Living organisms are constantly exposed to DNA damaging processes and agents from both endogenous (eg, replicative stress, reactive oxygen species, non-enzymatic methylation) and exogenous sources (eg, UV and ionizing radiation, environmental pollutants, products of combustion). Efficient removal or repair of DNA damage is essential to maintain genomic integrity and for the proper function and survival of cells. DNA damage activates the DNA damage response (DDR), an intricate intracellular network that sense, signal and control cellular responses to these lesions, including cell cycle arrest and damage repair, and impact on cell fate decisions, such as survival, cell death or senescence. DNA damage is also caused by some anticancer chemotherapeutic drugs and by radiations used for diagnostic and therapeutic purposes.

Our research group studies the role of the DNA damage response in determining whether cancer cells survive or die upon treatment with genotoxic chemotherapeutics. We are particularly interested on how proliferation of damaged cells after sub-lethal treatment impacts the dynamics of cancer evolution and acts as a substrate for tumour progression and development of chemo-resistance.