1982 BSc in Biochemistry, Sichuan University, P.R. China; ,1985 MSc in Cell and Molecular Biology, Cancer Institute, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, P. R. China, 1991 PhD in Cell and Molecular Biology, Imperial Cancer Research Fund and University College London, London, UK
Cancer Biology, tumour suppression, cell death, differentiation, gene suppression
Professor Xin Lu became the Director of the London Branch of the Ludwig Institute for Cancer Research in 2004 and in 2007 established LICR Oxford. She is an elected Member of the European Molecular Biology Organisation (EMBO), Honorary Fellow of the Royal College of Pathologists ((Hon), FRCPath), Fellow of the Society of Biology (FBS) and Fellow of the Academy of Medical Sciences (FMedSci). Professor Lu is actively collaborating with cancer research communities in Asia, in particular Hong Kong, Beijing and Shanghai, to study the cause of stomach, oesophageal and liver cancer and the responses to therapy.
Professor Lu’s research is focused on understanding tumour suppression and to identify molecular switches that selectively kill cancer cells. Cancer is a disease where cells grow in the wrong place at the wrong time. Regenerative medicine involves growing cells to replace the ones that were lost or damaged. Therefore, understanding molecular mechanisms that control cell growth is vital, both to stop cancer cell growth and to grow normal cells to replace the damaged ones. Professor Lu’s research team has been one of the major research groups in the world to study the regulation of the tumour suppressor function of the p53 protein whose function is lost in most human cancers. The majority of nuclear import pathways are mediated by importin-cargo interactions. Yet around 50% of all nuclear proteins do not use this pathway. Through a detailed understanding of the regulation of the ASPP proteins, Professor Lu’s group has identified a code that defines RaDAR as a novel nuclear import pathway of ankyrin repeats (AR) containing proteins. AR is a structural motif found in over 250 human proteins with diverse functions. The RaDAR (RanGDP/AR) pathway is acquired by the most common familial melanoma-associated CDKN2A mutation, leading to nuclear accumulation of mutant p16ink4a. It is frequently used by AR-containing transcriptional regulators, especially those regulating NF-ĸB/p53. All these suggest the existence of an Ankyrin repeats signaling and its role in infection and cancer.
Professor Lu studied Biochemistry at Sichuan University and then Cancer Research at Peking Union Medical School in Beijing where she obtained her MSc. She received a competitive research training fellowship from WHO and moved to the UK in 1986. Professor Lu completed her PhD and postdoctoral training and established her own research group at the LICR in 1993.
Tumour heterogeneity underlies differences in cancer progression and responses to therapy and is caused by genetic and cellular heterogeneity. Cellular heterogeneity is itself caused by cellular plasticity. Over 80% of human tumours originate from epithelial cells and these cells have the unique property of cell polarity, which acts as a first line of defence against infection and a barrier against cancer cell invasion. In this session we will discuss how epithelial cell plasticity is controlled by molecular switches operating at levels from cell polarity and cell adhesion that senses external signals such as infection to gene regulation by transcription factors and cell fate determination. We will also illustrate how single cell sequencing technology can enable us to study cellular heterogeneity in vivo in human tissues.