Siric > Research > SIRIC research programs > Tumour Escape: exploration of mechanisms and search for targets

A wide range of skills

The tumour escape program aims at characterizing molecular and cellular determinants of cancer resistance to treatment, in order to identify new synthetic lethal interactions which could be exploited to overcome declared resistance or obviate its emergence. As a final aim we want to devise new therapeutical strategies to be tested in preclinical and clinical tests.

The development of this program relies on the existence of wide ranging basic and applied research teams in Montpellier with strong expertise in the fields of the regulation of cell cycles, of DNA replication, metabolism of tumour cells and cancer stem cell biology. At the same time, links woven with clinical teams allow stakeholders in the Program to be part of a dynamic transfer of coordinated clinician-researcher information.

Guillaume_CartronCharles-TheilletThe TreatFail program is coordinated by Pr Guillaume Cartron, PU-PH, Department of Clinical Hematology CHU Montpellier, and Dr Charles Theillet, team leader of the research group ” Tumor identity and plasticity”.

Scientific objectives

cell 6The great diversity of mechanisms governing the resistance of cancer cells has made it difficult to set up effective treatment strategies. It requires an intimate insight into the biology of resistance to define new parameters for predicting tumor responsiveness. Given the tightly woven interactions between intrinsic alterations, cancer stem cells/tumor-initiating cells (CSC/TIC) phenotype and treatment failure, we decided to address these questions jointly and, within the framework of the SIRIC, to assemble research and clinical expertise to tackle fundamental, translational and clinical aspects of this critical issue.

The work undertaken within this frame covers the impact of basic biological mechanisms such as cell cycle control, DNA replication, repair and recombination, cellular metabolism, the maintenance of cancer stem cell/tumor initiating cell phenotypes, in the emergence of resistance to treatment.

Our unifying objective is to ultimately propose new treatment modalities for these frequently incurable cancers. To this effect, we have structured our program around 3 working goals:

Axis 1: Interplay between cell cycle chekpoints and DNA replication, repair and recombination

Axis 2: Impact of cell metabolism on genome integrity: focus on nucleotide biosynthesis and redox homeosasis in ancer progression and targeted therapies

Axis 3: Impact of epigenome modification on DNA replication and repair