About

William Aronson is a Professor-in-Residence in the Department of Urology at UCLA's David Geffen School of Medicine. His research activities and funding focus on the role of GPR120 and macrophages in dietary omega-3 fatty acid inhibition of prostate cancer. He has contributed to numerous studies related to prostate cancer, including the quantification of the impact of biochemical recurrence after radical prostatectomy on overall mortality, and the effects of omega-3 fatty acid treatment on prostate cancer progression. His work also encompasses the development of clinical-genomic risk systems for prognostication in patients with localized prostate cancer, as well as the influence of diet and lifestyle on prostate cancer outcomes. Aronson's research extends to evaluating racial disparities in prostate cancer pathology prediction models, the risk of progression after early androgen deprivation therapy, and the safety and efficacy of various treatments in diverse populations. His contributions are characterized by a focus on improving understanding of prostate cancer biology, risk assessment, and therapeutic strategies.

Research topics

• Internal medicine
• Medicine
• Urology
• Oncology
• Chemistry
• Food science
• Biochemistry
• Pharmacology

Selected publications

• IP38-04 COMPARISON OF EMBARK AND EAU CRITERIA TO IDENTIFY HIGH-RISK PATIENTS WITH BIOCHEMICAL RECURRENCE AFTER RADICAL PROSTATECTOMY

  The Journal of Urology · 2026-04-27

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  PublisherDOI

• IP74-03 COSTS OF CARE AND ONCOLOGIC OUTCOMES ASSOCIATED WITH BLUE LIGHT CYSTOSCOPY IN AN EQUAL ACCESS SETTING: RESULTS FROM THE BRAVO STUDY

  The Journal of Urology · 2026-04-27

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  PublisherDOI

• Consensus Recommendations for Disease- and Treatment-Related Fatigue in Patients With Advanced Prostate Cancer: A Modified Delphi Panel

  Journal of the National Comprehensive Cancer Network · 2026-03-31

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  BACKGROUND: Among patients with advanced prostate cancer (aPC), fatigue is a commonly experienced symptom that may be associated with the disease itself or occur as a side effect of treatment. We aimed to develop evidence-based, consensus-driven statements to support shared decision-making for managing fatigue in patients with aPC. METHODS: To identify potential fatigue-management strategies, we performed a targeted literature review followed by expert advisor interviews, and then conducted a modified Delphi panel. In both the interviews and the modified Delphi panel, participants included oncologists, urologists, exercise scientists, psychologists, nutritionists/dietitians, and nurse practitioners/nurses. The modified Delphi panel comprised 2 survey rounds, with a live panel discussion between them, intended to drive consensus on the statements. In determining consensus for the final statements, each strategy's effectiveness, accessibility for patients, and feasibility for both patients and health care providers were taken into account. Consensus was predefined as ≥75% agreement or disagreement with each statement. RESULTS: The targeted literature review identified 14 fatigue-management strategies derived from 32 articles. These strategies were further refined and expanded by the expert advisors and modified Delphi panelists, who ultimately compiled a final list of 15 statements, each achieving ≥75% agreement. The 15 statements were grouped into 4 categories of fatigue-management strategies: exercise (eg, endurance, strength, aerobic, and resistance training), diet and nutrition (eg, hydration and healthy eating), clinical management (eg, counseling and support groups), and "other strategies" (eg, acupuncture and adopting good sleep habits). CONCLUSIONS: These recommendations and considerations provide practical guidance-grounded in evidence and expert opinion-for managing fatigue in patients with aPC, with the goal of improving quality of life. Future research should prioritize high-quality studies evaluating fatigue-management strategies in aPC, particularly in areas where published evidence remains limited.

  PublisherDOI

• IP44-01 ARE WE OPERATING ON THE SAME PATIENTS OVER THE PAST 2 DECADES? 20-YEAR TRENDS IN RADICAL PROSTATECTOMY DEMOGRAPHICS, CLINICOPATHOLOGY, AND OUTCOMES FROM A TERTIARY ACADEMIC CENTER AND MULTI-INSTITUTIONAL COLLABORATIVE

  The Journal of Urology · 2026-04-27

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  PublisherDOI

• Costs of care and oncologic outcomes associated with blue light cystoscopy in an equal access setting: Results from the BRAVO study

  Urologic Oncology Seminars and Original Investigations · 2026-04-03

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  PublisherDOI

• IP44-10 A WEIGHTED SCALE TO IDENTIFY EMBARK-LIKE PATIENTS AT HIGH-RISK FOR PROGRESSION AND MORTALITY AFTER BIOCHEMICAL RECURRENCE (BCR) WHO MAY BENEFIT FROM EARLY INTENSIFIED ADT

  The Journal of Urology · 2026-04-27

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  PublisherDOI

• A high omega-3, low omega-6 diet with fish oil for men with prostate cancer on active surveillance: The CAPFISH-3 randomized clinical trial.

