Background and activities
My research explores the molecular mechanisms of antigen-driven lymphomagenesis.
My research carrer began when I earned a BA in Biochemistry at Portland State University in 2007. My undergraduate thesis in Dirk Iwata-Reuyl's lab dealt with enzymology and biosynthesis and was titled "NADPH-Binding in QueF, an Oxidoreductase Involved in Queuosine Biosynthesis."
After college, I worked at the Ulm University Hospital (Ulm, Germany) in Stephan Stilgenbauer's and Daniel Merten's groups in 2008-2009, researching chronic lymphocytic leukaemia. My research involved therapies that bypass p53 deficiency and NF-kB's role in oncogenesis.
Finally, I moved to NTNU to work with Hans Krokan. Here I began to work on genomic uracil and earned an MSc (2009-2011) and PhD (2011-2015) in Molecular Medicine. My MSc and PhD theses were titled, "Improved determination of genomic uracil content by high-performance liquid chromatography – tandem mass spectrometry," and, "Uracil in DNA - necessary intermediate for antibody maturation and mutagenic lesion," respectively.
My research focuses on genomic uracil, a DNA modification that is both a crucial intermediate for the body's adaptive immune response and a mutagenic lesion that can lead to cancer. During my MSc and PhD, I helped develop a method to accurately quantify genomic uracil and explored how it is both introduced and repaired in the genome.
My postdoc will focus on applying the findings of my PhD work to lymphoma patient samples to determine whether genomic uracil can be used as a biomarker in B-cell cancer development, treatment response, and/or disease progression.
Scientific, academic and artistic work
Displaying a selection of activities. See all publications in the database
- (2016) New results and ongoing research related to deaminases. 1st DeamiNET meeting . Svend Petersen-Mahrt IFOM; UFOM-Milano. 2016-11-10 - 2016-11-11.
- (2016) Genomic Uracil - Important carcinogenic mutagen but normal intermediate in adaptive immunity. The 10th International 3R (Replication, recombination and repair) Symposium, Matsue, Japan ; Matsue. 2016-11-13 - 2016-11-17.
- (2016) REGULATION OF BASE EXCISION REPAIR – CANONICAL AND NON-CANONICAL PROCESSING OF GENOMIC URACIL. 10th International Multiconference on Bioinformatics of Genome Regulation and Structure\Systems Biology . Russian Academy of Sciences, Siberian branch; Akademorodok, Novosibirsk. 2016-08-29 - 2016-09-03.
- (2016) Genomic uracil - Important carcinogenic mutagen but normal intermediate in adaptive immunity. Eurotox 2016 . Turkish Society of Toxicology.; Sivilla. 2016-09-04.
- (2016) Mitochondrial UNG1 supports class switch recombination in mouse B-cells. 10th 3R International Symposium . 10th 3R Symposium Organzing Committee; Matsue. 2016-11-13 - 2016-11-17.
- (2016) Telomere maintenance defects in mice deficient in SMUG1 uracil-DNA glycosylase. 10th 3R International Symposium . 10th 3R International Symposium Organizing Committee; Matsue. 2016-11-13 - 2016-11-17.
- (2016) UNG and SMUG1 complement each other in DNA uracil excision and DNA 5-hydroxymethyluracil originates from 5-hydroxymethylcytosine deamination in mice. 10th 3R International Symposium . 10th 3R International Symposium Organizing Committee; Matsue. 2016-11-13 - 2016-11-17.
- (2015) AID expression in B-cell lymphomas causes accumulation of genomic uracil and a distinct AID mutational signature. DNA Repair. vol. 25.
- (2015) Modulation of cell metabolic pathways and oxidative stress signaling contribute to acquired Melphalan resistance in multiple myeloma cells. PLoS ONE. vol. 10 (3).
- (2014) Expression and recruitment of uracil-DNA glycosylase are regulated by E2A during antibody diversification. Molecular Immunology. vol. 60 (1).
- (2013) A robust, sensitive assay for genomic uracil determination by LC/MS/MS reveals lower levels than previously reported. DNA Repair. vol. 12 (9).
- (2013) Genomic uracil - potent mutagen but normal intermediate in adaptive immunity. The FEBS Journal. vol. 280.
- (2013) An inverse switch in DNA base excision and strand break repair contributes to melphalan resistance in multiple myeloma cells. PLoS ONE. vol. 8 (2).