Anthony Williams, PhD

Division

• Anatomic and Molecular Pathology

Education

• BA, Kinesiology and Pre-Medical Studies: Occidental College
• PhD, Cancer Biology: University of Miami – Miller School of Medicine
• Postdoctoral Scholar: University of Chicago – Pritzker School of Medicine

Recognition

• Cell Press, “1000 Inspiring Black Scientists in America,” 2021
• Halo Awards, “40 Under 40 Scientist,” 2019
• Henry D. Strunk Family Fellow, University of Chicago Department of Medicine, 2018
• AACR “Minority Scholar in Cancer Research” Award, 2017

Research Interests

Mechanisms of castration-resistant prostate cancer development; Resistance to nuclear hormone receptor-targeted therapy in prostate cancer; dysregulated transcription factor biology in prostate cancer; biology of prostate cancer health disparities in African-American men.

Research Statement

The development of androgen receptor (AR)-targeted drug resistance in prostate cancer (PC) remains therapeutically challenging, and mechanisms of resistance owing to this challenge are likely to involve both AR-dependent and -independent signaling nodes. Genomic analyses performed by our group in ARSI-resistant PC cells reveals FOXP1, a transcription factor and tumor suppressor that negatively regulates AR signaling, as a dysregulated gene in this context. Loss of FOXP1 expression has been associated with poor survival in PC, and interestingly, an increased risk of aggressive PC disease particularly for African-American men. Through a comprehensive investigation of FOXP1-mediated biology in PC, the overarching objectives of our studies are to: 1) delineate the basis of irregular FOXP1 biology for AR-dependent and -independent transcriptional programming, 2) discover new drug targets that mitigate FOXP1 loss-mediated behavior, and 3) determine the extent to which FOXP1 loss drives ethnicity-dependent, aggressive PC. The work being conducted towards our objective employs a host of high-throughput, cutting-edge technologies such as ATAC-Seq, ChIP-Seq, ChIP-RIME, RNA-Seq, spatial transcriptomic profiling, genome-wide CRISPR screens and diverse drug compound screens to translate basic findings regarding FOXP1-mediated PC biology into actionable intelligence to maximize positive clinical outcomes. Through this work, we ultimately seek to develop FOXP1 loss as a bona fide driver and biomarker of aggressive PC, where we hope to demonstrate the efficacy of FOXP1 loss to serve as a predictor for sensitivity to novel therapies, particularly in AA men. Importantly, data resulting from our work will become a key resource upon which near-term clinical trials for improved PC patient management can be established, and future hypotheses that seek to study disparate PC biology among African-American men can be tested.

Selected Publications

Williams A, Gutgesell L, de Wet L, Selman P, Dey A, Avineni M, et al. SOX2 Expression in Prostate Cancer Drives Resistance to Nuclear Hormone Receptor Signaling Inhibition Through the WEE1/CDK1 Signaling Axis. Cancer Lett. 2023; Jul 1, 565: 216209.

de Wet L, Williams A, Gillard M, Kregel S, Lamperis S, Brown R, et al. SOX2 Mediates Metabolic Reprogramming of Prostate Cancer Cells. Oncogene. 2022; 41(8): 1190-1202.

McAuley EM, Mustafi D, Simons BW, Valek R, Zamora M, Markiewicz E, Lamperis S, Williams A, et al. Magnetic Resonance Imaging and Molecular Characterization of a Hormone-Mediated Murine Model of Prostate Enlargement and Bladder Outlet Obstruction. Am J Pathol. 2017; 187(11): 2378-2387.

Ao Z*, Shah SH*, Machlin L, Parajuli R, Miller P, Rawal S, Williams A, et al. Identification of Cancer-Associated Fibroblasts in Circulating Blood From Patients With Metastatic Breast Cancer. Cancer Res. 2015; 75(22): 4681-4687.

Zhou M-D*, Hao S*, Williams A*, Haraouaka R, Schrand B, Rawal S, et al. Separable Bilayer Microfiltration Device for Viable Label-Free Enrichment of Circulating Tumor Cells. Sci Rep. 2014; 4(7392).   [Asterisks indicate authors contributed equally]

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Assistant
Blerina Cuka
314-362-8788
bcuka@wustl.edu
BJCIH Room 3410