Efficacy of PSMA ligand PET-based radiotherapy for recurrent prostate cancer after radical prostatectomy and salvage radiotherapy.
Aged
Antigens, Surface
/ metabolism
Combined Modality Therapy
Follow-Up Studies
Glutamate Carboxypeptidase II
/ metabolism
Humans
Ligands
Male
Middle Aged
Neoplasm Metastasis
Neoplasm Recurrence, Local
/ diagnostic imaging
Positron-Emission Tomography
/ methods
Prognosis
Prostatectomy
Prostatic Neoplasms
/ diagnostic imaging
Radiotherapy, Image-Guided
Retrospective Studies
Salvage Therapy
/ methods
Survival Rate
Oligometastases
PSMA
Prostate cancer
Radical prostatectomy
Radiotherapy
Recurrence
Journal
BMC cancer
ISSN: 1471-2407
Titre abrégé: BMC Cancer
Pays: England
ID NLM: 100967800
Informations de publication
Date de publication:
29 Apr 2020
29 Apr 2020
Historique:
received:
20
01
2020
accepted:
21
04
2020
entrez:
1
5
2020
pubmed:
1
5
2020
medline:
23
1
2021
Statut:
epublish
Résumé
A substantial number of patients will develop further biochemical progression after radical prostatectomy (RP) and salvage radiotherapy (sRT). Recently published data using prostate-specific membrane antigen ligand positron emission tomography (PSMA - PET) for re-staging suggest that those recurrences are often located outside the prostate fossa and most of the patients have a limited number of metastases, making them amenable to metastasis-directed treatment (MDT). We analyzed 78 patients with biochemical progression after RP and sRT from a retrospective European multicenter database and assessed the biochemical recurrence-free survival (bRFS; PSA < nadir + 0.2 ng/ml or no PSA decline) as well as the androgen deprivation therapy- free survival (ADT-FS) using Kaplan-Meier curves. Log-rank test and multivariate analysis was performed to determine influencing factors. A total of 185 PSMA - PET positive metastases were detected and all lesions were treated with radiotherapy (RT). Concurrent ADT was prescribed in 16.7% (13/78) of patients. The median PSA level before RT was 1.90 ng/mL (range, 0.1-22.1) and decreased statistically significantly to a median PSA nadir level of 0.26 ng/mL (range, 0.0-12.25; p < 0.001). The median PSA level of 0.88 ng/mL (range, 0.0-25.8) at the last follow-up was also statistically significantly lower (p = 0.008) than the median PSA level of 1.9 ng/mL (range, 0.1-22.1) before RT. The median bRFS was 17.0 months (95% CI, 14.2-19.8). After 12 months, 55.3% of patients were free of biochemical progression. Multivariate analyses showed that concurrent ADT was the most important independent factor for bRFS (p = 0.01). The median ADT-FS was not reached and exploratory statistical analyses estimated a median ADT-FS of 34.0 months (95% CI, 16.3-51.7). Multivariate analyses revealed no significant parameters for ADT-FS. RT as MDT based on PSMA - PET of all metastases of recurrent prostate cancer after RP and sRT represents a viable treatment option for well-informed and well-selected patients.
Sections du résumé
BACKGROUND
BACKGROUND
A substantial number of patients will develop further biochemical progression after radical prostatectomy (RP) and salvage radiotherapy (sRT). Recently published data using prostate-specific membrane antigen ligand positron emission tomography (PSMA - PET) for re-staging suggest that those recurrences are often located outside the prostate fossa and most of the patients have a limited number of metastases, making them amenable to metastasis-directed treatment (MDT).
METHODS
METHODS
We analyzed 78 patients with biochemical progression after RP and sRT from a retrospective European multicenter database and assessed the biochemical recurrence-free survival (bRFS; PSA < nadir + 0.2 ng/ml or no PSA decline) as well as the androgen deprivation therapy- free survival (ADT-FS) using Kaplan-Meier curves. Log-rank test and multivariate analysis was performed to determine influencing factors.
