Vishva Dixit has conducted pioneering studies defining key components of the cell death pathway. His laboratory was among the first to: (i) show that caspases are components of the death receptor-induced apoptotic pathway; demonstrate that death receptors signal by an entirely novel mechanism of recruiting and activating a death protease (FLICE/caspase-8) by an induced proximity mechanism; (ii) identify the mammalian death protease equivalent to the CED3 protein in worms (YAMA/caspase-3) as well as other pro-apoptotic caspases including caspase-6, -7 and -9; (iii) show that the death domain-containing molecule MyD88 is a key signaling adaptor; (iv) discover paracaspases and metacaspases: two ancient families of caspase-related proteins, one of which plays a key role in MALT lymphoma; (v) discover the non-canonical inflammasome pathway. Vishva is currently Vice President of Research, runs an active research laboratory, and has published well over a hundred scientific articles. He also has a significant number of patents to his name. He is a Foreign Member, European Molecular Biology Organization, a member of the Institute of Medicine, the American Academy of Arts and Sciences and the National Academy of Sciences.
Professor Karen Vousden is the Director of the Cancer Research UK Beatson Institute in Glasgow. The Beatson Institute carries out a program of world-class science directed at understanding key aspects of cancer cell behavior, and provides a state of the art facility where basic and clinical scientists can work together to translate these discoveries into new therapies and diagnostic/prognostic tools to help cancer patients. Karen’s own research focuses on the regulation and function of the tumour suppressor protein p53. Karen received her Ph.D. in Genetics from the University of London, followed by postdoctoral fellowships with Chris Marshall at the Institute of Cancer Research in London and Douglas Lowy at the National Cancer Institute in the USA. After joining the Ludwig Institute for Cancer Research in London moved back to the NCI in 1995 where she was Chief of the Regulation of Cell Growth Laboratory, before taking up her current position in 2002. Karen has been elected to the Royal Society, the Royal Society of Edinburgh, EMBO, the Academy of Medical Sciences and the European Academy of Sciences, and received honorary DScs from the Universities of London and Strathclyde. She was awarded the Tenovus Gold Medal in 1998, the Sir Frederick Gowland Hopkins Medal in 2008, the Royal Medal from the Royal Society of Edinburgh in 2009 and was honoured as Commander of the British Empire in 2010. She is presently on the Board of Directors of the AACR
Martin Bushell completed his Ph.D. under Dr S. Morley (1996-1999) and first short post-doc under Prof. Mike Clemens (1999-2001) examining the mechanisms by which translation is inhibited during the induction of apoptosis. With a Wellcome Trust International Travelling Fellowship (2001-2005) he spent two years at Stanford University (USA) under Prof. P. Sarnow (the final year was located at University of Leicester with Prof. Willis). He investigated cDNA micro-array analysis of mRNAs that are polysomally associated during apoptosis and successfully identified 200 mRNAs that are co-ordinately regulated during this process and the mechanisms by which these mRNAs are selected for translation. Following a BBSRC David Phillips Fellowship, he was made an associate professor at University of Nottingham (2005-2010) to study the control of translation during apoptosis. Interestingly, his group found that all of the mRNAs translationally up-regulated during the induction of apoptosis possessed potential microRNA (miRNA) binding sites within their 3`UTR which led to investigating how miRNAs regulate gene expression. He is now at the MRC Toxicology Unit in Leicester (2010-present) and holds an MRC non-clinical senior fellowship, a program leader position within the Unit and a Readership within the University of Leicester. He is currently investigating how microRNAs and translations are involved in the response to toxic insults, including poor maternal diet and neuronal cell death. His group has determined the basic underlying mechanisms by which microRNAs control gene expression involving eIF4A2, inhibiting the scanning of the ribosome.
