**About the Editors**

**Angela C. Hirbe** is a graduate of the Washington University M.D. Ph.D. program and completed her residency in Internal Medicine and fellowship in Oncology as part of the Physician Scientist Training Program. She has had a longstanding interest in neurofibromatosis research; her post-doctoral work was performed in the laboratory of Dr. David Gutmann, where she used next-generation sequencing technologies to identify beta-III spectrin as a protein involved in malignant peripheral nerve sheath tumor (MPNST) pathogenesis and developed a mouse model for this deadly type of sarcoma. This work transitioned into her own lab when she joined the faculty at Washington University.

Dr. Hirbe is currently an Assistant Professor in the Division of Medical Oncology in the Departments of Medicine and Pediatrics at Washington University in St. Louis. Her laboratory continues to use genomics to identify drivers in MPNST pathogenesis that can be exploited as diagnostic biomarkers or therapeutic targets.

Clinically, Dr. Hirbe is a member of the sarcoma section and part of the Adolescent Young Adult Cancer Program and the Neurofibromatosis Center at Washington University. Her clinical practice is geared at caring for patients with cancer predisposition syndromes such as neurofibromatosis type 1 and Li–Fraumeni syndrome as well as treating patients with any type of sarcoma. She has particular expertise in the care of patients with MPNST.

**Christine A. Pratilas** is Director of the Pediatric Sarcoma Program at the Sidney Kimmel Comprehensive Cancer Center and Associate Professor of Oncology and Pediatrics at the Johns Hopkins University School of Medicine. She joined the Hopkins pediatric sarcoma and solid tumor team in 2014, after completing her fellowship and spending the early years of her career at Memorial Sloan Kettering Cancer Center.

During her years at MSKCC, Dr. Pratilas focused her research on signal transduction, the molecular events that both activate and negatively regulate cancer cell signaling pathways. This knowledge helps to determine how to best deploy novel targeted therapies and to predict how resistance to these agents may emerge over time. One of her most important contributions to date has been advancing our understanding of the molecular alterations in a protein called BRAF, how RAF inhibitors work to inhibit cancer cell growth, and how cancer cellular networks adapt to RAF and MEK inhibitors.

Her current laboratory research focuses on deregulated ERK signaling in solid tumors, including pediatric sarcomas. ERK signaling output is activated in many human tumors, including those with BRAF and RAS mutations and those with loss of NF1. Several pediatric solid tumors express these mutations, including a subset of rhabdomyosarcoma, neuroblastoma, and MPNST. Her lab is investigating whether MEK inhibition can effectively inhibit ERK output in pediatric sarcomas with activation of ERK signaling. A primary focus is to determine the biochemical and adaptive signaling response to MEK inhibition and other targeted therapies, to identify mechanisms by which tumors with loss of NF1 or mutations in RAS can evade MEK inhibition, and to identify targets for more effective and combination therapy.

Dr. Pratilas' clinical expertise is in the managemen<sup>t</sup> of children, adolescents, and young adults with all sarcomas, and specifically rhabdomyosarcoma and MPNST. In addition, she sees children with melanocytic neoplasms and melanoma and children with NF1-associated non-CNS neoplasms

and other rare pediatric cancers. She has a strong interest in pediatric cancer genetics and, together with the Clinical Genetics Service and the Comprehensive Neurofibromatosis Center at Johns Hopkins, provides care for children with Li–Fraumeni syndrome, neurofibromatosis type 1 (NF1), RAS-opathies, and other cancer predisposition syndromes.

**Rebecca D. Dodd** is an Assistant Professor of Internal Medicine in Hematology/Oncology and Bone Marrow Transplantation at the University of Iowa Holden Comprehensive Cancer Center. Dr. Dodd completed her Ph.D. and post-doctoral fellowship at Duke University, where she focused on sarcoma metastasis and MPNST biology.

Dr. Dodd's lab uses powerful in vivo model systems to address complex questions in cancer biology. Her research program uses CRISPR/Cap and Cre-loxP technology for translational oncology research. Over the past decade, her group has built new mouse models of MPNST to investigate events that are difficult to study in patient populations. These models include new approaches for in vivo modeling of cancer, including novel somatic CRISPR/Cas9-based tumorigenesis tools to generate MPNSTs in wild-type adult mice. Other areas of interest include (1) epigenetically targeted therapies, (2) novel gene-editing tools, and (3) the tumor microenvironment.
