Meet David Steiner
· Professor Executive Director, Johns Hopkins Institute for Education PolicyVerifiedJohns Hopkins University · Educational Policy and Politics
Active 1985–2024
About
David Steiner, PhD, is the executive director of the Johns Hopkins Institute for Education Policy and a professor of education at Johns Hopkins University. He has served in various prominent roles including commissioner of education for New York State, where he played a leading role in the state's successful $700 million Race to the Top application, supporting the redesign of standards, assessments, and teacher certification requirements. His efforts contributed to the launch of EngageNY, a widely consulted free online curriculum resource. Steiner has also served as the Klara and Larry Silverstein Dean at Hunter College School of Education, and as director of education at the National Endowment for the Arts. He holds degrees from Harvard University, including a PhD in political science, and from Balliol College at Oxford University, where he earned both a BA and an MA. Steiner is known for consulting regularly with federal and state education leaders, educational reform organizations, and universities, and has authored numerous articles and books, including his most recent publication, 'A Nation at Thought: Restoring Wisdom in America’s Schools' (2023). His research and professional focus center on education policy, standards, curriculum development, and educational reform.
Research topics
- Internal medicine
- Medicine
- Oncology
- Virology
- Geography
- Pathology
- Urology
Selected publications
Endocrine Practice · 2024-05-01
articleOpen accessSenior authorCancer Research · 2024-05-02 · 1 citations
articleAbstract Background: Targeting the androgen receptor (AR) with an oral selective agonist, enobosarm, is a novel approach to overcome ER and CDK4/6 resistance to suppress metastatic breast cancer (mBC). Preclinical studies in CDK4/6 inhibitor and estrogen blocking agent resistant PDX mBC models demonstrated that enobosarm alone or in combination with another CDK 4/6 inhibitor suppressed PDX mBC growth. In a subgroup analysis from a Phase 2 study, enobosarm demonstrated efficacy in the treatment of AR+ ER+ HER2- metastatic breast cancer in patients who had tumor progression on estrogen blocking agent and a CDK 4/6 inhibitor with a best overall response rate of 30% (2CRs and 1 PR). A Phase 3 ENABLAR-2 multi-center, open label, study evaluating enobosarm +/- abemaciclib is open and active for the treatment of HR+HER2- mBC. Methods: The two-staged Phase 3 ENABLAR-2, open-label, randomized, multicenter study is being conducted in AR+ER+ HER2- 2nd-line mBC who have progressed on estrogen blocking agent plus palbociclib or ribociclib. In the Stage 1 of the study (160 patients), five treatment arms will be assessed with the primary efficacy endpoint of ORR: enobosarm 9 mg QD, enobosarm 1 mg QD + abemaciclib, enobosarm 3 mg QD + abemaciclib, enobosarm 9 mg QD + abemaciclib, and an estrogen blocking agent, active control (a nonsteroidal AI, exemestane +/- everolimus, or SERD). Secondary efficacy endpoints include progression-free survival (PFS). In Stage 2 of the study, patients will be randomized to receive enobosarm +/- abemaciclib (based on outcome of ORR in Stage 1) or estrogen blocking agent, active control, with the primary endpoint of PFS and secondary efficacy endpoints including, ORR, CBR, OS, as well as changes in quality-of-life measurements (SPPB, EORTC-QLQ, body composition measured by DEXA). Randomization will be stratified by AR% nuclei staining and by line of treatment for metastatic disease. Subjects will receive study drug until disease progression is observed. Preliminary Results: To date, 3 patients have been treated with enobosarm 9 mg in combination with abemaciclib. The combination therapy was well tolerated with no new safety findings. There were no drug-drug interactions between enobosarm and abemaciclib. Two patients have achieved BOR of a partial response with up to 79% and 56% reduction in their target lesion recorded by local reads on day 224 post-treatment initiation (PTI). The third patient has achieved a stable disease and continues to receive treatment (on study 10+ months). Conclusions: Preliminary data of efficacy and safety of enobosarm in combination with abemaciclib are encouraging. The Phase 3 ENABLAR-2 study is underway to further evaluate enobosarm monotherapy or in abemaciclib combination therapy in 2nd-line metastatic breast cancer population. Clinical trial information: NCT05065411. Research Sponsor: Veru Inc Citation Format: Kristine Rinn, Hannah Linden, Lee Schwartzberg, Gary Barnette, Domingo Rodriguez, Itay Shalev, Mitchell Steiner, Adam Brufsky, Joyce O'Shaughnessy. Design of Active Phase 3 ENABLAR-2 Study Evaluating Enobosarm +/- Abemaciclib in Patients with AR+ER+HER2- 2nd-Line Metastatic Breast Cancer Following Tumor Progression on an Estrogen Blocking Agent Plus Palbociclib or Ribociclib [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO4-27-06.
