Selected Bibliography

• Phadwal Kanchan, Alegre-Abarrategui Javier, Scarth Watson Alexander, Pike Luke, Anbalagan Selvakumar, Hammond Ester M, Wade-Martins Richard, McMichael Andrew, Klenerman Paul, and Katharina Simon Anna (April 2012) A novel method for autophagy detection in primary cells: Impaired levels of macroautophagy in immunosenescent T cells Autophagy, 8:4.

• Anbalagan S, Pires I M, Blick C, Hill M A, Ferguson D J, Chan D A, and Hammond E M (2012) Radiosensitization of renal cell carcinoma in vitro through the induction of autophagy. Radiother Oncol.

• Fokas E, Prevo R, Pollard J R, Reaper P M, Charlton P A, Cornelissen B, Vallis K A, Hammond E M, Olcina M M, Gillies McKenna W, Muschel R J, and Brunner T B (2012) Targeting ATR in vivo using the novel inhibitor VE-822 results in selective sensitization of pancreatic tumors to radiation. Cell Death Dis, 3:e441.

• Pires I M, Olcina M M, Anbalagan S, Pollard J R, Reaper P M, Charlton P A, McKenna W G, and Hammond E M (2012) Targeting radiation-resistant hypoxic tumour cells through ATR inhibition. Br J Cancer.

• Coutts A S, Pires I M, Weston L, Buffa F M, Milani M, Li J-L, Harris A L, Hammond E M, and La Thangue N B (2011) Hypoxia-driven cell motility reflects the interplay between JMY and HIF-1alpha. Oncogene, 30(48):4835-42.

Ester Hammond

Recently it has been proposed that the DNA damage response acts as a barrier mechanism during the early stages of tumourigenesis. Markers commonly phosphorylated as a result of an active DNA damage pathway were identified in pre-neoplastic lesions and have been attributed to the early activation of oncogenes. Our hypothesis suggests that along with the activation of oncogenes, the DNA-damage response pathway could be initiated by other factors during early tumour progression, for example, oxidative changes to DNA bases, the production of reactive oxygen species and hypoxia.  Regions of hypoxia arise due to the malformed vessels induced by tumour angiogenesis and occur early in the development of all solid tumours. Many elegant studies have demonstrated that the degree of hypoxia within human cancers correlates with poor prognosis as a result of a more aggressive phenotype as well as resistance to both chemo and radio-therapy. Significantly, red cell flux instability within a tumour can lead to rapid re-oxygenation and also induces a DNA damage response.  My work has shown that both the ATR and ATM signal transduction pathways are activated by tumour hypoxia. The aim of my lab is to target the DNA damage response as a means of sensitizing cells to hypoxia/reoxygenation.

2012 University Research Lecturer, University of Oxford, UK

2011 Director of Graduate Studies, Gray Institute for Radiation Oncology and Biology, Oxford, UK

2007 Junior Group Leader, Gray Institute for Radiation Oncology and Biology, Oxford, UK

2003 Research Associate, Stanford University, USA

1999 Post doctoral Fellow, Stanford University, USA