The Role of Fast and Deep PSA Response in Castration-sensitive Prostate Cancer.


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
01 2022
Historique:
received: 28 07 2021
revised: 12 11 2021
accepted: 16 11 2021
entrez: 31 12 2021
pubmed: 1 1 2022
medline: 5 1 2022
Statut: ppublish

Résumé

Outcomes of castration-sensitive prostate cancer (CSPC) have improved owing to new therapies and early treatment, previously reserved for castration-resistant disease (CRPC). Prostatic-specific antigen (PSA) remains the most used marker to follow-up patients under treatment, but only limited data are available about the prognostic role of its changes over time and the impact of response to subsequent therapies. This analysis aims to assess the prognostic role of the magnitude and velocity of PSA response in CSPC and describe how this may affect the outcome to subsequent treatment outcomes in CRPC. A retrospective analysis was performed on patients with de novo CSPC referring to six oncology centers in Italy. Clinical and pathological features were recorded. PSA response (PSA50), defined as a decrease > 50% compared to baseline, PSA velocity (PSAv), defined as any decrease in PSA levels over time and the deep and fast PSA response (4mPSA50), defined as the PSA response reached within the threshold of 4 months from the beginning of androgen deprivation therapy (ADT) have been evaluated for their impact on survival. Survivals were estimated using the Kaplan-Meier method and compared across groups using the log-rank test. Cox proportional-hazard models, stratified according to baseline characteristics, were used to estimate hazard ratios for overall survival (OS). A totals of 94.4% of patients had PSA50, which was correlated to longer OS compared to patients without PSA50 (56.0 vs. 14.8 months; p<0.001). The median PSAv was 6.9 (ng/dl)/month, which was predictive for longer OS: Each decrease of 1 (ng/dl)/month was able to improve OS by 0.2% (HR=0.998, 95%CI=0.997-1.000; p=0.008). A total of 47.9% of patients reached 4mPSA50, with a median OS and progression-free survival (PFS) to ADT-based therapy of 101.0 and 23.4 months compared to 41.9 and 11.0 months for those who did not (p<0.001), respectively. The independent prognostic role of 4mPSA50 was retained even when evaluated in multivariable analysis adjusted for other baseline characteristics and early docetaxel for CSPC. In CRPC, 4mPSA50 evaluated during CSPC retains its prognostic role even if it does not predict a different outcome between patients treated with abiraterone/enzalutamide or taxanes. Achieving a deep and fast PSA response correlates with a better outcome in patients with de novo mCSPC, also positively influencing the prognosis of the subsequent first-line therapy for CRPC disease.

Sections du résumé

BACKGROUND
Outcomes of castration-sensitive prostate cancer (CSPC) have improved owing to new therapies and early treatment, previously reserved for castration-resistant disease (CRPC). Prostatic-specific antigen (PSA) remains the most used marker to follow-up patients under treatment, but only limited data are available about the prognostic role of its changes over time and the impact of response to subsequent therapies. This analysis aims to assess the prognostic role of the magnitude and velocity of PSA response in CSPC and describe how this may affect the outcome to subsequent treatment outcomes in CRPC.
PATIENTS AND METHODS
A retrospective analysis was performed on patients with de novo CSPC referring to six oncology centers in Italy. Clinical and pathological features were recorded. PSA response (PSA50), defined as a decrease > 50% compared to baseline, PSA velocity (PSAv), defined as any decrease in PSA levels over time and the deep and fast PSA response (4mPSA50), defined as the PSA response reached within the threshold of 4 months from the beginning of androgen deprivation therapy (ADT) have been evaluated for their impact on survival. Survivals were estimated using the Kaplan-Meier method and compared across groups using the log-rank test. Cox proportional-hazard models, stratified according to baseline characteristics, were used to estimate hazard ratios for overall survival (OS).
RESULTS
A totals of 94.4% of patients had PSA50, which was correlated to longer OS compared to patients without PSA50 (56.0 vs. 14.8 months; p<0.001). The median PSAv was 6.9 (ng/dl)/month, which was predictive for longer OS: Each decrease of 1 (ng/dl)/month was able to improve OS by 0.2% (HR=0.998, 95%CI=0.997-1.000; p=0.008). A total of 47.9% of patients reached 4mPSA50, with a median OS and progression-free survival (PFS) to ADT-based therapy of 101.0 and 23.4 months compared to 41.9 and 11.0 months for those who did not (p<0.001), respectively. The independent prognostic role of 4mPSA50 was retained even when evaluated in multivariable analysis adjusted for other baseline characteristics and early docetaxel for CSPC. In CRPC, 4mPSA50 evaluated during CSPC retains its prognostic role even if it does not predict a different outcome between patients treated with abiraterone/enzalutamide or taxanes.
CONCLUSION
Achieving a deep and fast PSA response correlates with a better outcome in patients with de novo mCSPC, also positively influencing the prognosis of the subsequent first-line therapy for CRPC disease.

Identifiants

pubmed: 34969722
pii: 42/1/165
doi: 10.21873/anticanres.15470
doi:

Substances chimiques

Prostate-Specific Antigen EC 3.4.21.77

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

165-172

Informations de copyright

Copyright © 2022 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Roberto Iacovelli (R)

Medical Oncology Unit, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy roberto.iacovelli@policlinicogemelli.it.

Chiara Ciccarese (C)

Medical Oncology Unit, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.

Orazio Caffo (O)

Department of Medical Oncology, Santa Chiara Hospital, Trento, Italy.

Ugo De Giorgi (U)

Department of Medical Oncology, Scientific Institute Romagnolo for the Study and Treatment of Cancer (IRST) IRCCS, Meldola, Italy.

Umberto Basso (U)

Medical Oncology Unit 1, Istituto Oncologico Veneto IOV IRCCS, Padua, Italy.

Marcello Tucci (M)

Division of Medical Oncology, Department of Oncology, University of Turin, San Luigi Gonzaga Hospital, Turin, Italy.

Claudia Mosillo (C)

Medical Oncology Unit, Azienda Ospedaliera Santa Maria di Terni, Terni, Italy.

Marco Maruzzo (M)

Medical Oncology Unit 1, Istituto Oncologico Veneto IOV IRCCS, Padua, Italy.

Francesca Maines (F)

Department of Medical Oncology, Santa Chiara Hospital, Trento, Italy.

Chiara Casadei (C)

Department of Medical Oncology, Scientific Institute Romagnolo for the Study and Treatment of Cancer (IRST) IRCCS, Meldola, Italy.

Michele Milella (M)

Medical Oncology Unit, Azienda Ospedaliera Universitaria Integrata (AOUI), Verona, Italy.

Giampaolo Tortora (G)

Medical Oncology Unit, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.

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Classifications MeSH