Finasteride and high-grade prostate cancer in the Prostate Cancer Prevention Trial.
💡 한 문장 핵심
Prostate Cancer Prevention Trial에서의 피나스테리드와 고등급 전립선암.
4/5 보강
TL;DR
Results suggest that high-grade cancer was detected earlier and was less extensive in the finasteride group than in the placebo group, and effects of finasterid on prostate volume and selective inhibition of low- grade cancer, rather than effects on tumor morphology, may have contributed to the increase in high- grade cancers with finasterides in the PCPT.
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· 인용됨 17
📑 인용한 논문 (6) ▾
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연도별 인용 (2012–2025) · 합계 129
OpenAlex 토픽 ·
Prostate Cancer Diagnosis and Treatment
Prostate Cancer Treatment and Research
Urinary Bladder and Prostate Research
Abstract 🌐 Abstract
[BACKGROUND] The Prostate Cancer Prevention Trial (PCPT) reported a decreased incidence of prostate cancer overall but an increase in the incidence of high-grade prostate cancer with finasteride compared with placebo. We assessed whether the increased high-grade prostate cancer associated with finasteride in the PCPT was due to finasteride's potential effects on tumor morphology or prostate size.
[METHODS] Prostate biopsies with Gleason score 8-10 (n = 90, finasteride; n = 52, placebo) were examined histologically for hormonal effects, and those with Gleason score 7-10 (n = 282, finasteride; n = 244, placebo) were examined for pathologic surrogates of disease extent. Prostate volumes were measured at biopsy. Samples from radical prostatectomies (n = 222, finasteride; n = 306, placebo) were examined for tumor grade and extent, and, where possible, grades at biopsy and prostatectomy were compared between the groups. Logistic regression was used to analyze differences between treatment groups with respect to pathologic criteria. All statistical tests were two-sided.
[RESULTS] Degenerative hormonal changes in high-grade biopsies were equivalent between the finasteride and placebo groups, but prostate volumes were lower in the finasteride group (median = 25.1 versus 34.4 cm3, P<.001). Pathologic surrogates for tumor extent were lower with finasteride than with placebo, including mean percentage of positive cores (34% versus 38%, P = .016), mean tumor linear extent (greatest [4.4 versus 4.8 mm, P = .19] and aggregate [7.6 versus 9.2 mm, P = .13]), bilaterality (22.8% versus 30.6%, P = .046), and perineural invasion (14.2% versus 20.3%, P = .07). Among patients who had prostatectomy, the finasteride-associated increase in high-grade disease (Gleason score > or = 7) at biopsy (42.7% finasteride versus 25.4% placebo, P<.001) was diminished at prostatectomy (46.4% finasteride versus 38.6% placebo, P = .10). Biopsy identified a greater proportion of patients with high-grade disease present at prostatectomy in the finasteride group than in the placebo group (69.7% versus 50.5%, P = .01). The rate of upgrading (from low-grade cancer at biopsy to high-grade cancer at prostatectomy) and pathologic stage at prostatectomy were similar in both groups.
[CONCLUSIONS] Effects of finasteride on prostate volume and selective inhibition of low-grade cancer, rather than effects on tumor morphology, may have contributed to the increase in high-grade cancers with finasteride in the PCPT. Although induction of high-grade cancer cannot be excluded, the results suggest that high-grade cancer was detected earlier and was less extensive in the finasteride group than in the placebo group.
[METHODS] Prostate biopsies with Gleason score 8-10 (n = 90, finasteride; n = 52, placebo) were examined histologically for hormonal effects, and those with Gleason score 7-10 (n = 282, finasteride; n = 244, placebo) were examined for pathologic surrogates of disease extent. Prostate volumes were measured at biopsy. Samples from radical prostatectomies (n = 222, finasteride; n = 306, placebo) were examined for tumor grade and extent, and, where possible, grades at biopsy and prostatectomy were compared between the groups. Logistic regression was used to analyze differences between treatment groups with respect to pathologic criteria. All statistical tests were two-sided.
