Atıf İçin Kopyala
Chen L. W., Tuaç Y., Li S., Leeman J. E., King M. T., Orio P. F., ...Daha Fazla
CANCERS, cilt.17, sa.7, ss.1-16, 2025 (SCI-Expanded)
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Yayın Türü:
Makale / Tam Makale
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Cilt numarası:
17
Sayı:
7
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Basım Tarihi:
2025
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Doi Numarası:
10.3390/cancers17071055
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Dergi Adı:
CANCERS
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Derginin Tarandığı İndeksler:
Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, CINAHL, EMBASE, Veterinary Science Database, Directory of Open Access Journals
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Sayfa Sayıları:
ss.1-16
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Ankara Üniversitesi Adresli:
Evet
Özet
Background: Gleason score (GS) 10 prostate cancer (PC) is a highly aggressive localized disease. Despite advances in treating high-risk PC, the clinical outcomes and molecular underpinnings of GS 10 remain unclear. This study aimed to determine whether GS 10 PC has distinct clinical outcomes from other “high-risk” cancers (i.e., Gleason 8–9) and identify genomic alterations driving its aggressive phenotype. Methods: A retrospective review of The Cancer Genome Atlas database identified patients with GS 8–10 PC who underwent radical prostatectomy. Clinical factors were compared between GS 10 and GS 8–9 cohorts. Time to biochemical recurrence (BCR) was analyzed using Kaplan–Meier and Cox regression. RNA sequencing identified differentially expressed genes, and protein–protein interaction networks identified hub genes. Results: Of 192 patients, 13 (6.8%) had GS 10 PC. After median follow-up of 37.87 months, GS 10 status was associated with significantly lower time to BCR (AHR, 2.67; 95% CI, 1.18–6.02; p = 0.018) compared to GS 8–9. Multiple genes (e.g., RAD54L, FAAH, AATK, MAST2) showed higher alteration frequencies, and high expression of RAD54L, MAST2, and CCHCR1 correlated with shorter disease-free survival. Six overlapping hub genes (CD8A, CDC20, E2F1, IL10, TNF, VCAM1) were overexpressed in GS 10 tumors, reflecting key pathways in tumor progression. Conclusions: GS 10 PC confers inferior time to BCR and displays a distinct genomic landscape compared to GS 8–9 disease, highlighting the need for biomarker-driven therapeutic strategies. Further studies are needed to validate these genomic targets and improve management for this very high-risk population.