RESULTS
RESULTS
A total of 185 PSMA - PET positive metastases were detected and all lesions were treated with radiotherapy (RT). Concurrent ADT was prescribed in 16.7% (13/78) of patients. The median PSA level before RT was 1.90 ng/mL (range, 0.1-22.1) and decreased statistically significantly to a median PSA nadir level of 0.26 ng/mL (range, 0.0-12.25; p < 0.001). The median PSA level of 0.88 ng/mL (range, 0.0-25.8) at the last follow-up was also statistically significantly lower (p = 0.008) than the median PSA level of 1.9 ng/mL (range, 0.1-22.1) before RT. The median bRFS was 17.0 months (95% CI, 14.2-19.8). After 12 months, 55.3% of patients were free of biochemical progression. Multivariate analyses showed that concurrent ADT was the most important independent factor for bRFS (p = 0.01). The median ADT-FS was not reached and exploratory statistical analyses estimated a median ADT-FS of 34.0 months (95% CI, 16.3-51.7). Multivariate analyses revealed no significant parameters for ADT-FS.
CONCLUSIONS
CONCLUSIONS
RT as MDT based on PSMA - PET of all metastases of recurrent prostate cancer after RP and sRT represents a viable treatment option for well-informed and well-selected patients.
Identifiants
pubmed: 32349700
doi: 10.1186/s12885-020-06883-5
pii: 10.1186/s12885-020-06883-5
pmc: PMC7191762
doi:
Substances chimiques
Antigens, Surface
0
Ligands
0
FOLH1 protein, human
EC 3.4.17.21
Glutamate Carboxypeptidase II
EC 3.4.17.21
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
362Références
Eur Urol. 2017 Apr;71(4):630-642
pubmed: 27591931
J Urol. 2013 Aug;190(2):441-9
pubmed: 23707439
Lancet Oncol. 2016 Jun;17(6):747-756
pubmed: 27160475
J Nucl Med. 2019 Jul;60(7):963-970
pubmed: 30552203
J Nucl Med. 2018 Feb;59(2):230-237
pubmed: 29123013
Int J Radiat Oncol Biol Phys. 2019 Jan 1;103(1):95-104
pubmed: 30201438
Eur Urol. 2018 Oct;74(4):455-462
pubmed: 30227924
Eur Urol. 2019 Jan;75(1):88-99
pubmed: 29673712
J Clin Oncol. 2018 Feb 10;36(5):446-453
pubmed: 29240541
Int J Radiat Oncol Biol Phys. 2019 Jul 15;104(4):801-808
pubmed: 30890448
J Clin Oncol. 2018 Apr 10;36(11):1080-1087
pubmed: 29384722
N Engl J Med. 2019 Jul 11;381(2):121-131
pubmed: 31157964
Eur Urol Oncol. 2018 Dec;1(6):531-537
pubmed: 31158100
Radiat Oncol. 2014 Jun 12;9:135
pubmed: 24920079
Eur Urol Oncol. 2019 Sep 23;:
pubmed: 31558422
Bioconjug Chem. 2012 Apr 18;23(4):688-97
pubmed: 22369515
Eur Urol. 2018 Feb;73(2):178-211
pubmed: 28655541
Prostate. 2018 Jul;78(10):753-757
pubmed: 29663462
Radiother Oncol. 2010 Jul;96(1):1-5
pubmed: 20566227
Eur J Nucl Med Mol Imaging. 2017 Jun;44(6):1014-1024
pubmed: 28283702
BJU Int. 2016 May;117(5):732-9
pubmed: 26683282
Nat Rev Urol. 2017 Jan;14(1):15-25
pubmed: 27725639
J Nucl Med. 2018 Jan;59(1):82-88
pubmed: 28646014
N Engl J Med. 2017 Feb 2;376(5):417-428
pubmed: 28146658
Br J Cancer. 2017 Jun 6;116(12):1520-1525
pubmed: 28449007
Lancet. 2018 Dec 1;392(10162):2353-2366
pubmed: 30355464
Eur J Nucl Med Mol Imaging. 2017 Aug;44(8):1258-1268
pubmed: 28497198
Lancet Oncol. 2018 Oct;19(10):e534-e545
pubmed: 30303127
Eur Urol. 2017 Apr;71(4):618-629
pubmed: 27568654
Eur Urol Focus. 2019 Sep 5;:
pubmed: 31495759
Crit Rev Oncol Hematol. 2019 Jun;138:24-28
pubmed: 31092381
Eur Urol Focus. 2019 Mar;5(2):144-146
pubmed: 30612936