dc.contributor.author | Bryce, AH | |
dc.contributor.author | Alumkal, JJ | |
dc.contributor.author | Armstrong, A | |
dc.contributor.author | Higano, CS | |
dc.contributor.author | Iversen, P | |
dc.contributor.author | Sternberg, CN | |
dc.contributor.author | Rathkopf, D | |
dc.contributor.author | Loriot, Y | |
dc.contributor.author | de Bono, J | |
dc.contributor.author | Tombal, B | |
dc.contributor.author | Abhyankar, S | |
dc.contributor.author | Lin, P | |
dc.contributor.author | Krivoshik, A | |
dc.contributor.author | Phung, D | |
dc.contributor.author | Beer, TM | |
dc.date.accessioned | 2017-03-01T12:14:37Z | |
dc.date.issued | 2017-06-01 | |
dc.identifier.citation | Prostate cancer and prostatic diseases, 2017, 20 (2), pp. 221 - 227 | |
dc.identifier.issn | 1365-7852 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/439 | |
dc.identifier.eissn | 1476-5608 | |
dc.identifier.doi | 10.1038/pcan.2016.71 | |
dc.description.abstract | BACKGROUND: Advanced prostate cancer is a phenotypically diverse disease that evolves through multiple clinical courses. PSA level is the most widely used parameter for disease monitoring, but it has well-recognized limitations. Unlike in clinical trials, in practice, clinicians may rely on PSA monitoring alone to determine disease status on therapy. This approach has not been adequately tested. METHODS: Chemotherapy-naive asymptomatic or mildly symptomatic men (n=872) with metastatic castration-resistant prostate cancer (mCRPC) who were treated with the androgen receptor inhibitor enzalutamide in the PREVAIL study were analyzed post hoc for rising versus nonrising PSA (empirically defined as >1.05 vs ⩽1.05 times the PSA level from 3 months earlier) at the time of radiographic progression. Clinical characteristics and disease outcomes were compared between the rising and nonrising PSA groups. RESULTS: Of 265 PREVAIL patients with radiographic progression and evaluable PSA levels on the enzalutamide arm, nearly one-quarter had a nonrising PSA. Median progression-free survival in this cohort was 8.3 months versus 11.1 months in the rising PSA cohort (hazard ratio 1.68; 95% confidence interval 1.26-2.23); overall survival was similar between the two groups, although less than half of patients in either group were still at risk at 24 months. Baseline clinical characteristics of the two groups were similar. CONCLUSIONS: Non-rising PSA at radiographic progression is a common phenomenon in mCRPC patients treated with enzalutamide. As restaging in advanced prostate cancer patients is often guided by increases in PSA levels, our results demonstrate that disease progression on enzalutamide can occur without rising PSA levels. Therefore, a disease monitoring strategy that includes imaging not entirely reliant on serial serum PSA measurement may more accurately identify disease progression. | |
dc.format | Print-Electronic | |
dc.format.extent | 221 - 227 | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | NATURE PUBLISHING GROUP | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0 | |
dc.subject | Humans | |
dc.subject | Disease Progression | |
dc.subject | Phenylthiohydantoin | |
dc.subject | Prostate-Specific Antigen | |
dc.subject | Antineoplastic Agents | |
dc.subject | Disease-Free Survival | |
dc.subject | Treatment Outcome | |
dc.subject | Proportional Hazards Models | |
dc.subject | Drug Resistance, Neoplasm | |
dc.subject | Aged | |
dc.subject | Middle Aged | |
dc.subject | Male | |
dc.subject | Prostatic Neoplasms, Castration-Resistant | |
dc.title | Radiographic progression with nonrising PSA in metastatic castration-resistant prostate cancer: post hoc analysis of PREVAIL. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2016-11-29 | |
rioxxterms.versionofrecord | 10.1038/pcan.2016.71 | |
rioxxterms.licenseref.uri | https://creativecommons.org/licenses/by-nc-sa/4.0 | |
rioxxterms.licenseref.startdate | 2017-06 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | Prostate cancer and prostatic diseases | |
pubs.issue | 2 | |
pubs.notes | No embargo | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Clinical Studies | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Clinical Studies/Prostate Cancer Targeted Therapy Group | |
pubs.organisational-group | /ICR/Primary Group/Royal Marsden Clinical Units | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Clinical Studies | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Clinical Studies/Prostate Cancer Targeted Therapy Group | |
pubs.organisational-group | /ICR/Primary Group/Royal Marsden Clinical Units | |
pubs.publication-status | Published | |
pubs.volume | 20 | |
pubs.embargo.terms | No embargo | |
icr.researchteam | Prostate Cancer Targeted Therapy Group | |
dc.contributor.icrauthor | De Bono, Johann | |