Selected Bibliography

• Bencokova Z, Kaufmann M R, Pires I M, Lecane P S, Giaccia A J, and Hammond E M (2009) ATM activation and signalling under hypoxic conditions. Mol Cell Biol.

• Rankin Erinn B, Giaccia Amato J, and Hammond Ester M (2009) Bringing H2AX into the angiogenesis family. Cancer Cell, 15(6):459-61.

• Ameri K, Hammond E M, Culmsee C, Raida M, Katschinski D M, Wenger R H, Wagner E, Davis R J, Hai T, Denko N, and Harris A L (2007) Induction of activating transcription factor 3 by anoxia is independent of p53 and the hypoxic HIF signalling pathway. Oncogene, 26(2):284-9.

• Hammond Ester M, Kaufmann Muriel R, Giaccia Amato J, and (2007) Oxygen sensing and the DNA-damage response. Curr Opin Cell Biol, 19(6):680-4.

• Freiberg Rachel A, Krieg Adam J, Giaccia Amato J, and Hammond Ester M (2006) Checking in on hypoxia/reoxygenation. Cell Cycle, 5(12):1304-7.

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 focus of my lab is the biological consequences of hypoxia initiating a DNA damage response in the absence of DNA damage.

2007 Junior Group Leader, ROB

2003 Research Associate, Stanford University, USA

1999 Post doctoral Fellow, Stanford University, USA