David N. Saenz
University of Texas MD Anderson Cancer Center
5 Papers
3 Citations
David N. Saenz is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Gene knockdown & Venetoclax. The author has an hindex of 4, co-authored 5 publications.
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Papers
RUNX1-targeted therapy for AML expressing somatic or germline mutation in RUNX1.
Christopher P. Mill,Warren Fiskus,Courtney D. DiNardo,Yimin Qian,Kanak Raina,Kimal Rajapakshe,Dimuthu Perera,Cristian Coarfa,Tapan M. Kadia,Joseph D. Khoury,Dyana T. Saenz,David N. Saenz,Anuradha Illendula,Koichi Takahashi,Steven M. Kornblau,Michael R. Green,Andrew Futreal,John H. Bushweller,Craig M. Crews,Kapil N. Bhalla +19 more
TL;DR: Novel expression-mimickers (EMs) were identified, which repressed RUNX1 and exerted in vitro and in vivo efficacy against AML cells expressing mtRUNX1, which highlighted novel therapeutic agents for AML expressing somatic or germline mtRunX1.
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Synergistic Pre-Clinical Activity of Targeted Inhibition of KDM1A and BET Proteins Against Human AML Blast Progenitor Cells
Warren Fiskus,Christopher P. Mill,Raffaella Soldi,Roulan Han,Dyana T. Saenz,Agnieszka J Nowak,Baohua Sun,David N. Saenz,Courtney D. DiNardo,Gautam Borthakur,Tapan M. Kadia,Wendy Jin,Thurika Ganesh,Vaishnavi Rao,Joseph D. Khoury,Sunil Sharma,Kapil N. Bhalla +16 more
TL;DR: It is determined that tet-inducible shRNA to KDM1A depleted protein levels of K DM1A, repressed c-Myc, but de-repressed p21, CD11b, CD86 and CEBPα, thereby inhibiting colony growth and modestly inducing lethality in genetically diverse cultured AML cell lines.
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Mechanisms Underlying Superior Efficacy of Co-Targeting BET Proteins and Anti-Apoptotic BCL2 or MCL1 Protein Against AML Blast Progenitor Cells
Christopher P. Mill,Tianyu Cai,Warren Fiskus,Gautam Borthakur,Steven M. Kornblau,Tapan M. Kadia,Courtney D. DiNardo,Agnieszka J Nowak,Dyana T. Saenz,David N. Saenz,Baohua Sun,Thurika Ganesh,Wendy Jin,Vaishnavi Rao,Joseph D. Khoury,Yu Shen,Marina Konopleva,Kapil N. Bhalla +17 more
TL;DR: Kadia et al. as discussed by the authors investigated the epigenetic mechanisms underlying transcriptional repression due to BETi treatment, as well as determined the anti-AML activity of co-treatment with BETi and venetoclax or A-1210477 against AML BPCs.
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Targeting nuclear β-catenin as therapy for post-myeloproliferative neoplasm secondary AML.
Dyana T. Saenz,Warren Fiskus,Taghi Manshouri,Christopher P. Mill,Yimin Qian,Kanak Raina,Kimal Rajapakshe,Cristian Coarfa,Raffaella Soldi,Prithviraj Bose,Gautam Borthakur,Tapan M. Kadia,Joseph D. Khoury,Lucia Masarova,Agnieszka J Nowak,Baohua Sun,David N. Saenz,Steven M. Kornblau,Steve Horrigan,Sunil Sharma,Peng Qiu,Craig M. Crews,Srdan Verstovsek,Kapil N. Bhalla +23 more
TL;DR: Preclinical findings highlight potentially promising anti-post-MPN sAML activity of the combination of β-catenin and BETP antagonists against post- MPsAML BPCs.
Superior efficacy of cotreatment with BET protein inhibitor and BCL2 or MCL1 inhibitor against AML blast progenitor cells.
Warren Fiskus,Tianyu Cai,Courtney D. DiNardo,Steven M. Kornblau,Gautam Borthakur,Tapan M. Kadia,Naveen Pemmaraju,Prithviraj Bose,Lucia Masarova,Kimal Rajapakshe,Dimuthu Perera,Cristian Coarfa,Christopher P. Mill,Dyana T. Saenz,David N. Saenz,Baohua Sun,Joseph D. Khoury,Yu Shen,Marina Konopleva,Kapil N. Bhalla +19 more
TL;DR: Compared to treatment with either agent alone, cotreatment with ABBV-075 and venetoclax was significantly more effective in reducing AML cell-burden and improving survival, without inducing toxicity, in AML-engrafted immune-depleted mice.