understanding of how oncogenes induce replication stress. It is widely appreciated that oncogenes can promote replication stress by de-regulating the cell cycle machinery to increase proliferation. However to promote proliferation, oncogenes also need to hyper-activate the basal transcription machinery. We use DNA fibre approaches to identify new mechanisms of oncogene-induced replication stress (Jones et al., 2013). 

We have evidence for transcription hyper-activation as an alternative and important replication stress mechanism. We recently reported that H-RasV12 induces replication-transcription conflicts, not by de-regulating the cell cycle, but by increasing expression of a general transcription factor (TBP) and global RNA synthesis (Kotsantis et al., 2016). We showed that TBP overexpression can promote replication stress independently of oncogenes.  We are further investigating the mechanisms of oncogene-induced transcription-replication conflicts. We are also investigating transcription-replication conflicts induced by a new class of cancer drugs called BET inhibitors (Bowry et al., 2018).



Homologous recombination at stalled replication forks

Homologous recombination (HR) is a remarkable genome maintenance pathway that brings together DNA replication and DNA repair. Because of this, it is absolutely central to diseases characterized by replication stress or treated with replication stress-inducing agents. 

It is increasingly evident that HR processes frequently occur at perturbed replication forks, where HR performs novel roles that are distinct from its classic function in DNA double-strand break repair. New insights into the roles of HR at stressed replication forks are relevant for cancer development and therapy. We are particularly interested in understanding how HR can slow and stall forks.


We use DNA fibre approaches to identify new roles for HR and the central HR factor RAD51 at stalled replication forks. We study how RAD51 modulates fork progression in response to classic chemotherapy, targeted cancer therapies, and environmental mutagens (Jones et al, 2014; Ronson et al., 2018)


Highlight publications

Piberger, L, Bowry, A, Kelly, R, Walker, A, Gonzalez-Acosta, D, Bailey, L, Doherty, A, Mendez, J, Morris, J, Bryant, HE & Petermann, E 2020, 'PrimPol-dependent single-stranded gap formation mediates homologous recombination at bulky DNA adducts', Nature Communications, vol. 11, no. 1, 5863. https://doi.org/10.1038/s41467-020-19570-7

Bowry, A, Piberger, AL, Rojas, P, Saponaro, M & Petermann, E 2018, 'BET inhibition induces HEXIM1- and RAD51-dependent conflicts between transcription and replication', Cell Reports, vol. 25, no. 8, pp. 2061–2069.e4. https://doi.org/10.1016/j.celrep.2018.10.079

Kotsantis, P, Marques Silva, L, Irmscher, S, Jones, R, Folkes, L, Gromak, N & Petermann, E 2016, 'Increased global transcription activity as a mechanism of replication stress in cancer', Nature Communications, vol. 7, no. 1, 13087. https://doi.org/10.1038/ncomms13087

Jones, R, Kotsantis, P, Stewart, G, Groth, P & Petermann, E 2014, 'BRCA2 and RAD51 promote double-strand break formation and cell death in response to Gemcitabine', Molecular Cancer Therapeutics, vol. 13, no. 10, pp. 2412-2421. https://doi.org/10.1158/1535-7163.MCT-13-0862

Jones, R, Mortusewicz, O, Afzal, I, Lorvellec, M, García, P, Helleday, T & Petermann, E 2012, 'Increased replication initiation and conflicts with transcription underlie Cyclin E-induced replication stress', Oncogene. https://doi.org/10.1038/onc.2012.387

Recent publications


Landsverk, HB, Sandquist, LE, Bay, LTE, Steurer, B, Campsteijn, C, Landsverk, OJB, Marteijn, JA, Petermann, E, Trinkle-Mulcahy, L & Syljuasen, RG 2020, 'WDR82/PNUTS-PP1 prevents transcription-replication conflicts by promoting RNA POLYMERASE II degradation on chromatin', Cell Reports, vol. 33, no. 9, 108469. https://doi.org/10.1016/j.celrep.2020.108469

Nazeer, R, Qashqari, F, Albalawi, A, Piberger, AL, Tilotta, M, Read, M, Hu, S, Davis, S, McCabe, C, Petermann, E & Turnell, A 2019, 'Adenovirus E1B 55-kilodalton protein targets SMARCAL1 for degradation during infection and modulates cellular DNA replication', Journal of virology, vol. 93, no. 13, e00402-19. https://doi.org/10.1128/JVI.00402-19

