
Cell Signalling
Why we focus on Cell Signalling
Cell signalling is the process by which our cells communicate with each other and with their environment. Pathways that govern how cells proliferate, move, survive and differentiate represent key targets in cancer biology. Targeting cell signalling has proven extremely successful in cancer treatment – drugs such as Glivec, Herceptin and Iressa, all discovered as a result of our increased understanding of cell signalling are being used to treat millions of patients worldwide.
What we do
- We study Phosphatidylinositol 3-kinase (PI3K) enzymes, key regulators of cell signalling pathways that are often deregulated in cancer and represent new drug targets for cancer and other diseases.
- We use novel proteomic approaches to study cell signalling pathways in unprecedented detail, allowing us to understand chemoresistance and cancer cell metabolism.
- We study compartmental signalling and how receptors, in particular c-Met, are trafficked within cancer cells, thus identifying novel pathways and therapeutic targets.
- We study Fibroblast Growth Factor Receptors and their impact on cancer cell behaviour, focusing on their nuclear trafficking and their oncogenic mutations.
- We study the role of voltage-gated proton channels in B-cell cancers and their role in supporting B Cell Receptor signalling.
Key Publications
- Beltran et al. Calpain interacts with class IA phosphoinositide 3-kinases regulating their stability and signaling activity. Proc Natl Acad Sci USA 2011; 108: 16217-22.
- Joffre et al. A direct role for Met endocytosis in tumorigenesis. Nat Cell Biol 2011; 13: 827-37.
- Foukas et al. Activity of any class IA PI3K isoform can sustain cell proliferation and survival. Proc Natl Acad Sci USA 2010; 107: 11381-6.
- Billottet et al. Inhibition of class I phosphoinositide 3-kinase activity impairs proliferation and triggers apoptosis in acute promyelocytic leukemia without affecting atra-induced differentiation. Cancer Res 2009; 69: 1027-36.
- Graupera et al. Angiogenesis selectively requires the p110alpha isoform of PI3K to control endothelial cell migration. Nature 2008; 453: 662-6.
- Grose et al. The role of fibroblast growth factor receptor 2b in skin homeostasis and cancer development. EMBO J 2007; 26: 1268-1278.
- Foukas et al. Critical role for the p110alpha phosphoinositide-3-OH kinase in growth and metabolic regulation. Nature 2006; 441: 366-70.
Who does the research
→ Click here for BCI senior researchers working on cell signalling.
Major Funders
- BBSRC
- Breast Cancer Campaign
- British Lung Foundation
- Cancer Research UK
- EU
- Leukaemia & Lymphoma Research
- MRC








