Professor Eva Petermann PhD

Professor Eva Petermann

Institute of Cancer and Genomic Sciences
Professor of Genome Stability

Contact details

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

Professor 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:

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


Career to date

2023 -           Professor of Genome Stability, University of Birmingham

2020 - 2023 Reader, University of Birmingham

2014 - 2020 Senior Lecturer, University of Birmingham

2010 - 2014 Lecturer, University of Birmingham

2007 - 2010 Postdoctoral researcher, University of Oxford

2004 - 2007 Postdoctoral researcher, University of Sussex

External Engagement

2021 -           Editorial Board, British Journal of Cancer

2013 -            UK Genome Stability Network Committee

2020 - 2022 Conference Theme Panel RAI, Biochemical Society

2020 - 2022 Member of funding committee

Member of junior PI recruitment panel


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

General doctoral research enquiries:


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). 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, Kotsantis et al., 2016, Bowry et al., 2021).

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, Bowry et al., 2021). 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 (Da Costa et al., 2013; 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; Piberger et al., 2020)


Highlight publications

Petermann, E, Lan, L & Zou, L 2022, 'Sources, resolution and physiological relevance of R-loops and RNA–DNA hybrids', Nature Reviews. Molecular Cell Biology, vol. 23, no. 8, pp. 521-540.

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.

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.

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.

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.

Recent publications


Blakemore, D, Vilaplana-Lopera, N, Almaghrabi, R, Gonzalez, E, Moya, M, Ward, C, Murphy, G, Gambus, A, Petermann, E, Stewart, GS & García, P 2021, 'MYBL2 and ATM suppress replication stress in pluripotent stem cells', EMBO Reports, vol. 22, no. 5, e51120.

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.

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.

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.

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.,

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.

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.


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.

Review article

Petermann, E 2022, 'Conflicts with transcription make early replication late', Molecular Cell, vol. 82, no. 18, pp. 3315-3317.

Bowry, A, Kelly, R & Petermann, E 2021, 'Hypertranscription and replication stress in cancer', Trends in Cancer, vol. 7, no. 9, pp. 863-877.

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.

View all publications in research portal