Effectiveness of Primary Androgen-Deprivation Therapy for Clinically Localized Prostate Cancer
Open accessAbstract
Purpose: Primary androgen-deprivation therapy (PADT) is often used to treat clinically localized prostate cancer, but its effects on cause-specific and overall mortality have not been established. Given the widespread use of PADT and the potential risks of serious adverse effects, accurate mortality data are needed to inform treatment decisions. Methods: We conducted a retrospective cohort study using comprehensive utilization and cancer registry data from three integrated health plans. All men were newly diagnosed with clinically localized prostate cancer. Men who were diagnosed between 1995 and 2008, were not treated with curative intent therapy, and received follow-up through December 2010 were included in the study (n = 15,170). We examined all-cause and prostate cancer-specific mortality as our main outcomes. We used Cox proportional hazards models with and without propensity score analysis. Results: Overall, PADT was associated with neither a risk of all-cause mortality (hazard ratio [HR], 1.04; 95% CI, 0.97 to 1.11) nor prostate-cancer–specific mortality (HR, 1.03; 95% CI, 0.89 to 1.19) after adjusting for all sociodemographic and clinical characteristics. PADT was associated with decreased risk of all-cause mortality but not prostate-cancer–specific mortality. PADT was associated with decreased risk of all-cause mortality only among the subgroup of men with a high risk of cancer progression (HR, 0.88; 95% CI, 0.78 to 0.97). Conclusion: We found no mortality benefit from PADT compared with no PADT for most men with clinically localized prostate cancer who did not receive curative intent therapy. Men with higher-risk disease may derive a small clinical benefit from PADT. Our study provides the best available contemporary evidence on the lack of survival benefit from PADT for most men with clinically localized prostate cancer.
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Preclinical studies suggest that FBZ exerts anticancer effects through a wide variety of mechanisms.
“Preclinical studies suggest that FBZ exerts its anticancer effects through a wide variety of mechanisms.”
From Fenbendazole as an Anticancer Agent? A Case Series of Self-Administration in Three Patients. (2025) · cites this paper as [4]
The Discussion addresses primary androgen-deprivation therapy for clinically localized prostate cancer, not preclinical anticancer effects of FBZ. Searches for FBZ, fenbendazole, and anticancer mechanisms found no passage addressing the claim in our copy. (LLM, conf=0.77)
Experimental — accuracy not yet measuredBenzimidazoles, including FBZ, exert anticancer effects through several mechanisms, including disruption of microtubule polymerization, induction of apoptosis, cell cycle arrest at G2/M, inhibition of angiogenesis, and interference with glucose and glutamine metabolic pathways.
“Benzimidazoles, including FBZ, exert anticancer effects through several mechanisms: they disrupt microtubule polymerization, induce apoptosis, arrest the cell cycle at the G2/M phase, inhibit angiogenesis, and interfere with both glucose [3] and probably also glutamine [4] metabolic pathways.”
From Fenbendazole as an Anticancer Agent? A Case Series of Self-Administration in Three Patients. (2025) · cites this paper as [4]
The Introduction and Discussion address primary androgen-deprivation therapy for localized prostate cancer, not benzimidazoles or fenbendazole. Searches for FBZ, microtubule disruption, apoptosis, and glucose and glutamine metabolic pathways found no passage addressing the mechanisms attributed to this source. (LLM, conf=0.78)
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- Authors
- Potosky, A. L., Haque, R., Cassidy-Bushrow, A. E., Ulcickas Yood, M., Jiang, M., Tsai, H.-T., Luta, G., Keating, N. L., Smith, M. R., & Van Den Eeden, S. K.
- Affiliations
- Boston University (US)
- Arnold L. Potosky, Huei-Ting Tsai, George Luta, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC; Reina Haque, Kaiser Permanente Southern California, Pasadena; Stephen K. Van Den Eeden, Kaiser Permanente Northern California, Oakland, CA; Andrea E. Cassidy-Bushrow, Henry Ford Hospital, Detroit, MI; Marianne Ulcickas Yood, Boston University School of Public Health; Nancy L. Keating, Brigham and Women's Hospital and Harvard Medical School; Matthew R. Smith,...
- Venue
- Journal of Clinical Oncology
- Published
- 2014-05-01
- Volume
- 32
- Issue
- 13
- Pages
- 1324-1330
- ISSN
- 0732-183X (ISSN-L)
- 1527-7755
- PMC
- PMC3992722
- OpenAlex
- W2030240052
- Cited by
- 75
- References
- 36
- Citations by year
- 2025: 1 · 2024: 4 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 9 · 2019: 5 · 2018: 9 · 2017: 9 · 2016: 4 · 2015: 14 · 2014: 15
- FWCI
- 11.23
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Oncology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5k24ca121990-07)
- National Cancer Institute (R01CA142934, RC1CA146238, K24-CA121990, P30CA051008)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Diagnosis and Treatment
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Keywords
- localized prostate cancer, prostate cancer-specific mortality, all-cause mortality, survival benefit, cancer progression risk, treatment effectiveness, curative treatment
- MeSH terms
- Adult, Aged, Aged, 80 and over, California, Humans, Gonadotropin-Releasing Hormone, Male, Michigan, Middle Aged, Neoplasms, Hormone-Dependent, Orchiectomy, Prostatectomy, Prostatic Neoplasms, Registries, Retrospective Studies, Cohort Studies, Proportional Hazards Models, Treatment Outcome, SEER Program, Radiotherapy, Adjuvant, Antineoplastic Agents, Hormonal, Neoadjuvant Therapy
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