Endocrine Practice · 2024-05-01
articleOpen accessSenior authorCancer Research · 2024-05-02
articleAbstract Background: Targeting the androgen receptor (AR) with an oral selective AR agonist, enobosarm, is a novel approach to overcome ER and CDK4/6 inhibitor resistance to suppress AR+ER+HER2- metastatic breast cancer (mBC). Preclinical studies in CDK4/6 inhibitor and estrogen blocking agent resistant PDX mBC models demonstrated that enobosarm alone suppressed tumor growth. In a small subgroup analysis of patients with ER+HER2- mBC who progressed on estrogen blocking agent and a CDK 4/6 inhibitor from the Phase 2 802 study, enobosarm treatment resulted in a best overall response rate of 30% (2 CRs and 1 PR) and a 6-month clinical benefit rate (CBR) of 50%. Methods: The clinical activity of enobosarm 9mg alone was evaluated compared to standard of care (SOC) in the Phase 3 ARTEST, open-label, randomized, multicenter study in AR+ER+HER2-mBC who have progressed on 2 or greater lines of prior therapies, including estrogen blocking agents and CDK4/6 inhibitors. The study was discontinued for administrative reasons not related to efficacy or safety. Results: At the time study was discontinued, 34 patients with confirmed AR positivity were randomized to either enobosarm (n=16) or SOC control (n=18). SOC control treatment group received an average of 2.6 (range 1-5) and enobosarm 9mg monotherapy an average of 2.9 (range 1-5) prior lines of treatment. On average, enobosarm or the SOC control was given in the 4th line treatment for AR+ER+HER2- metastatic breast cancer. In the evaluable population, two partial responses were observed in the enobosarm treatment arm versus no responses in the SOC control arm. In patients with ≤3 lines of prior endocrine therapy, the best objective response rate (ORR) was 18.8% for enobosarm and 0% for control. In patients with ≤3 lines of prior endocrine therapy with ≤1 prior treatment with CDK 4/6 inhibitor, best ORR was 33% in the enobosarm group versus no responses in the SOC control (Table 1). CBR on day 180 was 33.3% (4/12) in the enobosarm group vs 0% (0/11) in the control group. Enobosarm treatment was well tolerated without masculinizing adverse events and no increases in hematocrit changes. Conclusions: Activity of enobosarm in this heavily pretreated patient population is encouraging and supports further clinical investigation. The Phase 3 ENABLAR-2 study is underway to further evaluate enobosarm alone or in combination with abemaciclib for the second-line treatment of AR+ER+HER2- metastatic breast cancer in patients who have received a prior estrogen blocking agent and a CDK 4/6 inhibitor. Clinical trial information: NCT04869943. Research Sponsor: Veru Inc. Table 1. Responses in patients with enobosarm versus SOC treatment. Citation Format: Kristine Rinn, Elisa Krill Jackson, Gary Barnette, Domingo Rodriguez, Itay Shalev, Mitchell Steiner, Joyce O'Shaughnessy, Hope Rugo, Adam Brufsky. Clinical Results of Subjects Remaining in the Phase 3 ARTEST Study Enobosarm Therapy in AR+ER+HER2- Metastatic Breast Cancer with 3 or Greater Prior Lines of Therapy [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO2-27-03.
