The Marie Curie fellowship has enabled me to work on fundamental questions related to cancer and metastasis.
Indeed, metastasis is the primary cause of cancer deaths. Yet, for most of cancers, the identification and the mechanisms by which the metastatic initiating cells (MICs) successfully establish a secondary tumor at a distant site from their primary tumor remains elusive.
Understanding these mechanisms is fundamental in developing clinical applications that would enable the treatment of patients suffering from advanced-stage cancers. The understanding of such mechanisms would also enable a preventive approach for cancers detected early enough.
The classical view of the metastatic process posits that MICs need to lose their cell-cell contact with the neighbors, detach from the primary tumor, intravasate into the blood circulation, circulate through the body, stop, extravasate and colonize distant organs, in which they reform a new mass of proliferative cells. With the tremendous heterogeneity of tumors and the limited capacity to trace multiple genetic clones in parallel with the traditional reporter mice , new animal models are needed to better understand the clonal dynamic and molecular mechanisms guiding different steps of the metastatic cascades in vivo.
The overall objective of this project was to to investigate primary tumour heterogeneity and contribution of cancer clones to metastasis, as well as the role of microenvironment in regulating metastasis. This knowledge aids the design of new methods for early diagnosis and the monitoring of patients with metastasis, and will lead to new strategies that target or prevent metastasis.
