About the Editors
UK, Oxford - 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 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.
KEYWORDS: apoptosis, p53, EBV, ASPP proteins, Ankyrin repeats signaling
Italy, Rome and UK, Cambridge - Ivano Amelio is currently an AIRC Start-Up Group Leader at the TOR Centre of Excellence of the University of Rome “Tor Vergata” (Italy) and an Assistant Professor in the School of Life Sciences at the University of Nottingham (UK). His work aims to understand the molecular basis of tumour suppression signalling with a particular focus on the role of p53 family members, microenvironmental hypoxia and metabolic alterations.
His training started at the University of Rome Tor Vergata (Italy) where in 2011 he received the PhD in Biochemistry and Molecular Biology, elucidating a novel microRNA-mediated mechanism regulating the balance of epidermal cell proliferation/differentiation. His research activity then continued at the MRC Toxicology Unit, University of Cambridge (UK), where in 2016 he received the appointment of Senior Investigator Scientist. His major contributions include the identification of specific functions for p53 family members in cellular stress response, mediated by p73 regulation of cancer metabolism, angiogenesis, and development. More recently, he revealed a novel gain-of-function effect of p53 mutants in hypoxic tumours.
Ivano is a member of the board of directors of the European Cell Death Organisation (ECDO) and member of a number of international advisory boards. He has served as Editor-in-Chief of Cell Death Discovery since 2018 and as member of the editorial board of Cell Death & Disease and Molecular and Cellular Oncology since 2017 and 2014 respectively.
KEYWORDS: p53, DNA damage response, hypoxia, miR, skin biology
The Cell Death Discovery international Editorial Board spans the breadth of the coverage of the journal – view the full Editorial Board.