Benedict, B, van Harn, T, Dekker, M, Hermsen, S, Kucukosmanoglu, A, Pieters, W, Delzenne-Goette, E, C Dorsman, J, Petermann, E, Foijer, F & te Riele, H 2018, 'Loss of p53 suppresses replication-stress-induced DNA breakage in G1/S checkpoint deficient cells', eLife, vol. 7, e37868. https://doi.org/10.7554/eLife.37868

Bayley, R, Blakemore, D, Cancian, L, Dumon, S, Volpe, G, Ward, C, Al Maghrabi, R, Gujar, J, Reeve, N, Raghavan, M, Higgs, M, Stewart, G, Petermann, E & Garcia, P 2018, 'MYBL2 supports DNA double strand break repair in haematopoietic stem cells', Cancer Research, vol. 78, no. 20, pp. 5767-5779. https://doi.org/10.1158/0008-5472.CAN-18-0273

Ronson, G, Piberger, AL, Higgs, M, Olsen, A, Stewart, G, McHugh, P, Petermann, E & Lakin, N 2018, 'PARP1 and PARP2 stabilise replication forks at base excision repair intermediates through Fbh1-dependent Rad51 regulation', Nature Communications, vol. 9, no. 1, 746. https://doi.org/10.1038/s41467-018-03159-2

Kwok, M, Davies, N, Agathanggelou, A, Smith, E, Oldreive, C, Petermann, E, Stewart, G, Brown, J, Lau, A, Pratt, G, Parry, H, Taylor, M, Moss, P, Hillmen, P & Stankovic, T 2016, 'ATR inhibition induces synthetic lethality and overcomes chemoresistance in TP53 or ATM defective chronic lymphocytic leukemia cells', Blood, vol. 127, no. 5, pp. 582-595. https://doi.org/10.1182/blood-2015-05-644872

Chapter (peer-reviewed)

Kotsantis, P, Jones, R, Higgs, M & Petermann, E 2015, Cancer Therapy and Replication Stress: Forks on the Road to Perdition. in GS Makowski (ed.), Advances in Clinical Chemistry. vol. 69, Academic Press (Elsevier), pp. 91-138. <http://www.sciencedirect.com/science/article/pii/S0065242314000420>


Petermann, E 2018, Homologous Recombination at Replication Forks. in R Grand & J Reynolds (eds), DNA Repair and Replication: Mechanisms and Clinical Significance. Routledge.


Bowry, A, Piberger, AL & Petermann, E 2018, 'BET inhibition induces transcription-replication conflicts that depend on HEXIM1 and RAD51', RNA and genome maintenance, Mainz, Germany, 10/10/18 - 13/10/18.

Piberger, AL & Petermann, E 2018, 'Mechanisms of Benzo[a]pyrene-induced recombination', 42nd Annual Meeting of the United Kingdom Environmental Mutagen Society (UKEMS), Oxford, United Kingdom, 2/09/18 - 5/09/18.

Tang, HM, Kotsantis, P, Gromak, N & Petermann, E 2018, 'RNA/DNA hybrid metabolism and replication stress in cancer', RNA and genome maintenance, Mainz, Germany, 10/10/18 - 13/10/18.

Kotsantis, P, Marques Silva, L, Irmscher, S, Jones, R, Folkes, L, Gromak, N & Petermann, E 2017, 'Increased global transcription activity as a mechanism of oncogene-induced replication stress', 2nd DNA Replication as a Source of DNA Damage Conference, Rome, Italy, 3/07/17 - 6/07/17.

Kotsantis, P, Marques Silva, L, Irmscher, S, Jones, R, Folkes, L, Gromak, N & Petermann, E 2016, 'Increased global transcription activity as a mechanism of replication stress in cancer', Mutagenesis Gordon Research Conference, Girona, Spain, 5/06/16 - 10/06/16.

Kotsantis, P, Irmscher, S, Jones, R, Gromak, N & Petermann, E 2015, 'Oncogenic RAS causes replication stress by deregulating transcription', Keystone Symposium DNA Replication and Recombination, Whistler, Canada, 1/03/15 - 6/03/15.

Review article

Kotsantis, P, Petermann, E & Boulton, SJ 2018, 'Mechanisms of oncogene-induced replication stress: jigsaw falling into place', Cancer Discovery, vol. 8, no. 5, pp. 537-555. https://doi.org/10.1158/2159-8290.CD-17-1461

View all publications in research portal