Kevin B. Jones, MD

Kevin B. Jones, MD

Leader, Huntsman Cancer Institute Sarcoma Disease Center

Division Chief, Sarcoma, Department of Orthopaedics

Professor, Department of Orthopaedics and Adjunct Professor of Oncological Sciences

As an orthopaedic surgeon specialized in the care of pediatric and adult patients with sarcoma, I see first-hand the limitations and frank failures of the currently available treatment options. Not only do we fail to cure far too many young patients with sarcomas, but the long-term effects of our treatments create other major challenges to the health of the survivors in the long term.

With protected time for basic investigation, I dedicate my entire laboratory to the study of pediatric and young adult fusion oncogene-associated sarcomas. In efforts always angling toward improved targeted therapies, we use mouse genetic models of sarcomagenesis to dissect pathways of importance to initiation and progression of tumors. This work utilizes conditional activation of translocation-associated fusion oncogenes as well as manipulation of additional modifying genes directed toward improved understanding of the conditions that promote or inhibit sarcomagenesis. This work has led to generous experience with comparative genomics and epigenomics.

The simple genetic changes that drive translocation-associated sarcomas make a strong argument for cancer being defined as a transcriptional state for cells, rather than a state of accumulated mutations or genetic losses and gains. The study of the epigenetic determinants of this transcriptional state in cells that harbor very few genetic code alterations has already revealed important knowledge that pertains to more complex genome cancer types as well as to transcriptional biology more generally.

I also believe firmly in the synergy possible in collaborative team science. Such efforts are required for progress toward improved treatments for rare malignancies that can never be studied with optimal efficacy in a silo. With such collaborative work as direct goal, I have participated in and assembled teams to work on pediatric sarcomas both within my institution and internationally.

Research Statement

With 80 percent protected time for academic pursuits, and an independent laboratory at the Huntsman Cancer Institute, I focus most of my research on dissecting the genetic and epigenetic underpinnings of sarcoma initiation. Although sarcomas are rare cancers, the tissues which give rise to sarcomas when they become cancerous are the predominant tissues in the human body, the muscles, tendons, bones, vessels, fat, etc. These tissues derive from mesenchyme or mesoderm. While many organ-based cancer cells gain some characteristics of mesenchyme or mesoderm as they become malignant, turning mesenchyme itself into cancer is much more difficult. The intrinsic resistance to transformation (the process of becoming cancerous) in mesenchyme has brought particular focus to any factor capable of overcoming that resistance and forming cancers from connective tissues.Thus, sarcomas--not only in spite of, but actually because of their low frequency in the general population--have played a central role in the fundamental discoveries of cancer biology. For example, radium dial painters developing osteosarcomas led to the discovery that radiation causes cancer. Oncogenes, the tumor causing genes, were discovered by study of a virus that caused sarcomas in birds. Tumor suppressor genes, the genes that when turned off lead to cancer, were discovered because families had too many sarcomas (Even two is way too common in any one family!) We therefore pursue sarcoma biology vigorously not only because we need to generate better treatment strategies for this horrible group of cancers that impacts young people disproportionately, but also because sarcoma will likely yet teach us much more about cancer biology in general, especially its beginnings.

Kevin B. Jones, MD Profile in University of Utah Website