Pierre Sonveaux #


Pierre Sonveaux is a Pharmacist and a PhD in Pharmaceutical Sciences. He was recently appointed Research Associate of the Fonds National de la Recherche Scientifique (F.R.S.-FNRS) and Assistant Professor in the Pole of Pharmacology at the University of Louvain (UCL) Medical School in Brussels, Belgium.

After graduation as a Pharmacist in 1998, Pierre Sonveaux joined the Ludwig Institute for Cancer Research (LICR, Brussels branch) to perform a Master degree in tumor immunogenetics. In 2000, he joined the team of Prof. Olivier Feron at UCL to perform a PhD in vascular oncology. Pierre’s PhD thesis dissertation (The tumor vasculature: functional reactivity and therapeutic implications, 2004) reports the development of new anticancer strategies that exploit the tumor vascular reactivity to radio- and chemo- sensitize tumors. These approaches have now collectively been termed ‘provascular’. As a post-doc and fellow of the Belgian American Educational Foundation (BAEF), Pierre joined the Radiation Oncology group of Prof. Mark W. Dewhirst at Duke University in North Carolina, USA. There, he gained new knowledge in tumor metabolism that he translated in a career as a senior post-doc and more recently as a young independent investigator when he joined back the Pole of Pharmacology at UCL.

Pierre Sonveaux is the author of about 30 papers, some of them in prominent journals such as Cancer Research, Circulation Research, Molecular Cell and the Journal of Clinical Investigation, and the inventor of 1 granted patent and of 3 pending patent applications. He received prestigious awards, among which the National Prize of the Belgian Society of Pharmaceutical Sciences (2005), the ESTRO Varian-Juliana Denekamp award (2007), the FECS-EJC award (2008) and the EACR Highly Commended Award (2010). Pierre currently holds an ERC Starting Independent Researcher Grant (#243188 - TUMETABO), which by itself speaks for the highly innovative and provocative aspects of Pierre Sonveaux’s researches at the European level.


Hypoxic tumor cells are particularly resistant to conventional anticancer treatments owing to poor oxygenation (resistance to radiotherapy and DNA-damaging agents), the distance from blood vessels (limited bioavailability of circulating anticancer agents) and high genetic instability promoting the emergence of resistant cell populations. These cells account for treatment failure, tumor recurrence and metastasis. Sonveaux et al.1 recently found that the existence of a hypoxic tumor cell compartment primarily relies on a metabolic symbiosis by which glycolytic/hypoxic and oxidative/oxygenated tumor cells mutually regulate their access to energy metabolites. The symbiosis involves lactate recycling: oxidative tumor cells use lactate preferentially to glucose as an oxidative fuel, allowing glucose to optimally fuel glycolytic tumor cells that produce lactate abundantly. Sonveaux et al. identified monocarboxylate transporter 1 (MCT1) as the prominent path for lactate uptake by oxidative tumor cells. Inhibiting MCT1 pharmacologically or with genetic approaches induces a switch from lactate-fueled respiration to glycolysis in these cells. Consequently, MCT1 inhibition retards tumor growth in vivo as the hypoxic/glycolytic tumor cells die from glucose starvation. Through the oxygen effect coupled to the glycolytic conversion, MCT1 inhibition also synergizes with radiotherapy. Finally, Sonveaux et al. found MCT1 to be expressed in an array of primary human tumors and MCT1 inhibition to have limited toxicity in mice, suggesting a high clinical potential for the new anticancer treatment.


Sonveaux P, Végran F, Schroeder T, Wergin MC, Verrax J, Rabbani ZN, De Saedeleer CJ, Kennedy KM, Diepart C, Jordan BF, Kelley MJ, Gallez B, Wahl MW, Feron O, Dewhirst MW. Targeting lactate-fueled respiration selectively kills hypoxic tumor cells in mice. J. Clin. Invest. 2008;118:3930-3942.
Imprint Privacy policy « This page (revision-3) was last changed on Thursday, 28. September 2017, 13:00 by Kaiser Dana
  • operated by