[RESULTS] Degenerative hormonal changes in high-grade biopsies were equivalent between the finasteride and placebo groups, but prostate volumes were lower in the finasteride group (median = 25.1 versus 34.4 cm3, P<.001). Pathologic surrogates for tumor extent were lower with finasteride than with placebo, including mean percentage of positive cores (34% versus 38%, P = .016), mean tumor linear extent (greatest [4.4 versus 4.8 mm, P = .19] and aggregate [7.6 versus 9.2 mm, P = .13]), bilaterality (22.8% versus 30.6%, P = .046), and perineural invasion (14.2% versus 20.3%, P = .07). Among patients who had prostatectomy, the finasteride-associated increase in high-grade disease (Gleason score > or = 7) at biopsy (42.7% finasteride versus 25.4% placebo, P<.001) was diminished at prostatectomy (46.4% finasteride versus 38.6% placebo, P = .10). Biopsy identified a greater proportion of patients with high-grade disease present at prostatectomy in the finasteride group than in the placebo group (69.7% versus 50.5%, P = .01). The rate of upgrading (from low-grade cancer at biopsy to high-grade cancer at prostatectomy) and pathologic stage at prostatectomy were similar in both groups.
[CONCLUSIONS] Effects of finasteride on prostate volume and selective inhibition of low-grade cancer, rather than effects on tumor morphology, may have contributed to the increase in high-grade cancers with finasteride in the PCPT. Although induction of high-grade cancer cannot be excluded, the results suggest that high-grade cancer was detected earlier and was less extensive in the finasteride group than in the placebo group.
- 표본수 (n) 90
- p-value P<.001
- p-value P = .016
Results suggest that high-grade cancer was detected earlier and was less extensive in the finasteride group than in the placebo group, and effects of finasterid on prostate volume and selective inhibi
APA 7
Lucia, M. S., Epstein, J. I., Goodman, P. J., Darke, A. K., Reuter, V. E., Civantos, F., Tangen, C. M., Parnes, H. L., Lippman, S. M., FG, L. R., Kattan, M. W., Crawford, E. D., Ford, L. G., Coltman, C. A., & Thompson, I. M. (2007). Finasteride and high-grade prostate cancer in the prostate cancer prevention trial.. Journal of the National Cancer Institute, 99(18), 1375-83. https://doi.org/10.1093/jnci/djm117
Vancouver
Lucia MS, Epstein JI, Goodman PJ, Darke AK, Reuter VE, Civantos F, et al. Finasteride and high-grade prostate cancer in the Prostate Cancer Prevention Trial. Jour. Nati. Canc. Inst.. 2007;99(18):1375-83. doi:10.1093/jnci/djm117
AMA 11
Lucia MS, Epstein JI, Goodman PJ, Darke AK, Reuter VE, Civantos F, et al. Finasteride and high-grade prostate cancer in the Prostate Cancer Prevention Trial. Jour. Nati. Canc. Inst.. 2007;99(18):1375-83. doi:10.1093/jnci/djm117
Chicago
Lucia, M. S., Epstein, J. I., Goodman, P. J., Darke, A. K., Reuter, V. E., Civantos, F., Tangen, C. M., Parnes, H. L., Lippman, S. M., FG, L. R., and .... 2007. "Finasteride and high-grade prostate cancer in the Prostate Cancer Prevention Trial." Journal of the National Cancer Institute 99 (18): 1375-83. https://doi.org/10.1093/jnci/djm117
MLA 9
Lucia, M. S., et al. "Finasteride and high-grade prostate cancer in the Prostate Cancer Prevention Trial." Journal of the National Cancer Institute, vol. 99, no. 18, 2007, pp. 1375-83. doi:10.1093/jnci/djm117.
PMID
17848673 ↗
🏷️ 키워드 / MeSH 📖 같은 키워드 OA만
- Black or African American
- Aged
- Anticarcinogenic Agents
- Bias
- Biopsy
- Needle
- Confounding Factors
- Epidemiologic
- Enzyme Inhibitors
- Finasteride
- Humans
- Incidence
- Logistic Models
- Male
- Middle Aged
- Prostate-Specific Antigen
- Prostatectomy
- Prostatic Neoplasms
- Severity of Illness Index
- United States
- White People
인용 관계
그래프 OA 노드: 8/8 (100%)
· 참조 0편 · 후속 8편
이 논문을 인용한 후속 연구 17
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- Case-only Methods Identified Genetic Loci Predicting a Subgroup of Men with Reduced Risk of High-gra…
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같은 제1저자의 인용 많은 논문 (3)
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