- Investigator, Genetics Branch
Dr. Caplen was awarded her Ph.D. from the University of London (Kings College Hospital Medical School) for studies on the genetics of type I diabetes and its complications. Dr. Caplen's Postdoctoral training began at St Mary's Hospital Medical School, Imperial College, where she focused on the development of gene therapy approaches for cystic fibrosis (CF) during which she was involved in some of the first pre-clinical and clinical studies of cationic lipid mediated gene therapy for CF. In 1996, Dr. Caplen came to the National Human Genome Research Institute (NHGRI) at NIH as a Visiting Fellow, where she initially conducted studies investigating hybrid viral vector systems for the delivery of genes. It was while at NHGRI that Dr. Caplen developed a research interest in the newly identified gene silencing mechanism, RNA interference (RNAi) leading to her studies that help establish the presence of RNAi in mammalian cells. Dr. Caplen joined CCR, NCI in 2004 as a Senior Scientist, where she pioneered approaches for exploiting RNAi to investigate cancer biology and treatment and helped establish a trans-NIH facility for genome-wide RNAi screening. Dr. Caplen was appointed a Tenure-Track Investigator in CCR’s Genetics Branch in January 2016. Her current research focuses on using functional genetic methods to interrogate specific aspects of the genetic, transcriptional, and signaling alterations observed in cancers driven by fusion oncogenes.
- (2020). Cancer biology functional genomics: From small RNAs to big dreams. MOLECULAR CARCINOGENESIS.
- (2020). CDK9 Blockade Exploits Context-dependent Transcriptional Changes to Improve Activity and Limit Toxicity of Mithramycin for Ewing Sarcoma. MOLECULAR CANCER THERAPEUTICS. 19(5), 1183-1196.
- (2019). Fusion transcripts: Unexploited vulnerabilities in cancer?. Wiley Interdisciplinary Reviews-RNA.
- (2019). HNRNPH1-dependent splicing of a fusion oncogene reveals a targetable RNA G-quadruplex interaction. RNA. 25(12), 1731-1750.
- (2019). MAP kinase and autophagy pathways cooperate to maintain RAS mutant cancer cell survival. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 116(10), 4508-4517.
- (2018). EWS-FLI1 reprograms the metabolism of Ewing sarcoma cells via positive regulation of glutamine import and serine-glycine biosynthesis. MOLECULAR CARCINOGENESIS. 57(10), 1342-1357.
- (2017). BRD4 facilitates DNA damage response and represses CBX5/Heterochromatin protein 1 (HP1). 8(31), 51402-51415.
- (2016). Functional Genomic Screening Reveals Splicing of the EWS-FLI1 Fusion Transcript as a Vulnerability in Ewing Sarcoma. Cell Reports. 14(3), 598-610.
- (2016). Identification of therapeutic targets applicable to clinical strategies in ovarian cancer. BMC CANCER. 16,
- (2015). Targeting MPS1 Enhances Radiosensitization of Human Glioblastoma by Modulating DNA Repair Proteins. MOLECULAR CANCER RESEARCH. 13(5), 852-862.