Dr. Gius is on Doximity
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Office
7979 Wurzbach Road
San Antonio, TX 78229Phone+1 210-450-5648
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 ConsortiumResidency, Radiation Oncology, 1994 - 1997
- University of MichiganResidency, Radiation Oncology, 1993 - 1994
- University of Chicago Medical CenterInternship, Preliminary Year, 1992 - 1993
- Loyola University Chicago Stritch School of MedicineClass of 1992
- University of ChicagoPhD, Tumor Virology, 1985 - 1990
- University of Illinois College of MedicineB.S., Chemistry, 1980 - 1983
Certifications & Licensure
- TX State Medical License 2020 - 2025
- IL State Medical License 1992 - 2020
- TN State Medical License 2010 - 2012
- 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
- Member Alpha Omega Alpha (AOA) Honor Medical Society, 2014
- Alpha Omega Alpha 2014
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Publications & Presentations
PubMed
- 324 citationsHonokiol blocks and reverses cardiac hypertrophy in mice by activating mitochondrial Sirt3Vinodkumar B. Pillai, Sadhana Samant, Nagalingam R. Sundaresan, H. Raghuraman, Gene Kim
Nature Communications. 2015-04-14 - 11 citationsSystemic application of honokiol prevents cisplatin ototoxicity without compromising its antitumor effectXiaodong Tan, Yingjie Zhou, Aditi Agarwal, Michelle Lim, Yingyue Xu
American Journal of Cancer Research. 2020-12-01 - 625 citationsSIRT3 Is a Mitochondria-Localized Tumor Suppressor Required for Maintenance of Mitochondrial Integrity and Metabolism during StressHyun-Seok Kim, Krish Patel, Kristi Muldoon-Jacobs, Kheem S. Bisht, Nukhet Aykin-Burns
Cancer Cell. 2010-01-19
Journal Articles
- ATRIP Deacetylation by SIRT2 Drives ATR Checkpoint Activation by Promoting Binding to RPA-ssDNAZhang 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 DiabetesWang 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 micePillai 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
Press Mentions
- Mays Cancer Center Radiation Oncologist Recognized as Outstanding Mentor to Next Generation LeadersOctober 11th, 2024
- Study: Dysregulation in Bioenergetic Process Linked to Rapid Onset of Non-Alcoholic Fatty Liver DiseaseAugust 20th, 2024
- Study Says Long-Term Consumption Accelerates Organ AgingMay 21st, 2024
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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
- Member
Other Languages
- Spanish
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