Professor Katia Scotlandi
Katia Scotlandi, Chief of the Experimental Oncology Lab, Istituto Ortopedico Rizzoli, Bologna, Italy
Katia Scotlandi graduated in Biomedical Science at the University of Bologna, where she received her training in experimental oncology. thanks to a fellowship from the Italian Association for Cancer Research. In 1990 she moved to the Rizzoli Orthopedic Institute, one of the most important orthopedic Institute in the world with a Dept devoted to the study and the cure of bone and soft tissue sarcomas. In 1996, she received her specialization in Clinical Pathology.
Since 2001 she served as adjunct Professor in molecular biology at the faculty of Pharmacological Science at University of Bologna.
During her training she spent several periods abroad as fellow or visiting Professor either in Europe or US ( Department of Pathology, University of Valencia (Spain), June 14-28, 2009; Hospital University Centre, INSERM, Unit 343, Nice (Prof. A. Bernard), September 17-22, 2001; The Thomas Jefferson University, Kimmel Cancer Institute (Prof. R. Baserga), June 23-26, 1999; The University of Illinois at Chicago, College of Medicine, Department of Genetics (Prof. Igor B. Roninson), April-May 1997. Research Project: Multidrug resistance and in situ RT-PCR).
She has received theTina Anselmi Award, Bologna, March 6, 2019 and the Oswald Van der Veken 2011 Award, Bruxelles, November 7, 2011 for her studies on bone tumors.
Her research work has been focused on pediatric solid tumors particularly bone sarcomas. The goal of her research activity is to contribute to the definition of biomarkers of risk and response that allow more personalized therapeutic approaches against Ewing sarcoma and osteosarcoma and to pave the way for accelerating the discovery of the most promising biologically and epigenetically-targeted drug.
Katia Scotlandi has long been committed to advancing research and scientific interest in the field of IGF and insulin system. Her scientific group has demonstrated the importance of the related signalling pathway in sarcomas, particularly in Ewing sarcoma and participated to the development of rationale strategies to inhibit the IGF1R-mediated signalling at preclinical level. She has also highlighted the role of the insulin receptor in the rapid development of resistance to antibodies targeting IGF1R. More recently, she has introduced the concept that the RNA-binding protein IGF2BP3 may regulate the cell sensitivity to anti-IGF1R agents. In addition she has contributed hard to the identification of novel biomarkers of risk and prognosis, including CCN3, as well as of new therapeutic targets for these tumors. More recently, she has developed a platform for sequencing and establishment of complex preclinical models to accelerate our understanding of bone sarcomas.
Starting from 2005, the Scotlandi’s lab has been involved in several European networks and granted projects. At national level, from 2016 to 2019, dr. Scotlandi served as Secretary of the Working Group Sarcoma inside the Italian Alliance against Cancer, the oncologic network of the Italian Ministry of Health, to coordinate preclinical research activities that will ameliorate the diagnosis of sarcomas and facilitate the harmonization of treatments.
Not less important, it is her mentoring activity inside the academia. Over the years, she followed over seventy among graduate students, post-doctoral fellows and junior faculty members, contributing to the career development of young researchers and diffusing knowledge on pediatric oncology.
On the occasion of the ICCNS-Springer Award, Professsor Katia Scotlandi will give a presentation entitled:
Ewing’s sarcoma: embracing complexity to identify new therapeutic vulnerabilities
Genome instability and mutations are key elements of cancer initiation and progression. However, non-mutational epigenetic reprogramming can also help the acquisition of the cancer hallmark. This is particularly true for pediatric tumors, which usually derive from incompletely differentiated progenitor cells that are blocked during differentiation by a genetic alteration that freeze transformed cells into a proliferative, stem-like cell state, with unlocked plastic potential. These tumors are suitable models to study critical mediators of gene-regulatory architecture involved in oncogenic and developmental programs responsible of tumor initiation and disease progression. Ewing sarcoma, an aggressive developmental pediatric tumor, is a paradigm of tumors in which malignant progression is based on non-mutational epigenetic reprograming rather than genomic instability. EwS results from a chromosomal translocation that fuses the EWSR1 gene with an ETS family member, most frequently the FLI1 gene , forming the oncogenic driver EWSR1::FLI1. EWSR::FLI1 binds to DNA. EWSR1::FLI1 reprograms the genetic landscape of EwS, affecting many key cellular processes (i.e. cell cycle, apoptosis, angiogenesis, metabolism, and cell migration) and is the oncogenic driver of this tumor. However, its presence is a necessary but not sufficient condition. Other molecules, such as CD99 and RNA binding proteins, have been demonstrated to have a crucial role in the regulation of Ewing sarcoma malignancy, offering a general vision of how tumors can be dynamically shaped. In fact, although genetically transformed, cancer cells may be actively controlled by the dynamic interactions between the microenvironment elements and nuclear elements that modify chromatin accessibility at transcription factor binding sites and enhancer-promoter interactions. The study of this dynamic interplay will help the development of novel therapeutic strategies.