Dr Michaela Frye is a Principal Investigator at the Department of Genetics, Wellcome Trust MRC Cambridge Stem Cell Institute, University of Cambridge. Her scientific focus is dedicated to stem cells that are established during development and remain present in adulthood allowing the body to replace, restore and regenerate dead, damaged or diseased cells. Stem cells continuously maintain their population (self-renewal) while generating progeny (differentiation). During self-renewal stem cells have to avoid cell cycle exit and differentiation; whereas during differentiation stem cells must evade uncontrolled proliferation. Dissecting the regulatory pathways controlling the balance between these two states is fundamental to understanding how stem cell mis-regulation causes human diseases. Dr Frye explores whether modulation of RNA-methylation pathways can help to protect from human diseases such as cancer.
Doug Green is the Peter C. Doherty Endowed Chair of Immunology at St Jude Children’s Research Hospital. Prior to this he was Head of the Division of Cellular Immunology at the La Jolla Institute for Allergy and Immunology. Professor Green received his PhD from Yale University. His research has focused on the process of active cell death and cell survival. His research extends from the role of cell death in the regulation of cancer and immune responses in the whole organism to the fundamental molecular events directing the death of the cell. He has published over 450 papers, chapters, and books, and is an ISI “highly cited” investigator. His recent book is “Means to an End: Apoptosis and Other Cell Death Mechanisms,” published in 2011 by Cold Spring Harbor Laboratory Press and available at Amazon.
Sharad Kumar is the co-Director of the Centre for Cancer Biology, a Research Professor and Chair of Cancer Biology at the University of South Australia, and an affiliate Professor at the University of Adelaide. His laboratory discovered a number of key genes/proteins, including the developmentally regulated Nedd genes, such as Nedd1, a key centrosomal protein required for y-tubulin recruitment; Nedd2 (caspase-2), one of the first mammalian caspases; Nedd4, the first and the founding member of the WW-HECT type of ubiquitin-protein ligase family; Nedd5 (Sept2), the first characterised mammalian septin; and Nedd8, a ubiquitin-like protein involved in a protein modification pathway, now widely known as neddylation. The laboratory also discovered a large part of the Drosophila cell death machinery, including four caspases and both Bcl-2-like proteins, and defined a caspase-independent, autophagy-depended cell death process. Other discoveries from his group include Ndfips as regulators of the Nedd4 family of ubiquitin ligases, the functions of Nedd4 family of ubiquitin ligases and Ndfips in regulating ion channels and transporters, and an unexpected role of caspase-2 as a tumour suppressor. His group continues to study caspase biology and functions, mechanisms of developmentally programmed cell death, and the physiological functions and regulation of the Nedd4 family members. He is a Fellow of the Australian Academy of Science and 2013 ASBMB Lemberg Medallist. His work has also been recognised through the 2003 ASBMB Amersham Biosciences Award, the 2009 Ranbaxy Research Award and the 2013 FAOBMB Research Excellence Award.
The Lowe laboratory is interested in understanding how the genetic alterations in cancer cells contribute to tumorigenesis, alter treatment response, and create vulnerabilities that may be targeted therapeutically. To facilitate our research, we are combining genetic and genomic tools that enable us to explore various aspects of cancer biology in a comprehensive way. We have recently developed mouse cancer models based on the genetic manipulation of stem and progenitor cells ex vivo followed by transplantation of the altered cells into the appropriate organ of syngeneic recipient mice. This approach allows us to study the impact of many genes and gene combinations on tumorigenesis in a “mosaic” setting where tumor-initiating cells are embedded in normal tissues. Furthermore, we have developed powerful new transgenesis methods for using RNAi to suppress gene function in vivo in either a stable or reversible manner. Current efforts strive to integrate mosaic mouse models, RNA interference, and genomics to identify new components of these networks and characterize their impact on tumorigenesis and treatment response. In addition, we are developing new RNAi methods to explore the role of tumor suppressor genes in tumor maintenance, and cell death mechanisms involved in tumor regression.
