Paul Andreassen completed his PhD in Experimental Pathology from the University of Washington (Seattle, WA) while working at the Fred Hutchinson Cancer Research Center (Seattle) and the Institut de Biologie Structurale (Grenoble, France). Dr. Andreassen then completed a research fellowship at the Dana-Farber Cancer Institute (Boston, MA) before moving to Cincinnati Children’s Hospital Medical Center in 2004.
BS: Willamette University, Salem, Oregon, 1984.
PhD: University of Washington, Seattle, Washington, 1995.
Fanconi anemia; breast cancer susceptibility; genetic variants; genome instability; DNA damage responses; replication stress; relationship of DNA repair and chromatin; mitosis; radiation biology; cell biology
Experimental Hematology and Cancer Biology, Cancer and Blood Diseases
Identification of new RAD51D-regulating microRNAs that also emerge as potent inhibitors of the Fanconi anemia/homologous recombination pathways. Human Molecular Genetics. 2022; 31:4241-4254.
Active DNA damage response signaling initiates and maintains meiotic sex chromosome inactivation. Nature Communications. 2022; 13:7212.
Head and Neck Cancer Susceptibility and Metabolism in Fanconi Anemia. Cancers. 2022; 14.
Meiotic sex chromosome inactivation and the XY body: a phase separation hypothesis. Cellular and Molecular Life Sciences. 2022; 79:18.
RNF8 is not required for histone-to-protamine exchange in spermiogenesis†. Biology of Reproduction. 2021; 105:1154-1159.
The Initiation of Meiotic Sex Chromosome Inactivation Sequesters DNA Damage Signaling from Autosomes in Mouse Spermatogenesis. Current Biology. 2020; 30:408-420.e5.
NF1 patient missense variants predict a role for ATM in modifying neurofibroma initiation. Acta Neuropathologica. 2020; 139:157-174.
CRISPR-Cas9 fusion to dominant-negative 53BP1 enhances HDR and inhibits NHEJ specifically at Cas9 target sites. Nature Communications. 2019; 10:2866.