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In This Section
Dr. Felix uses molecular, biochemical, cellular and in vivo methods to investigate the pathobiology of leukemias with KMT2A (MLL) translocations. Leukemias with these translocations affect infants and young children or occur as a complication of type II topoisomerase (TOP2) poison chemotherapies used for anti-cancer treatment. She aims to develop better treatment and prevention approaches for these leukemias, which have a poor prognosis.
The pathobiology of leukemias with KMT2A (MLL) translocations is the central focus of Dr. Felix’s dynamic research program. A pioneer in panhandle polymerase chain reaction (PCR) cloning strategies as well as new high-throughput sequencing technology, Dr. Felix aims to better understand those translocations in order to develop more effective treatments and preventative strategies.
In addition, Dr. Felix and her team are investigating molecularly targeted agents to surmount cell death resistance, and are developing models in zebrafish embryos as a developmental tool to recapitulate leukemogenesis in infants.
Her KMT2A-R leukemia research program encompasses TOP2 DNA damage mechanisms, molecular epidemiology, disease biomarkers, and developmental origins of the translocations and novel treatments.
Among her career achievements, Dr. Felix:
- Invented panhandle PCR technologies to clone KMT2A genomic translocation breakpoint junctions and KMT2A fusion transcripts and, using this technology, discovered new KMT2A partner genes and traced origins of translocations
- Discovered that KMT2A translocation breakpoints are TOP2 cleavage sites in vitro and in cells
- Invented high-throughput sequencing technology to surmount key challenge of removing covalently attached DNA from TOP2 enzyme at the cleavage site in order to be able to resolve TOP2 cleavage at single base precision genome-wide in cells
- Made major discoveries with new high-throughput sequencing technology indicating that TOP2A cleavage is associated with genes involved in oncogenic translocations, and with key factors in the transcriptome and epigenome
- Discovered that targeting EIF4E with ribavirin reduces proliferation and survival, downregulates EIF4E targets and enhances chemosensitivity in infant acute lymphoblastic leukemia
Education and Training
BS, Boston College (Biology/Chemistry), 1977
MD, Boston University, 1981
Titles and Academic Titles
Leader, Normal and Malignant Hematopoiesis Research Affinity Group
Joshua Kahan Endowed Chair in Pediatric Leukemia Research
Professor of Pediatrics
Association of American Physicians, 2006-
ASPHO Young Investigator Award, 1990
ASCO Young Investigator Award, 1992
Eastern PA Chapter LLS Distinguished Leadership Award, 2000
Eagles Fly for Leukemia Award for Excellence in Treatment of Pediatric Cancer, 2006