Education & Certifications


  • MPH, Harvard University, Public Health Epiemiology (2021)
  • MS, Indiana University Bloomington, Business Analytics (2018)
  • MBA, Indiana University Bloomington, Business Management (2018)
  • PharmD, University of Minnesota - Twin Cities, Pharmacy (2014)
  • BA, University of Minnesota - Twin Cities, Chemistry (2011)

Stanford Advisors


  • Lu Tian, Master's Program Advisor

Current Clinical Interests


  • Clinical Pharmacy Information Systems
  • Personalized Medicine
  • Epidemiology
  • Pharmacoepidemiology

Work Experience


  • Consultant, Data Analytics and Market Access, Valuate Health Consultancy (June 1, 2021 - Present)

    Location

    Boston, MA

  • Pharmacy Informatics Specialist, Salinas Valley Memorial Healthcare System (December 2, 2019 - Present)

    Location

    Salinas, CA

  • Hospital Pharmacist, CHI St. Alexius Health Medical Center (July 1, 2014 - June 30, 2019)

    Location

    Williston, ND

All Publications


  • Mapping Structurally Defined Guanine Oxidation Products along DNA Duplexes: Influence of Local Sequence Context and Endogenous Cytosine Methylation JOURNAL OF THE AMERICAN CHEMICAL SOCIETY Ming, X., Matter, B., Song, M., Veliath, E., Shanley, R., Jones, R., Tretyakova, N. 2014; 136 (11): 4223-4235

    Abstract

    DNA oxidation by reactive oxygen species is nonrandom, potentially leading to accumulation of nucleobase damage and mutations at specific sites within the genome. We now present the first quantitative data for sequence-dependent formation of structurally defined oxidative nucleobase adducts along p53 gene-derived DNA duplexes using a novel isotope labeling-based approach. Our results reveal that local nucleobase sequence context differentially alters the yields of 2,2,4-triamino-2H-oxal-5-one (Z) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (OG) in double stranded DNA. While both lesions are overproduced within endogenously methylated (Me)CG dinucleotides and at 5' Gs in runs of several guanines, the formation of Z (but not OG) is strongly preferred at solvent-exposed guanine nucleobases at duplex ends. Targeted oxidation of (Me)CG sequences may be caused by a lowered ionization potential of guanine bases paired with (Me)C and the preferential intercalation of riboflavin photosensitizer adjacent to (Me)C:G base pairs. Importantly, some of the most frequently oxidized positions coincide with the known p53 lung cancer mutational "hotspots" at codons 245 (GGC), 248 (CGG), and 158 (CGC) respectively, supporting a possible role of oxidative degradation of DNA in the initiation of lung cancer.

    View details for DOI 10.1021/ja411636j

    View details for Web of Science ID 000333435500024

    View details for PubMedID 24571128

    View details for PubMedCentralID PMC3985951