Byeongyeob Choi, Ph.D.

Federal

Funding Agency NIH-National Institute on Aging Title Identification of a missing key element underlying apoE2 neuroprotection in Alzheimer?s disease and the aging brain Status Active Period 9/2018 - 6/2023 Role Co-Investigator Grant Detail   Funding Agency NIH/NCI Title (PQ3) Novel Tumor Intrinsic PD-L1 Signals Direct Tumor Status Active Period 6/2017 - 6/2022 Role Co-Investigator Grant Detail Assist in the analysis of data from ERβ-centered signaling axis indicating a previously unrecognized molecular handle for mobilizing tumor-extrinsic antitumor activity of ERβ in immune cells Funding Agency Department of Defense Title Early detection of castration-resistant prostate cancer by assessing interactions between circulating tumor cells and accompanying immune cells Status Active Period 9/2018 - 8/2021 Role Co-Investigator Grant Detail To develop a procedure to early identify CR patients with a risk score based on mechanical/ immunocytochemical profiling of blood-isolated cells. For its future clinical use, collection and analysis of cells? mechanical parameters, vetted for essentiality in this study, will be condensed into a bed side device. Specific Aims: 1 ? We will determine the role of EMT in mechanical fitness of CTCs by measuring their mechanical properties with atomic force microscopy (AFM). We will recapitulate the EMT in cell culture to follow mechanical fitness related biophysical and gene expression changes in model CTCs. Aim 2 ? We will define the role of CTC-macrophage interactions in mechanical fitness of CTCs. We will classify the macrophage populations and determine mechanical and gene expression phenotypes of interacting CTCs. We will recapitulate the interactions in cell culture and follow phenotypic changes in model CTCs contacting macrophages. Aim 3 - We will construct a model for patients? stratification predicting the risk of castration resistance based on the mechanical fitness of CTCs collected before the start of ADT. Funding Agency NIH, NCI Title Cancer Therapy & Research Center at UTHSCSA, P30 Status Active Period 8/1997 - 7/2019 Role Co-Investigator Grant Detail Support research efforts of Cancer Center investigators. Funding Agency NIH-Diabetes/Digestive/Kidney Diseases Title Sglt2 Inhibition and Stimulation of Endogenous Glucose Status Active Period 7/2016 - 6/2018 Role Consultant Grant Detail We and others have demonstrated that glucosuria produced by inhibition of the renal sodium-glucose transporter-2 (SGLT2) lowers the fasting plasma glucose (FPG) concentration but causes a ?paradoxical? increase in endogenous glucose production (EGP). Although the increase in EGP can be viewed as a compensatory mechanism that opposes urinary glucose loss and prevents the development of hypoglycemia in NGT individuals, in T2DM individuals it occurs while the plasma glucose concentration is still in the hyperglycemic range. Moreover, it offsets by ~50% the urinary glucose loss produced by SGLT2 inhibitors and attenuates their glucose lowering ability. The increase in EGP following SGLT2 inhibition is associated with an increase in plasma glucagon concentration and decrease in plasma insulin concentration. Because renal glucose production is stated to be unresponsive to an increase in the plasma glucagon concentration, it is likely that the liver contributes, at least in part, to the increase in EGP [which is triggered by glucosuria]. However, an increase in glucose production by the kidney cannot be excluded. We hypothesize that there is a previously unrecognized, [completely novel] ?reno-hepatic? interaction that participates in the regulation of plasma glucose concentration. Funding Agency NIH/NCATS Title Institute for Integration of Medicine & Science: A Partnership to Improve Health (Clinical and Translational Science Award) Status Active Period 5/2013 - 4/2018 Role Co-Investigator Grant Detail This Clinical and Translational Science Award (CTSA) provides a broad range of infrastructure support across the institution and its CTSA partners. This UL1 component provides all CTSA support except for the KL2 Career Development Award and TL1 Training Award, which are listed separately. I served as the NIH Contact PI and Director of the IIMS. Note that this 2013-2018 CTSA comprises a new award (with a different grant number) from the 2008-2013 CTSA, due to a change in the NIH sponsoring center from NCRR to NCATS. Also note that due to NIH delays the period from 05/2013 to 09/2013 was funded by an extension of the prior award, but for consistency those funds are included in the first year amount reported here.

Private

Funding Agency V Foundation Title A novel therapeutic approach for endocrine resistant breast cancer by inhibiting a targeted epigenetic program Status Active Period 11/2017 - 10/2020 Role Co-Investigator Grant Detail Develop a novel therapeutic approach for endocrine resistant breast cancer by inhibiting a targeted epigenetic program.

State

Funding Agency Cancer Prevention Research Institute of Texas (CPRIT) Title Mechanisms and treatment of hippocampal cognitive impairment associated with androgen deprivation therapy for prostate cancer Status Active Period 3/2018 - 2/2021 Role Co-Investigator Grant Detail This project will identify mechanisms of cognitive impairment after ADT that may be viable therapeutic targets, inform a potential new use for vortioxetine in treating it, and ultimately improve the quality of life of prostate cancer survivors treated by ADT.

Funding Agency NIH-Diabetes/Digestive/Kidney Diseases Title Durability of Early Combination Therapy vs Conventional Status Active Period 9/2015 - 8/2018 Role Consultant Grant Detail The hypothesis is that the initiation of combination therapy with a glucagon-like peptide-1 analogue (liraglutide) plus a thiazolidinedione (pioglitazone) in type 2 diabetic subjects poorly controlled blood glucose levels on metformin plus sulfonylurea (SU) will achieve superior and more durable glycemic control with fewer side effects compared to basal-bolus insulin. Accordingly we will compare the efficacy and safety of initiating combination therapy with liraglutide plus pioglitazone versus basal (glargine) plus premeal insulin in type 2 diabetic subjects who are suboptimally controlled (HbA1c > 7.0%) with metformin plus SU on the achievement of optimal glycemic control (HbA1C