• Prof. Alix-Panabieres Catherine

CV

Catherine Alix-Panabières is Professor of Oncology and Director of the Laboratory of Rare Human Circulating Cells and Liquid Biopsy (LCCRH) at Montpellier University Hospital and the Faculty of Medicine. Since 2022, she has also been Professor at the University of Hamburg, Germany. A pioneer in circulating tumor cell (CTC) research for over 25 years, she introduced the term liquid biopsy in 2010 together with Prof. Pantel. She teaches internationally, has organized numerous conferences, and has contributed over 170 publications, book chapters, and patents. Her landmark work demonstrated the clinical utility of CTCs in breast cancer. Prof. Alix-Panabières has received multiple national and international awards, including the “Gallet et Breton” Prize (2012) and the “Berthe Péan, Antoine et Claude Béclère” Prize (2023) from the French Academy of Medicine. In 2020, Nature highlighted her contributions to liquid biopsy as a major cancer research breakthrough of the past two decades.

ABSTRACT

Unravelling the biology of metastasis-competent circulating tumor cells: insights into the metastatic cascade

The characterization of circulating tumor cells (CTCs) offers valuable opportunities for precision medicine, as these cells serve as important clinical indicators of treatment efficacy and disease progression. We established the first—and still only—nine permanent colon CTC lines from peripheral blood samples of a patient with metastatic colon cancer, collected at different time points during therapy and progression. The study aimed (i) to compare gene expression profiles across these CTC lines and (ii) to identify features acquired under treatment pressure. A higher number of genes were upregulated in post-treatment CTC lines, reflecting adaptive mechanisms for survival. Among them, genes involved in the mTOR and PI3K/AKT signaling pathways were significantly enriched. Notably, cytidine deaminase expression was increased after failure of 5-fluorouracil-based regimens, suggesting enzymatic drug inactivation. Enzymes implicated in xenobiotic metabolism were also upregulated, indicating the activation of detoxification mechanisms in response to chemotherapy. Furthermore, aldolase B was markedly overexpressed in CTC lines obtained after treatment withdrawal, consistent with a liver metastasis origin. Beyond transcriptional changes, I will present complementary data on epigenomic reprogramming, describe the major hallmarks of CTCs, and highlight the mechanobiological properties that underlie their capacity to seed metastases. Collectively, these unique CTC lines provide critical insights into tumor evolution, drug resistance, and metastatic potential.