Mariia Yuneva

Oncogenes and Tumour Metabolism Laboratory

Metabolic changes are thought to provide tumour cells with a proliferation and survival advantage over healthy cells. However, these alterations can also make tumour cells selectively dependent upon certain nutrients and metabolic pathways, making tumour metabolism an attractive therapeutic target.

Both the genetic lesions and the tissue of origin are known to be critical factors that determine tumour metabolism (Figure 1). However, the relationship between these factors and their contributions to the metabolic requirements of different tumour types in the context of the whole organism remain largely unknown and are the focus of our research.

We are employing genetics and stable isotope-based metabolomics approaches to investigate how metabolism is changed in tumours induced by specific pro-tumourigenic events in various mammalian tissues. We are seeking to understand the molecular mechanisms of tissue-specific regulation of metabolic pathways by different oncogenes as well as how oncogenes induce the metabolic dependence of transformed cells in vivo. Finally, we are interested in exploring the relationship between oncogenes and metabolic changes in various types of human cancers.

Figure 1

Figure 1. Oncogenic lesions are among the factors determining tumour metabolism. Liver tumours induced by the MYC oncogene (center) have a significantly higher uptake of glucose than normal livers (left) or liver tumours induced by the MET oncogene (right). Glucose uptake is evaluated by positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG). The intensity of the color reflects the intensity of 18F-FDG signal. (Click to view larger image)

Selected publications

Yuneva, MO; Fan, TWM; Allen, TD; Higashi, RM; Ferraris, DV; Tsukamoto, T; Mates, JM; Alonso, FJ; Wang, C; Seo, Y; Chen, X and Bishop, JM (2012) The metabolic profile of tumours depends on both the responsible genetic lesion and tissue type Cell Metabolism 15, 157-170

Yuneva, M (2008) Finding an "Achilles' heel" of cancer: the role of glucose and glutamine metabolism in the survival of transformed cells Cell Cycle7, 2083-2089

Yuneva, M; Zamboni, N; Oefner, P; Sachidanandam, R and Lazebnik, Y (2007) Deficiency in glutamine but not glucose induces MYC-dependent apoptosis in human cells. Journal of Cell Biology 178, 93-105

Mariia Yuneva
+44 (0)20 379 61651

  • 2002 - PhD in Biochemistry, M.V. Lomonosov, Moscow State University, Moscow, Russia
  • 2002-2005 - Postdoctoral Fellow, Cold Spring Harbor Laboratory, NY, USA
  • 2005-2013 - Postdoctoral Fellow, University of California San Francisco, USA
  • 2013 - Group Leader, Medical Research Council National Institute for Medical Research, London UK
  • 2015 - Group Leader, The Francis Crick Institute, London, UK