Performance of clinicopathologic models in men with high risk localized prostate cancer: impact of a 22-gene genomic classifier.


Journal

Prostate cancer and prostatic diseases
ISSN: 1476-5608
Titre abrégé: Prostate Cancer Prostatic Dis
Pays: England
ID NLM: 9815755

Informations de publication

Date de publication:
12 2020
Historique:
received: 28 10 2019
accepted: 09 03 2020
revised: 24 01 2020
pubmed: 2 4 2020
medline: 18 9 2021
entrez: 2 4 2020
Statut: ppublish

Résumé

Prostate cancer exhibits biological and clinical heterogeneity even within established clinico-pathologic risk groups. The Decipher genomic classifier (GC) is a validated method to further risk-stratify disease in patients with prostate cancer, but its performance solely within National Comprehensive Cancer Network (NCCN) high-risk disease has not been undertaken to date. A multi-institutional retrospective study of 405 men with high-risk prostate cancer who underwent primary treatment with radical prostatectomy (RP) or radiation therapy (RT) with androgen-deprivation therapy (ADT) at 11 centers from 1995 to 2005 was performed. Cox proportional hazards models were used to determine the hazard ratios (HR) for the development of metastatic disease based on clinico-pathologic variables, risk groups, and GC score. The area under the receiver operating characteristic curve (AUC) was determined for regression models without and with the GC score. Over a median follow-up of 82 months, 104 patients (26%) developed metastatic disease. On univariable analysis, increasing GC score was significantly associated with metastatic disease ([HR]: 1.34 per 0.1 unit increase, 95% confidence interval [CI]: 1.19-1.50, p < 0.001), while age, serum PSA, biopsy GG, and clinical T-stage were not (all p > 0.05). On multivariable analysis, GC score (HR: 1.33 per 0.1 unit increase, 95% CI: 1.19-1.48, p < 0.001) and GC high-risk (vs low-risk, HR: 2.95, 95% CI: 1.79-4.87, p < 0.001) were significantly associated with metastasis. The addition of GC score to regression models based on NCCN risk group improved model AUC from 0.46 to 0.67, and CAPRA from 0.59 to 0.71. Among men with high-risk prostate cancer, conventional clinico-pathologic data had poor discrimination to risk stratify development of metastatic disease. GC score was a significant and independent predictor of metastasis and may help identify men best suited for treatment intensification/de-escalation.

Sections du résumé

BACKGROUND
Prostate cancer exhibits biological and clinical heterogeneity even within established clinico-pathologic risk groups. The Decipher genomic classifier (GC) is a validated method to further risk-stratify disease in patients with prostate cancer, but its performance solely within National Comprehensive Cancer Network (NCCN) high-risk disease has not been undertaken to date.
METHODS
A multi-institutional retrospective study of 405 men with high-risk prostate cancer who underwent primary treatment with radical prostatectomy (RP) or radiation therapy (RT) with androgen-deprivation therapy (ADT) at 11 centers from 1995 to 2005 was performed. Cox proportional hazards models were used to determine the hazard ratios (HR) for the development of metastatic disease based on clinico-pathologic variables, risk groups, and GC score. The area under the receiver operating characteristic curve (AUC) was determined for regression models without and with the GC score.
RESULTS
Over a median follow-up of 82 months, 104 patients (26%) developed metastatic disease. On univariable analysis, increasing GC score was significantly associated with metastatic disease ([HR]: 1.34 per 0.1 unit increase, 95% confidence interval [CI]: 1.19-1.50, p < 0.001), while age, serum PSA, biopsy GG, and clinical T-stage were not (all p > 0.05). On multivariable analysis, GC score (HR: 1.33 per 0.1 unit increase, 95% CI: 1.19-1.48, p < 0.001) and GC high-risk (vs low-risk, HR: 2.95, 95% CI: 1.79-4.87, p < 0.001) were significantly associated with metastasis. The addition of GC score to regression models based on NCCN risk group improved model AUC from 0.46 to 0.67, and CAPRA from 0.59 to 0.71.
CONCLUSIONS
Among men with high-risk prostate cancer, conventional clinico-pathologic data had poor discrimination to risk stratify development of metastatic disease. GC score was a significant and independent predictor of metastasis and may help identify men best suited for treatment intensification/de-escalation.

