2016Journal of Clinical OncologyRequires access

Identifying candidates for prednisone to dexamethasone switch amongst patients with castration-resistant prostate cancer undergoing abiraterone therapy.

Vanessa Sarah Arciero, Kelly Lien, Erica J. McDonald, Esther K. Lee, Phillip Blanchette, Urban Emmenegger

Open publisher page 1 citations

Abstract

e16568 Background: Abiraterone plus prednisone (AA+P) delays symptomatic progression, palliates symptoms, and improves survival of pts with castration-resistant prostate cancer (CRPC). While inherent or acquired therapeutic resistance limits the benefit of AA+P, emerging data suggest that a switch from prednisone to dexamethasone (D) may achieve durable biochemical responses in CRPC pts progressing on AA+P. Methods: To better understand who may benefit from a steroid switch, we analyzed the outcome of pts switched to AA+D upon biochemical progression on AA+P, among CRPC pts treated at Sunnybrook Odette Cancer Centre, Toronto, Canada. Pts were included if they had undergone AA+D therapy (D 0.5 or 1.0 mg po daily) for at least 12 weeks. