Dr Katiuscia Bianchi

PhD
Lecturer
Group Leader
Research Focus

My research aims to reveal how cancer cells evolve to proliferate and evade cell death in order to develop new therapeutic strategies, in particular for the treatment of breast cancer. I am interested in understanding the contribution of cellular metabolism to cancer cell survival and proliferation.

Key Publications

The Ripoptosome, a signaling platform that assembles in response to genotoxic stress and loss of IAPs. Mol Cell (2011) 43 (3): 432-48. PMID: 21737329

A tangled web of ubiquitin chains: breaking news in TNF-R1 signaling. Mol Cell (2009) 36(5):736-42. Review. PMID: 20005838

Chaperone-mediated coupling of endoplasmic reticulum and mitochondrial Ca2+ channels. J Cell Biol (2006) 175(6):901-11 *co-author. PMID: 17178908

Major Funding
  • 2017-2020- Barts Charity, Creating a facility for metabolic flux analysis, £497,691.00
Other Activities
  • Founder of The London Inflammation Network- Bringing together the wider community of scientists working on inflammation, an exciting opportunity for junior investigators to present their work and network.
Research

Cancer cells evolve to proliferate and evade cell death. Tumours indeed not only have an amazing ability to adapt to any kind of environment and nutrient condition, but they can actually re-program themselves to take advantage of any situation to grow and proliferate.

I hope to reveal how cancer cells can achieve this sheltered status in order to develop new therapeutic strategies, in particular for the treatment of breast cancer. Specifically, I am interested in understanding the contribution of cellular metabolism to cancer cell survival and proliferation.

The vast majority of tumours rely on a switch in metabolism towards anaerobic glycolysis to produce enough building blocks for their growth and successive divisions. Anaerobic glycolysis is a metabolic choice of diverting substrates away from the mitochondria despite the presence of oxygen, to allow the biosynthesis of all the components required for growth starting from glycolytic metabolic intermediates.

Another central aspect of cancer cell biology that I am investigating is inflammation driven malignant transformation. Cancer and inflammation have a close, complex relationship; my research aims to investigate whether inflammation can rewire cellular metabolism, causing malignant transformation.

The final scope of this line of my research is to design better combination therapy to limit inflammation driven malignant transformation, possibly combining anti-inflammatory drugs with drugs targeting different metabolic pathways.

Major Funding
  • 2017-2020- Barts Charity, Creating a facility for metabolic flux analysis, £497,691.00
  • 2016-2018- CRUK Pioneer Award, Reducing intracellular concentration of serine for the treatment of cancer, £188,000
  • 2014-2017- Barts Charity, Exploiting novel links between inflammation and cellular metabolism to prevent tumorigenesis and tumour development, £252,017.00

Recent Publications

The unconventional myosin CRINKLED and its mammalian orthologue MYO7A regulate caspases in their signalling roles. Orme MH, Liccardi G, Moderau N et al. Nat Commun (2016) 7(2) 10972
https://www.ncbi.nlm.nih.gov/pubmed/26960254

Aerobic glycolysis: beyond proliferation. Jones W, Bianchi K Front Immunol (2015) 6(2) 227
https://www.ncbi.nlm.nih.gov/pubmed/26029212

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015. Galluzzi L, Bravo-San Pedro JM, Vitale I et al. Cell Death Differ (2015) 22(2) 58-73
https://www.ncbi.nlm.nih.gov/pubmed/25236395

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015 Galluzzi L, Bravo-San Pedro JM, Vitale I et al. Cell Death and Differentiation (2014) (7)

Ubiquitin-mediated regulation of RhoGTPase signalling: IAPs and HACE1 enter the fray. Orme M, Bianchi K, Meier P EMBO J (2012) 31(2) 1-2
https://www.ncbi.nlm.nih.gov/pubmed/22215447

The Ripoptosome, a Signaling Platform that Assembles in Response to Genotoxic Stress and Loss of IAPs Tenev T, Bianchi K, Darding M et al. Molecular Cell (2011) 43(7) 689

The Ripoptosome, a signaling platform that assembles in response to genotoxic stress and loss of IAPs. Tenev T, Bianchi K, Darding M et al. Mol Cell (2011) 43(2) 432-448
https://www.ncbi.nlm.nih.gov/pubmed/21737329

Molecular determinants of Smac mimetic induced degradation of cIAP1 and cIAP2. Darding M, Feltham R, Tenev T et al. Cell Death Differ (2011) 18(2) 1376-1386
https://www.ncbi.nlm.nih.gov/pubmed/21331077

Synchronous intra-Golgi transport induces the release of Ca2+ from the Golgi apparatus Micaroni M, Perinetti G, Di Giandomenico D et al. Experimental Cell Research (2010) 316(7) 2071-2086

A tangled web of ubiquitin chains: breaking news in TNF-R1 signaling. Bianchi K, Meier P Mol Cell (2009) 36(2) 736-742
https://www.ncbi.nlm.nih.gov/pubmed/20005838

For additional publications, please click here
Team

Postdoctoral Researchers
Dr Ruoyan Xu

PhD Students
Mr William Jones

Biography

I obtained my PhD in Molecular Medicine (2006) in Ferrara, Italy, studying the role of mitochondrial signalling and metabolism in different pathophysiological conditions, under the supervision of Prof. Rosario Rizzuto. I then moved for a short postdoctoral period to the INSERM in Paris, to study the role of the mitochondria in hepatocellular tumour formation.

In 2007 I obtained a FEBS long-term postdoctoral fellowship to join the apoptosis laboratory at the Institute of Cancer Research, London, led by Prof. Pascal Meier. During my post-doctoral training, I focused on the family of protein IAPs (Inhibitor of Apoptosis) and their role in inflammation and cancer. As their name suggests, this family of proteins has a strong anti-apoptotic role and we studied their role in chemotherapy-induced death of cancer cells. Thus we identified the Ripoptosome, a newly described protein complex, which plays a crucial role in cell death induction, both via apoptosis and necroptosis.