Identifiants

pubmed: 32231245
doi: 10.1038/s41391-020-0226-2
pii: 10.1038/s41391-020-0226-2
pmc: PMC10184170
mid: NIHMS1893915
doi:

Substances chimiques

Biomarkers, Tumor 0
KLK3 protein, human EC 3.4.21.-
Kallikreins EC 3.4.21.-
Prostate-Specific Antigen EC 3.4.21.77

Types de publication

Journal Article Multicenter Study Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

646-653

Subventions

Organisme : NCI NIH HHS
ID : P50 CA186786
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA180984
Pays : United States
Organisme : NCI NIH HHS
ID : P50CA186786
Pays : United States

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Auteurs

Jeffrey J Tosoian (JJ)

Department of Urology, University of Michigan, Ann Arbor, MI, USA.

Samuel R Birer (SR)

Department of Radiation Oncology, University of Michigan, Ann Arbor, MI, USA.

R Jeffrey Karnes (R)

Department of Urology, Mayo Clinic, Rochester, MN, USA.

Jingbin Zhang (J)

Decipher Biosciences, Vancouver, BC, Canada.

Elai Davicioni (E)

Decipher Biosciences, Vancouver, BC, Canada.

Eric E Klein (EE)

Glickman Urological Institute, Cleveland Clinic, Cleveland, OH, USA.

Stephen J Freedland (SJ)

Department of Urology, Cedars-Sinai, Los Angeles, CA, USA.

Sheila Weinmann (S)

Center for Health Research, Kaiser Permanente, Portland, OR, USA.

Bruce J Trock (BJ)

Department of Urology, Johns Hopkins, Baltimore, MD, USA.

Robert T Dess (RT)

Department of Radiation Oncology, University of Michigan, Ann Arbor, MI, USA.

Shuang G Zhao (SG)

Department of Radiation Oncology, University of Michigan, Ann Arbor, MI, USA.

William C Jackson (WC)

Department of Radiation Oncology, University of Michigan, Ann Arbor, MI, USA.

Kosj Yamoah (K)

Department of Radiation Oncology, Moffitt Cancer Center, Tampa, FL, USA.

Alan Dal Pra (A)

Department of Radiation Oncology, University of Miami, Miami, FL, USA.

Brandon A Mahal (BA)

Department of Radiation Oncology, Brigham Women's Hospital, Boston, MA, USA.

Todd M Morgan (TM)

Department of Urology, University of Michigan, Ann Arbor, MI, USA.

Rohit Mehra (R)

Department of Pathology, University of Michigan, Ann Arbor, MI, USA.

Samuel Kaffenberger (S)

Department of Urology, University of Michigan, Ann Arbor, MI, USA.

Simpa S Salami (SS)

Department of Urology, University of Michigan, Ann Arbor, MI, USA.

Christopher Kane (C)

Department of Urology, University of California San Diego, San Diego, CA, USA.

Alan Pollack (A)

Department of Radiation Oncology, University of Miami, Miami, FL, USA.

Robert B Den (RB)

Department of Radiation Oncology, Thomas Jefferson, Philadelphia, PA, USA.

Alejandro Berlin (A)

Department of Radiation Oncology, Princess Margaret Hospital, Toronto, ON, Canada.

Edward M Schaeffer (EM)

Department of Urology and Polsky Urologic Cancer Institute, Northwestern University, Chicago, IL, USA.

Paul L Nguyen (PL)

Department of Radiation Oncology, Brigham Women's Hospital, Boston, MA, USA.

Felix Y Feng (FY)

Department of Radiation Oncology, University of California San Francisco, San Francisco, CA, USA.

Daniel E Spratt (DE)

Department of Radiation Oncology, University of Michigan, Ann Arbor, MI, USA. sprattda@med.umich.edu.

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Classifications MeSH