Frederic G. Barr, M.D., Ph.D.
Laboratory of Pathology
Building 10 - Magnuson CC, Room 3B55
Bethesda, MD 20892-1500
Dr. Barr's research interest is molecular genetics of cancer with a focus on recurrent chromosomal alterations in sarcomas. His research team has most recently been conducting a multidisciplinary approach to understand the biological consequences of these genetic events in rhabdomyosarcoma, a family of pediatric soft tissue cancers. Major focal points of this research program are fusions of the PAX3 or PAX7 gene with the FOXO1 (FKHR) gene to generate fusion oncoproteins, the amplification of several oncogenic loci, and genome-wide changes in DNA methylation. These studies revealed that the gene fusions result in an aberrant gene expression program that contributes to tumorigenesis. Amplification events involving known and new candidate oncogenes occur in specific gene fusion subsets and are associated with distinct clinical outcomes. Distinct DNA methylation patterns are associated with the fusion-positive and fusion-negative subtypes of rhabdomyosarcoma. Current studies are examining tumorigenic effects, functional domains, downstream targets, regulation of gene expression, and clinical applications.
Dr. Barr received his undergraduate education at Williams College, and then attended Washington University School of Medicine, where he obtained his M.D. and Ph.D. degrees. Subsequently, he received residency training in anatomic pathology at the Hospital of the University of Pennsylvania and performed postdoctoral research in the Division of Human Genetics and Molecular Biology at the Children's Hospital of Philadelphia. Before coming to the NIH, Dr. Barr was a faculty member in the Department of Pathology and Laboratory Medicine at the University of Pennsylvania School of Medicine. In addition to his research activities, Dr. Barr serves on the Steering Committee of the Soft Tissue Sarcoma Committee of the Children's Oncology Group, and is the Senior Associate Editor for the Journal of Molecular DIagnostics.
Pandey PR, Chatterjee B, Olanich ME, Khan J, Miettinen MM, Hewitt SM, Barr FG. PAX3-FOXO1 is essential for tumour initiation and maintenance but not recurrence in a human myoblast model of rhabdomyosarcoma. J Pathol. 2017;241(5):626-637.
Olanich ME, Sun W, Hewitt SM, Abdullaev Z, Pack SD, Barr FG. CDK4 Amplification Reduces Sensitivity to CDK4/6 Inhibition in Fusion-Positive Rhabdomyosarcoma. Clin Cancer Res. 2015;21(21):4947-59.
Sun W, Chatterjee B, Wang Y, Stevenson HS, Edelman DC, Meltzer PS, Barr FG. Distinct methylation profiles characterize fusion-positive and fusion-negative rhabdomyosarcoma. Mod Pathol. 2015;28(9):1214-24.
Shern JF, Chen L, Chmielecki J, Wei JS, Patidar R, Rosenberg M, Ambrogio L, Auclair D, Wang J, Song YK, Tolman C, Hurd L, Liao H, Zhang S, Bogen D, Brohl AS, Sindiri S, Catchpoole D, Badgett T, Getz G, Mora J, Anderson JR, Skapek SX, Barr FG, Meyerson M, Hawkins DS, Khan J. Comprehensive genomic analysis of rhabdomyosarcoma reveals a landscape of alterations affecting a common genetic axis in fusion-positive and fusion-negative tumors. Cancer Discov. 2014;4(2):216-31.
Skapek SX, Anderson J, Barr FG, Bridge JA, Gastier-Foster JM, Parham DM, Rudzinski ER, Triche T, Hawkins DS. PAX-FOXO1 fusion status drives unfavorable outcome for children with rhabdomyosarcoma: a children's oncology group report. Pediatr Blood Cancer. 2013;60(9):1411-7.
Related Scientific Focus Areas
Genetics and Genomics
Molecular Biology and Biochemistry
This page was last updated on September 13th, 2019