Joshua Saldivar, Ph.D.

  • Assistant Professor of Division of Oncological Sciences, School of Medicine
  • Assistant Professor, CEDAR, OHSU Knight Cancer Institute, School of Medicine

Biography

Our group studies how nuclear processes such as DNA replication, transcription, and repair are coordinated during the cell cycle. We integrate powerful microscopy approaches with cutting-edge sequencing technologies to uncover the elegant and dynamic biology of chromatin and how it both controls and is controlled by the cell cycle. These dynamics become disrupted in cancer and destabilize genetic and epigenetic information resulting in cell lineage instability and malignant transformation.

We have a particular interest in the ATR (ataxia telangiectasia and Rad3-related) pathway (Saldivar et al., 2017), which signals the cellular response to replication stress and replication – transcription conflicts (Hamperl et al., 2017) and controls key cell cycle checkpoints (Saldivar et al., 2018).

We are looking for talented graduate students and postdocs to join our group. Email me at saldivaj@ohsu.edu for more information.

Saldivar JC, Cortez D, Cimprich KA. The essential kinase ATR: ensuring faithful duplication of a challenging genome. Nat Rev Mol Cell Biol. 2017; 18(10):622-36.

Hamperl S, Bocek MJ, Saldivar JC, Swigut T, Cimprich KA. Transcription-replication conflict orientation modulates R-loop levels and activates distinct DNA damage responses. Cell. 2017; 170(4):774-86. 

Saldivar JC, Hamperl S, Bocek MJ, Chung M, Bass TE, Cisneros-Soberanis F, Samejima K, Xie L, Paulson JR, Earnshaw WC, Cortez D, Meyer T, Cimprich KA. An intrinsic S/G2 checkpoint enforced by ATR. Science. 2018; 361(6404):806-10.

MyBibliography: https://www.ncbi.nlm.nih.gov/myncbi/1n9DnlZAnu75C/bibliography/public/

Education and training

  • Degrees

    • B.S., 2005, University of Arkansas
    • M.S., 2007, University of Arkansas
    • Ph.D., 2013, Ohio State University

  • Fellowship

    • Postdoctoral Fellow, Stanford University School of Medicine (2013-2018)
    • American Cancer Society Postdoctoral Fellowship (2016-2018)

Memberships and associations:

  • American Association for Cancer Research
  • American Society for Biochemistry and Molecular Biology

Areas of interest

  • Epigenomic instability, DNA replication stress, transcription regulation, nuclear bodies

Honors and awards

  • Postdoctoral Enrichment Award, Burroughs Wellcome Fund (2014-2018)

Publications

Selected publications

  • Saldivar JC, Hamperl S, Bocek MJ, Chung M, Bass TE, Cisneros-Soberanis F, Samejima K, Xie L, Paulson JR, Earnshaw WC, Cortez D, Meyer T, Cimprich KA. An intrinsic S/G2 checkpoint enforced by ATR. Science. 2018; 361(6404):806-810.
  • Saldivar JC and Cimprich KA. A new mitotic activity comes into focus. Science. 2018; 359(6371):30-31.
  • Saldivar JC, and Park D. Mechanisms shaping the mutational landscape of the FRA3B/FHIT-deficient cancer genome. Genes Chromosomes Cancer. 2019; 58(5):317-323.
  • Saldivar JC, Cortez D, Cimprich KA. The essential kinase ATR: ensuring faithful duplication of a challenging genome. Nature Rev. Mol. Cell Biol. 2017; 18(10):622-36.
  • Hamperl S, Bocek MJ, Saldivar JC, Swigut T, Cimprich KA. Transcription-replication conflict orientation modulates R-loop levels and activates distinct DNA damage responses. Cell. 2017; 170(4):774-86.
  • Waters CE, Saldivar JC, Amin ZA, Schrock MS, Huebner K. FHIT loss-induced DNA damage creates optimal APOBEC substrates: Insights into APOBEC-mediated mutagenesis. Oncotarget. 2015; 6(5):3409-19.
  • Saldivar JC, Miuma S, Bene J, Hosseini SA, Shibata H, Sun J, Wheeler LJ, Mathews CK, Huebner K. Initiation of genome instability and preneoplastic processes through loss of Fhit expression. PLoS Genetics. 2012; 8(11):e1003077.

Publications