Professor Xin Lu studied Biochemistry at Sichuan University and then Cancer Research at Peking Union Medical School in Beijing. She was awarded an IARC WHO fellowship to come to the Imperial Cancer Research Fund in London in 1986 and studied for her PhD under Birgit Lane. In 1993 she joined the Ludwig Institute for Cancer Research (LICR), St. Mary’s Branch, Imperial College as an Assistant Member and was progressively promoted to LICR Full Member and Professor at Imperial College in 2000. In 2004, she was appointed as the Director of the LICR’s UCL Branch but moved the unit to Oxford in 2007. She is an elected Member of EMBO and Fellow of the Academy of Medical Sciences.
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 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.
Tak W. Mak is the Director of the Campbell Family Institute for Breast Cancer Research at the Princess Margaret Cancer Centre, and a University Professor in the Departments of Medical Biophysics and Immunology at the University of Toronto. Dr. Mak received his B.Sc. and M.Sc. degrees from the University of Wisconsin (Madison) and his Ph.D. degree from the University of Alberta. His postdoctoral work was performed at the Ontario Cancer Institute under the supervision of Dr. Ernest McCulloch. Dr. Mak’s research interests center on immune cell recognition/regulation, molecular mechanisms underlying the survival and death of normal or malignant cells, as well as the role of inflammation in the progression of autoimmune disease and cancer. He is best known as the lead scientist of the group that first cloned the genes of the human T cell antigen receptor, a discovery that provided essential insights into the molecular basis of cellular immunity. In addition, Dr. Mak has devoted a large portion of his research to investigating the pathogenesis of cancer. In particular, he is interested in mechanisms of metabolic transformation in order to identify potential targets for novel cancer therapeutics. Dr. Mak has published over 800 peer-reviewed research papers and holds many patents. His many accomplishments have been recognized by the scientific community through numerous prestigious awards and honours, such as the, Emil von Behring Prize, Gairdner International Award, King Faisal International Prize for Medicine, Sloan Prize, and Novartis Immunology Prize. He is a Fellow of the Royal Society of London, a Foreign Associate of the National Academy of Sciences (USA), an Officer of the Orders of Ontario and Canada and a Fellow of American Association for Cancer Research Academy (USA).
Professor Owen Sansom, FRSE, FMedSci is the Director of the Cancer Research UK Beatson Institute
Colorectal cancer is the third most common cancer in the UK and the second most common cause of cancer mortality. The focus of Professor Sansom’s group is to understand the early changes associated with intestinal neoplasia in order to identify novel markers of the disease as well as new targets for therapy. The key intestinal tumour suppressor is the APC gene that is mutated in approximately 80% of sporadic cancers. Central to our work is the use of novel inducible models of intestinal tumourigenesis that allow us to study the functions of specific tumour suppressor genes.
María S. Soengas embarked upon her scientific career first as an undergraduate student at the Universidad de La Coruña and later at the Universidad Autónoma de Madrid, where she graduated in Molecular Biology. There she received her PhD with First Class Honours for her studies on molecular mechanisms of DNA replication at the laboratory of M. Salas, Centro de Biología Molecular “Severo Ochoa”. In 1997 Soengas moved to the S. Lowe´s group at the Cold Spring Harbor Laboratory, New York (USA), where she assessed the role of apoptosis as a tumour suppressor mechanism, with special focus on melanoma. She then joined the Department of Dermatology at the University of Michigan in 2002 to develop a basic research programme in Melanoma. Her group defined new molecular mechanisms underlying human melanoma initiation, progression and chemoresistance. Since 2008, Soengas leads the Melanoma Group at the CNIO. The main objective of her team is to translate basic research in melanoma to the clinic by identifying novel markers of this disease and targets for drug development. Soengas has been recipient of fellowships and awards from both the Human Frontiers in Science Programme and the Leukemia and Lymphoma Society of America. She has also received a Life Science Biomedical Scholar Award from the University of Michigan, the Diana Ashby Young Investigator Award from the Society for Melanoma Research as well as Career Development Awards from the American Dermatology Foundation, the Elsa V. Pardee Foundation and the V Foundation for Cancer Research. She has also been honoured with the Premio M. Josefa Wonenburger from the Xunta de Galicia.
