Joshua Saldivar, Ph.D.

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

Biography

We study how challenges that arise during DNA replication promote tumorigenesis, particularly in lung and prostate cancer. We are interested in how replication stress alters the epigenetic landscape of pre-malignant cells and links oncogene activation to epigenetic reprogramming. 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 use diverse approaches and ex vivo models, including genetically-engineered organoids derived from primary cells, and advanced microscopy platforms to model and study epigenetic instability and lineage plasticity at the onset of tumorigenesis.

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

  • 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)

Honors and awards

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

Memberships and associations

  • American Association for Cancer Research

Areas of interest

  • Genome instability, DNA replication stress, epigenetic plasticity, cell cycle control, lung cancer, prostate cancer

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

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