2023-03-31
preprintOpen accessSupplementary Data from A Phase Ib/II Study of Sabizabulin, a Novel Oral Cytoskeleton Disruptor, in Men with Metastatic Castration-resistant Prostate Cancer with Progression on an Androgen Receptor–targeting Agent
2023-03-31
preprintOpen access<p>Supplementary Figures and Tables - PDF file 898K, Supplementary Table ST1: AKR1C3 over-expression in HEK-293 cells reduces IC50 of androgens. Supplementary Table ST2: Finasteride increases the testosterone formation. Supplementary Figure S1: Over-expression of AKR1C3 increases LNCaP xenograft growth in intact mice. Supplementary Figure S2: AR target FKBP51, but not AR, protein expression is increased in LNCaP-AKR1C3 xenograft tumors. Supplementary Figure S3: AKR1C3 translocation to nucleus requires AR. Top panel. NIH3T3-AKR1C3 cells infected with adenovirus LacZ. Bottom panel. NIH3T3-AKR1C3 cells infected with adenovirus AR.Supplementary Figure S4: AKR1C3 migrates with AR. Supplementary Figure S5: Duolink assay demonstrates interaction between AR and AKR1C3 in LNCaP-AKR1C3 cells. Supplementary Figure S6: AKR1C3 synergizes with SRC-2 in AR transactivation assay. Supplementary Figure S7: AKR1C3 dependent- androgen induced- AR transactivation is not cell type dependent. Transient transactivation studies conducted in COS-1 cells Supplementary Figure S8: AKR1C3-dependent increase in transactivation is selective to AR. Supplementary Figure S9: R1881 induced- AKR1C3 dependent- AR transactivation is not observed with other AKR1C. Supplementary Figure-S10: Different domains mediate the enzymatic and activator functions of AKR1C3. Supplementary Figure S11: GTx-560 is specific for AKR1C3. Supplementary Figure S12: HEK-293-AKR1C3 enzyme activity. Supplementary Figure S14: GTx-560 inhibits AKR1C3-dependent A�dione-induced AR transactivation at all concentration of AKR1C3. Supplementary Figure S15: Expression of steroidogenic enzymes in VCaP cells</p>
2023-03-31
preprintOpen accessSupplementary Figure from A Phase Ib/II Study of Sabizabulin, a Novel Oral Cytoskeleton Disruptor, in Men with Metastatic Castration-resistant Prostate Cancer with Progression on an Androgen Receptor–targeting Agent
2023-03-31
preprintOpen accessSupplementary Data from A Phase Ib/II Study of Sabizabulin, a Novel Oral Cytoskeleton Disruptor, in Men with Metastatic Castration-resistant Prostate Cancer with Progression on an Androgen Receptor–targeting Agent
2023-03-31
preprintOpen accessSupplementary Figure from A Phase Ib/II Study of Sabizabulin, a Novel Oral Cytoskeleton Disruptor, in Men with Metastatic Castration-resistant Prostate Cancer with Progression on an Androgen Receptor–targeting Agent
2023-03-31
preprintOpen access<div>Abstract<p><b>Purpose:</b> Castration-resistant prostate cancer (CRPC) may occur by several mechanisms including the upregulation of androgen receptor (AR), coactivators, and steroidogenic enzymes, including aldo keto reductase 1C3 (AKR1C3). AKR1C3 converts weaker 17-keto androgenic precursors to more potent 17-hydroxy androgens and is consistently the major upregulated gene in CRPC. The studies in the manuscript were undertaken to examine the role of AKR1C3 in AR function and CRPC.</p><p><b>Experimental Design:</b> LNCaP cells stably transfected with AKR1C3 and VCaP cells endogenously expressing AKR1C3 were used to understand the effect of AKR1C3 on prostate cancer cell and tumor growth in nude mice. Chromatin immunoprecipitation, confocal microscopy, and co-immunoprecipitation studies were used to understand the recruitment of AKR1C3, intracellular localization of AKR1C3 and its interaction with AR in cells, tumor xenograft, and in Gleason sum 7 CRPC tissues. Cells were transiently transfected for AR transactivation. Novel small-molecule AKR1C3-selective inhibitors were synthesized and characterized in androgen-dependent prostate cancer and CRPC models.</p><p><b>Results:</b> We identified unique AR-selective coactivator- and prostate cancer growth-promoting roles for AKR1C3. AKR1C3 overexpression promotes the growth of both androgen-dependent prostate cancer and CRPC xenografts, with concomitant reactivation of androgen signaling. AKR1C3 interacted with AR in prostate cancer cells, xenografts, and in human CRPC samples and was recruited to the promoter of an androgen-responsive gene. The coactivator and growth-promoting functions of AKR1C3 were inhibited by an AKR1C3-selective competitive inhibitor.</p><p><b>Conclusions:</b> AKR1C3 is a novel AR-selective enzymatic coactivator and may represent the first of more than 200 known nuclear hormone receptor coactivators that can be pharmacologically targeted. <i>Clin Cancer Res; 19(20); 5613–25. ©2013 AACR</i>.</p></div>
Recent grants
NIH · $483k · 1997
NIH · $1.8M · 2003
Frequent coauthors
- 53 shared
Robert H. Getzenberg
Nova Southeastern University
- 46 shared
K. Gary Barnette
- 43 shared
Mark C. Markowski
- 43 shared
Mario A. Eisenberger
- 38 shared
Ronald Tutrone
Chesapeake Urology Associates
- 36 shared
James T. Dalton
University of Rochester Medical Center
- 35 shared
Emmanuel S. Antonarakis
University of Minnesota
- 33 shared
Domingo Rodrı́guez
University of Puerto Rico System
Labs
Johns Hopkins Institute for Education PolicyPI
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