Thanos Halazonetis Group
Department of Molecular Biology - Faculty of Science, University of Geneva
Project at a glance
The long-term goal of our research is to understand cancer at the molecular level and then use this knowledge to develop novel cancer therapies.
Towards this goal we have found that while in the majority of normal cells the DNA damage checkpoint pathway is not active (because in normal cells the DNA is not damaged), in human precancerous and cancerous tissues, the DNA damage checkpoint pathway is constitutively activated (implying the presence of DNA damage in cancer cells).
We have further identified DNA replication stress as the cause for constitutive activation of the DNA damage checkpoint pathway in cancer cells. DNA replication stress is a term that refers to problems with DNA replication.
Normally, replication forks replicate the genomic DNA without stalling. However, in cancer cells the replication forks stall or even completely collapse, leading to DNA damage. If one could prevent re-start of collapsed DNA replication forks in cancer cells, then these cells would be unable to complete replication of their DNA.