Régulation de la signalisation de cassures d'ADN double brin dans le cancer cervical

 

Amélie Fradet-Turcotte

Centre de recherche du Centre hospitalier universitaire de Québec

 

Domaine : cancer

Programme chercheurs-boursiers - Junior 1

Concours 2015-2016

Human papillomaviruses (HPV) are small viruses that infect the cells of the epithelium that composes the skin and mucus membranes. While our immune system efficiently eliminates most HPV infections, the persistent ones lead to the appearance of cervical lesions, the precursors of cervical cancer in many patients. Infections that are caused by the ''high risk'' type of HPV are required but not sufficient for the development of cervical cancer. Indeed, the infected cells need to undergo additional changes to transition into cancer cells. These alterations are acquired when cells accumulate DNA damage or mutations. In healthy cells, the integrity of the genetic information stored in the DNA is safeguarded by a group of proteins that work together to rapidly detect and repair DNA damage. When the lesions are not faithfully repaired, the genetic information is modified and the cell becomes cancerous.

The main goal of our research is to understand how the virus disrupts detection and repair of the DNA lesions and how this process contributes to the development of cervical cancer. Specifically, we want to identify the mechanisms by which the virus hijacks the proteins that are required to detect and repair the DNA damage that leads to cancer development. Furthermore, we will investigate changes in the intracellular environment caused by viral infection challenges the capacity of the cell to choose the right DNA repair pathway and how these changes affect the reaction of the cells to anti-cancer treatments. To achieve these objectives, we will use techniques such as microscopy to track the proteins that detect DNA damage and experimental systems that will allow us to follow the different DNA repair pathways in cervical cancer cells.