  Journal of Clinical Oncology · 2025-02-10 · 1 citations

  article1st authorCorresponding

  312 Background: Men on active surveillance for prostate cancer are extremely interested in dietary changes or supplements to prevent progression of their disease. There are presently no prospective trials supporting such changes. We sought to determine if a high omega-3, low omega-6 fatty acid diet with fish oil capsules (D+FO) decreases proliferation (Ki-67) in prostate biopsies in men with prostate cancer on active surveillance over a 1-year time period. Methods: In this Phase II, prospective randomized trial, men (N=100) with grade group 1 or 2 prostate cancer that elected active surveillance were randomized to the D+FO or a control group. Same site prostate biopsies were obtained at baseline and 1-year tracked using an image-fusion device. The primary endpoint was the change in Ki-67 index from baseline to 1-year from same site biopsies compared between the groups. Ki-67 index was determined using multiplex immunofluorescence analysis. Secondary outcomes included compliance, grade group, maximum tumor length, the Decipher 22 gene score, serum PSA, lipid levels, and adverse events. Results: The Ki-67 index decreased in the D+FO group by approximately 15% from baseline to 1-year (1.34% at baseline, 1.14% at 1-year) and increased in the control group by approximately 24% from baseline to 1-year (1.23% at baseline, 1.52% at 1-year) resulting in a statistically significant difference in the change of Ki-67 index between the groups (95% CI 2%, 52%, p=0.043). There was no significant difference in the secondary outcomes grade group, tumor length, decipher genomic score or PSA between the two groups. There was a significant decrease in serum triglyceride (p=0.016) and serum colony stimulating factor-1 (p=0.017) in the D+FO group compared to control. Four patients in the D+FO group were withdrawn from the trial due to adverse events related to the FO. Conclusions: A high omega-3, low omega-6 diet with FO for 1-year resulted in a significant reduction in Ki-67 index (compared to the control group), a biomarker for prostate cancer progression, metastasis and death. These findings support future Phase III trials incorporating this intervention in men on active surveillance. Clinical trial information: NCT02176902 .

  PublisherDOI

• WHAT CLINICAL FACTORS PREDICT OUTCOMES IN RECURRENT METASTATIC CASTRATE-SENSITIVE PROSTATE CANCER? RESULTS FROM THE SEARCH DATABASE

  Urologic Oncology Seminars and Original Investigations · 2025-02-27

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  PublisherDOI

• Comparing progression following systemic and tumor-directed therapy for <i>de novo</i> versus recurrent PSMA PET–defined oligo-M1 prostate cancer: A pooled analysis of SOLAR and SATURN clinical trials.

  Journal of Clinical Oncology · 2025-02-10

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  64 Background: Therapeutic strategies for oligometastatic castration sensitive prostate cancer (omCSPC) combining treatment of the primary and metastases with short-term intensified systemic therapy aim to improve survival and local control while minimizing toxicity from indefinite systemic therapy. This post-hoc analysis of the SOLAR (NCT03298087) and SATURN (NCT03902951) trials, which evaluated systemic and tumor-directed therapy in PSMA-PET defined oligo-M1 (≤5 metastases) de novo and recurrent omCSPC, respectively, aims to draw inferences on biology and oncologic outcome. Methods: All patients were treated with 6 months of systemic therapy: leuprolide, abiraterone acetate with prednisone, and apalutamide in conjunction with SBRT to oligometastatic sites. SOLAR patients were treatment naïve and underwent either radical prostatectomy (RP) with lymph node dissection followed by post-operative radiotherapy for high-risk features, or definitive radiotherapy (dRT). SATURN patients all had recurrent disease after RP with or without postoperative radiotherapy and may have also had prior hormone or metastasis-directed therapy. The primary endpoint (response rate) was the percentage of patients with an undetectable PSA (&lt;0.05 ng/mL) for post-RP patients, or a PSA &lt;2 ng/mL for post-dRT patients, six months after recovery of testosterone to &gt;150 ng/dl. Secondary endpoints included progression-free survival (PFS) and eugonadal PFS starting from time of testosterone recovery. Kaplan-Meier assessed differences in time-to-event endpoints from initiation of systemic therapy. Fischer’s Exact Test compared proportional outcomes. Results: Analysis included data from 24 SOLAR and 26 SATURN patients. Overall, median follow-up was 32 months (interquartile range 28.25-36.75 months). Response rates were higher for de novo versus oligorecurrent patients (20/24 [83%] versus 13/26 [50%], p=0.018). PFS and eugonadal PFS were also significantly longer (median not reached versus 17 months and median not reached versus 13 months, respectively, p&lt;0.05). PFS was shorter for oligorecurrent patients with prior exposure to hormone therapy (median 10 months versus not reached, p&lt;0.05). There was no PFS difference comparing patients treated in the de novo setting versus the recurrent setting who were naive to hormonal therapy (p=0.23). Conclusions: Patients with recurrent omCSPC PSMA-PET defined M1 disease had a worse response rate and shorter PFS following intensified systemic and metastasis-directed SBRT than those with de novo omCSPC. The difference was driven by recurrent patients with prior exposure to hormonal therapy, suggesting a continuum of treatment resistances over repeated courses of hormonal therapy. The majority of patients with de novo omCSPC remain in remission after gonadal recovery. Clinical trial information: NCT03298087 , NCT03902951 .

  PublisherDOI

• Quantifying the Impact of Biochemical Recurrence After Radical Prostatectomy on Overall Mortality by Years of Life Lost: Results from the SEARCH Database

  European Urology Oncology · 2025-12-01

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  PublisherDOI

Recent grants

• Career Enhancement Program

  NIH · $35.9M · 2002–2025

• Role of GPR120 and Macrophages in Dietary Omega-3 Fatty Acid Inhibition of Prostate Cancer

  NIH · $1.7M · 2018–2023

• Role of GPR120 and Macrophages in Dietary Omega-3 Fatty Acid Inhibition of Prostate Cancer

  NIH · $445k · 2018–2023

• NIH Grant M01RR000865

  NIH · $41.8M · 2011

Frequent coauthors

• Stephen J. Freedland

  Durham VA Medical Center

  1015 shared

• Martha K. Terris

  875 shared

• Christopher J. Kane

  University of California, San Diego

  770 shared

• Christopher L. Amling

  Oregon Health & Science University

  700 shared

• Joseph C. Presti

  Kaiser Permanente San Francisco Medical Center

  550 shared

• Matthew R. Cooperberg

  307 shared

• Lauren E. Howard

  258 shared

• David Elashoff

  University of California, Los Angeles

  127 shared

Education

• MD, Medicine

  Washington University in St. Louis