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Sonia Franco, M.D., Ph.D.
Associate Professor of Radiation Oncology and Molecular Radiation Sciences
Research Interests: Radiobiology; Immunodeficiency; Mouse genetics; DNA repair
Dr. Sonia Franco is an assistant professor of radiation oncology and molecular radiation sciences and oncology at the Johns Hopkins University School of Medicine. Her areas of expertise include DNA repair, mouse genetics, immunodeficiency and radiobiology.
Dr. Franco earned her M.D. and Ph.D. in molecular biology and genetics from Autonoma University in Madrid, Spain. She completed her residency in pediatrics at University of Chicago and performed fellowships in pediatric hematology and oncology at Memorial Sloan-Kettering Cancer Center and a postdoctoral research fellowship at Harvard University.
Her research focuses on the use of mouse models to identify the cellular factors and pathway that repair DNA damage. She is interested in understanding how these factors interact at sites of DNA damage to suppress tumor development. She also aims at defining novel targets for future individualized cancer therapies.
- Associate Professor of Radiation Oncology and Molecular Radiation Sciences
- Associate Professor of Oncology
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Centers & Institutes
Research & Publications
Dr. Franco’s research objectives focus on the use of mouse models to identify the cellular factors and pathway that repair DNA damage. She and her team have an interest in understanding how these factors interact at sites of DNA damage to suppress tumor development. Their work also aims at defining novel targets for future individualized cancer therapies.
The goal of Dr. Franco’s lab is to define the cellular pathways used by mammalian cells to maintain genomic integrity. She and her team use mouse models to understand how DNA double-strand breaks are detected, signaled and repaired in mammalian cells.
Using a series of knock-out and transgenic mouse models, her team defines the regulation of the DNA Damage Response (DDR) and the Nonhomologus End-Joining (NHEJ) pathway in the repair of DNA double-strand breaks in distinct cellular contexts.
- Rybanska-Spaeder I, Reynolds T, Chou J, Prakash M, Jefferson T, Huso DL, Desiderio S, Franco S. "53BP1 is limiting for nonhomologous end-joining-mediated repair in ATM-deficient cells subjected to oncogenic stress or radiation." Mol Cancer Res 11:1223-34, 2013.
- Rybanska I, Ishaq O, Chou J, Prakash M, Bakhsheshian J, Huso DL, Franco S. "PARP1 and DNA-PKcs synergize to suppress p53 mutation and telomere fusions during T lineage lymphomagenesis." Oncogene. doi:10.1038/onc.2012. 199, 2012.
- Orsburn B, Escudero B, Prakash M, Gesheva S, Liu G, Huso DL, Franco S. "Differential requirement for H2AX and 53BP1 in organismal development and genome maintenance in the absence of PARP1." Mol. Cell. Biol. 30(10):, 2010.
- Schenten D*, Kracker S*, Esposito G*, Franco S., Klein U, Murphy MM, Alt FW, Rajewsky K. "Pol zeta ablation in B cells impairs the germinal center reaction, class switch recombination, DNA break repair and genomic stability." J. Exp. Med. 206:477-490, 2009.
- Li G, Alt FW, Cheng H-L, Brush JW, Goff PH, Murphy MM, Franco S., Zhang Y, Zha S. "Lymphocyte –specific compensation for XLF/Cernunnos end-joining functions in V(D)J recombination." Mol. Cell, 205:1949-57, 2008.