Professor Ester Hammond

PhD Birmingham


Ester Hammond, PhD, is Professor of Molecular Cancer Biology and a CRUK Senior Group Leader at the CRUK/MRC Oxford Institute for Radiation Oncology. She completed her PhD at the School for Cancer Sciences, University of Birmingham then accepted a post as a postdoctoral fellow within the Molecular Oncology Group at the University of Cambridge School of Clinical Medicine before moving to the USA to join the Department of Radiation Oncology at Stanford University, first as a postdoctoral fellow then a research associate. She returned to the UK to join the Oxford Institute in 2007 as a CRUK junior group leader.


In order to progress beyond a certain size, tumours need to develop their own blood supply for nutrients and oxygen. Although tumours are able to create their own blood supply this process is not perfect and so tumours have regions which do not receive enough oxygen. Hypoxia is the term used to describe any situation where there is insufficient oxygen. Most solid tumours have regions of hypoxia, which is significant because many studies have shown that the more hypoxic a tumour is, the worse the patient does. Importantly, this is independent of the therapy type the patient receives. Hypoxic tumours are resistant to both chemotherapy and radiotherapy as well as being more likely to spread and are therefore the most aggressive and hardest to treat. To improve the effectiveness of cancer therapy it is vital that we target the hypoxic part of tumours. My group has three approaches to this problem:

  1. We are investigating the biological response to hypoxia and in particular a pathway known as the DNA damage response. This pathway is active in hypoxic conditions despite a lack of detectable hypoxia-induced DNA damage. There are many drugs to target this pathway and it is possible that they will prove particularly useful in killing hypoxic cells when combined with standard therapies such as radiation.
  2. We are developing novel drugs which only work in the absence of oxygen and so can be used to target the hypoxic areas of tumours. This approach allows us to use potentially toxic drugs as the normal cells in the body are unaffected. This work is done in collaboration with Professor Stuart Conway in the Department of Chemistry.
  3. Finally, it is vital that novel inhibitors/drugs are tested in conditions which mimic those found in tumours.  Therefore, we test drugs in conditions which more closely resemble those found in tumours, including low oxygen, to determine if they are likely to be effective.


Ribonucleotide reductase requires subunit switching in hypoxia to maintain DNA replication. Iosifina P. Foskolou, Christian Jorgensen, Katarzyna B. Leszczynska, Monica M. Olcina, Hanna Tarhonskaya, Bauke Haisma, Vincenzo D’Angiolella, William K. Myers, Carmen Domene, Emily Flashman and Ester M. Hammond. Mol Cell. 2017 Apr 20;66(2):206-220

Preclinical testing of an ATR inhibitor demonstrates improved response to standard therapies for esophageal cancer. Katarzyna B. Leszczynska, Greg Dobrynin, Rhea E. Leslie, Jonathan Ient, A.J. Boumelha, Joana M. Senra, Maria A. Hawkins, Tim Maughan, Somnath Mukherjee and Ester M. Hammond. Radiother Oncol. 2016 Nov;121(2):232-238

Mechanisms and consequences of ATMIN repression in hypoxic conditions: roles for p53 and HIF-1. Katarzyna B. Leszczynska, Eva-Leonne Göttgens, Deborah Biasoli, Monica M. Olcina, Jonathan Ient, Selvakumar Anbalagan, Stephan Bernhardt, Amato J. Giaccia and Ester M. Hammond. Sci Rep. 2016 Feb 15;6:21698

Design, synthesis and evaluation of molecularly targeted hypoxia-activated prodrugs.  O'Connor LJ, Cazares-Körner C, Saha J, Evans CN, Stratford MR, Hammond EM, Conway SJ.  Nat Protoc. 2016 Apr;11(4):781-94.

H3K9me3 facilitates hypoxia-induced p53-dependent apoptosis through repression of APAK.  Olcina MM, Leszczynska KB, Senra JM, Isa NF, Harada H, Hammond EM.  Oncogene. 2016 Feb 11;35(6):793-9.

Leszczynska KB, Foskolou IP, Abraham AG, Anbalagan S, Tellier C, Haider S, Span PN, O'Neill EE, Buffa FM, Hammond EM. Hypoxia-induced p53 modulates both apoptosis and radiosensitivity via AKT. J Clin Invest. 2015 Jun;125(6):2385-98. 

Replication stress and chromatin context link ATM activation to a role in DNA replication. Olcina MM, Foskolou IP, Anbalagan S, Senra JM, Pires IM, Jiang Y, Ryan AJ, Hammond EM. Mol Cell. 2013 Dec 12;52(5):758-66.