Brigitta Stockinger, FMedSci, FRS, is a molecular immunologist in the Francis Crick Institute London. Following a PhD in Biology at the University of Mainz, she worked at the Basel Institute for Immunology (Member) as well as in the Division of Molecular Immunology, MRC National Institute for Medical Research (Head) before joining the Crick. She was elected a member of EMBO in 2008 and Fellow of the Royal Society in 2013 for understanding the regulation and maintenance of peripheral T cell immune responses. She defined the mechanisms underlying the differentiation of Th17 cells and demonstrated substantial pasticity in TH17 cell function depending on the inflammatory environment. Stockinger identified the Aryl hydrocarbon receptor (AhR) as connector between the immune system and environmental stimuli, showing that it shapes the functional differentiation of Th17 effector cells. The AhR links their role in host defence as well as their role in autoimmunity to environmental factors. Research into the physiological roles of AhR in the immune system and in toxicology provides a major cue also in cancer research.
Following his 1995 PhD at the Imperial Cancer Research Fund, UK (Cancer Research UK since 2002), Dr Swanton became Member of the Royal College of Physicians in 2002 and in 2004 established his own laboratory at the London Research Institute, Cancer Research UK. Since 2015 he is Group Leader at the Francis Crick Institute, London, UK. The Swanton laboratory focuses on mechanisms generating cancer genetic diversity and its consequences on clinical outcome. Through next generation sequencing studies, he has demonstrated that the principles of Darwinian evolution apply to the growth and adaptation of human tumours. In fact, he has demonstrated that intratumour heterogeneity, through tumour sampling bias, impacts upon our ability to successfully qualify cancer biomarkers for clinical use. Based on his findings on DNA replication stress, genome doubling events and the APOBEC mutational process, he investigates intratumour heterogeneity and accelerated cancer evolution (TRACERx study, the DARWIN trial, Deciphering Anti tumour Response With INtratumour heterogeneity) with a specific focus on non-small cell lung cancer, in order to develop deeper scientific insight for patient benefit.
Ashok is the Ursula Zoellner Professor of Cancer Research at the University of Cambridge, and the Director of the Medical Research Council (MRC) Cancer Unit. He trained in medicine at the Christian Medical College, Vellore, India, before completing his PhD at University College London. Ashok was a faculty member at the Medical Research Council’s Laboratory of Molecular Biology in Cambridge, before appointment to the Zoellner Professorship in 1998. Ashok is widely recognized for his contributions to understanding the genetics and biology of cancer, particularly in elucidating the impact of genome instability on carcinogenesis and cancer therapy. His research has not only illuminated the fundamental mechanisms governing genome repair, replication and segregation during cell division, but has also provided insight into their connections with cancer pathogenesis and treatment. Translation of these insights to clinical practice is a major focus in Ashok’s current work. He has been instrumental in establishing initiatives that link chemists, physicists, structural biologists, cancer biologists and clinicians in Cambridge and elsewhere, with the aim to pioneer innovative new approaches for the discovery and early clinical development of next-generation medicines. Ashok was elected a Fellow of the Academy of Medical Sciences, London, in 2001 and a Member of the EMBO European academy, Heidelberg, in 2004.
Professor Anne Willis obtained a BSc in Biochemistry from the University of Kent (1984). She holds a PhD in Biochemistry (1987) from University of London (Imperial College). Her PhD was carried out in the CRUK laboratories at Clare Hall. She then worked in the University of Cambridge, Department of Biochemistry (1988-1992) and held a Junior Research Fellowship (1988-1992) and a College Lectureship (1991-1992) at Churchill College Cambridge. She moved to the University of Leicester in 1992 to take up a Lectureship (1992-2000), Readership (2002-2004) and Chair (2004) in the department of Biochemistry. She was also awarded a BBSRC Advanced Fellowship during this period (2000-2005). She moved to the University of Nottingham as Professor of Cancer Cell Biology in 2004 and was appointed BBSRC Professorial Fellow (2008-2013). Her laboratory is interested in post-transcriptional control of gene expression, particularly translational control, and how this process adapts to allow cell recovery following exposure to agents that induce stress.