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Nathaniel H. Boyd
Researcher at University of Alabama at Birmingham
Publications - 15
Citations - 413
Nathaniel H. Boyd is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Tumor microenvironment & Glioma. The author has an hindex of 8, co-authored 14 publications receiving 264 citations. Previous affiliations of Nathaniel H. Boyd include Emory University & Georgia State University.
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Journal ArticleDOI
Addition of carbonic anhydrase 9 inhibitor SLC-0111 to temozolomide treatment delays glioblastoma growth in vivo
Nathaniel H. Boyd,Kiera Walker,Joshua Fried,James R. Hackney,Paul C. McDonald,Gloria A. Benavides,Raffaella Spina,Alessandra Audia,Sarah E. Scott,Catherine J. Libby,Anh Nhat Tran,Mark O. Bevensee,Corinne E. Griguer,Susan Nozell,G. Yancey Gillespie,Burt Nabors,Krishna P. Bhat,Eli E. Bar,Victor M. Darley-Usmar,Bo Xu,Emily R Gordon,Sara J. Cooper,Shoukat Dedhar,Anita B. Hjelmeland +23 more
TL;DR: It is determined that SLC-0111 improves the efficacy of temozolomide to extend survival of GBM-bearing mice and should be explored as a treatment strategy in combination with current standard of care.
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Inhibition of HDAC1 and DNMT1 modulate RGS10 expression and decrease ovarian cancer chemoresistance
TL;DR: The results suggest that HDAC1 and DNMT1 contribute to the suppression of RGS10 during acquired chemoresistance and support inhibition of HDAC 1 andDNMT1 as an adjuvant therapeutic approach to overcome ovarian cancer chemores resistance.
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Glioma stem cells and their roles within the hypoxic tumor microenvironment.
Nathaniel H. Boyd,Anh Nhat Tran,Joshua D. Bernstock,Tina Etminan,Amber Jones,G. Yancey Gillespie,Gregory K. Friedman,Anita B. Hjelmeland +7 more
TL;DR: The impact of hypoxia and acidic stress on GSC signaling and biologic phenotypes, and potential methods to inhibit these pathways are summarized.
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YAP/TAZ Transcriptional Coactivators Create Therapeutic Vulnerability to Verteporfin in EGFR-mutant Glioblastoma.
Krishanthan Vigneswaran,Nathaniel H. Boyd,Se-Yeong Oh,Shoeb Lallani,Andrew B. Boucher,Stewart G. Neill,Jeffrey J. Olson,Renee Read +7 more
TL;DR: The benzoporphyrin derivative verteporfin, a disruptor of YAP/TAZ-TEAD–mediated transcription, preferentially induced apoptosis of cultured patient-derived EGFR-amplified/mutant GBM cells, and conferred significant survival benefit in an orthotopic xenograft GBM model.
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NOS Expression and NO Function in Glioma and Implications for Patient Therapies.
TL;DR: These multifaceted effects of NO and NOS on gliomas both in vitro and in vivo suggest the potential of modulating the pathway for antiglioma patient therapies.