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David Gius, MD, Radiation Oncology, San Antonio, TX

DavidRoyGiusMDMD, PhD

Radiation Oncology San Antonio, TX

Breast Cancer

Professor, Department of Radiation Oncology, Assistant Dean of Research Joe R. & Teresa Lozano Long School of Medicine, Associate Cancer Center Director The Mays Cancer Center at UT Health San Antonio

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Summary

  • The central theme of the laboratory is the potential relationship of intracellular pro-proliferative / pro-survival factors and how tumor cells respond to therapeutic modalities. The overarching goal of my research is an extension of the hypothesis that tumor cells use pre-existing pro-survival signaling pathways, up-regulated as a result of transformation or tumor micro-environment, to evade the damaging and cytotoxic effects of anti-cancer agents. These signaling factors are involved in the transmission of inter- and intracellular information through multiple transduction cascades and it has been suggested that one function is the activation of preprogrammed reparative or protective cellular processes responding to intracellular stress. Tumor cells likely activate these pathways responding to dys-regulated cell division and the increased demands on multiple cellular processes including increased replication, transcription, translation, protein trafficking and the production of metabolites (oxidative stress) that must be scavenged to prevent cell damage. Thus, we hypothesize that specific pro-repair and pro-survival pathways, alone and likely in combination, and their upstream signaling factors are potential molecular targets to improve the cytotoxic effects of anti-cancer agents including but to ionizing radiation. These challenges have led our laboratory to concentrate its efforts into the investigation of the mechanistic connection between aging, cellular and/or mitochondrial metabolism, and carcinogenesis focusing on the Sirtuin gene family and the connection between this protein family and breast carcinogenesis and breast cancer tumor cell resistance.

Education & Training

  • Washington University/B-JH/SLCH Consortium
    Washington University/B-JH/SLCH ConsortiumResidency, Radiation Oncology, 1994 - 1997
  • University of Michigan Health System
    University of Michigan Health SystemResidency, Radiation Oncology, 1993 - 1994
  • University of Chicago Medical Center
    University of Chicago Medical CenterInternship, Preliminary Year, 1992 - 1993
  • Loyola University Chicago Stritch School of Medicine
    Loyola University Chicago Stritch School of MedicineClass of 1992
  • University of Chicago
    University of ChicagoPhD, Tumor Virology, 1985 - 1990
  • University of Illinois College of Medicine
    University of Illinois College of MedicineB.S., Chemistry, 1980 - 1983

Certifications & Licensure

  • TX State Medical License
    TX State Medical License 2020 - 2025
  • IL State Medical License
    IL State Medical License 1992 - 2020
  • TN State Medical License
    TN State Medical License 2010 - 2012
  • MI State Medical License
    MI State Medical License 1993 - 1994
  • American Board of Radiology Radiation Oncology

Awards, Honors, & Recognition

  • Established Investigator Award Recruitment Award Chemo-Prevention Research Institute of Texas CPRIT, 2020
  • Alpha Omega Alpha 2014
  • Member Alpha Omega Alpha (AOA) Honor Medical Society, 2014
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Publications & Presentations

PubMed

Journal Articles

  • ATRIP Deacetylation by SIRT2 Drives ATR Checkpoint Activation by Promoting Binding to RPA-ssDNA  
    Zhang H, Li X, Daddacha W, Pan Y, Madden WZ, Park S-H, Duong DM, Xie M, Yu1 B, Warren MD, Liu EA, Deng X, Seyfried NT, Yu DS, Cell Reports, 1/1/2016
  • G Protein-Coupled Bile Acid Receptor TGR5 Activation Inhibits Kidney Disease in Obesity and Diabetes  
    Wang XX, Edelstein MH, Gafter U, Qiu L, Luo Y, Dobrinskikh E, Lucia S, Adorini L, D'Agati VD, Levi J, Rosenberg A, Kopp JB, Saleem MA, Levi M, J Am Soc Nephrology, 1/30/2015
  • Honokiol is an activator of SIRT3 that protects the heart from pressure overload mediated cardiac hypertrophy in mice  
    Pillai VB, Samant S, Sundaresan NR, Raghuraman H, Kim G, Bonner M, Arbiser J, Gupta MP, Nature Communications, 1/1/2015
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Books/Book Chapters

Grant Support

  • Loss Of Mtsirt3, Decreased Mnsod Activity, And IR Induced Genomic InstabilityNational Cancer Institute2010–2012
  • SIRT3 Is A Mitochondrial Tumor Suppressor In Er/Pr Positive Mammary TumorsNational Cancer Institute2011
  • SIRT3 Is A Genomically Expressed Mitochondrial TSGNational Cancer Institute2010
  • Epigenetic Regulation Of Gene Expression And Resistance In Tumor CellsNational Cancer Institute2010
  • SIRT3 Is A Genomically Expressed Mitochondrial TSGDivision Of Basic Sciences - Nci2009
  • Epigenetic Regulation Of Gene Expression And Resistance In Tumor CellsDivision Of Basic Sciences - Nci2009
  • Epigenetic Regulation Of Gene Expression And Resistance In Tumor CellsNational Cancer Institute2008
  • HSP90 As A Molecular Target For Ionizing RadiationNational Cancer Institute2007–2008
  • Epigenetic Regulation Of Of Gene Expression And Multi-Modality Resistance In TumNational Cancer Institute2007
  • Epigenetic Regulation Of Of Gene Expression And Multi-MoDivision Of Basic Sciences - Nci2005–2006
  • HSP90 As A Molecular Target For Ionizing RadiationDivision Of Basic Sciences - Nci2003–2006
  • Sulfhydryl Switches And Free-Radical Scavenger InvolvemeDivision Of Basic Sciences - Nci2003–2005
  • Epigenetic Regulation Of Gene Expression And Multi-ModalDivision Of Basic Sciences - Nci2003
  • Redox Signaling &Cell Response To Ionizing RceladiationDivision Of Basic Sciences - Nci2002
  • Methylation Mechanism For Resistant PheotypeDivision Of Basic Sciences - Nci2002
  • HSP As Molecular Targets For Nsaids And GeldanamycinDivision Of Basic Sciences - Nci2002
  • GI Restriction Point &Tcr Activation Induced ApoptosisNational Cancer Institute1998–2000
  • G1 Restriction Point &Tcr Activation Induced ApoptosisNational Cancer Institute1997

Professional Memberships

Other Languages

  • Spanish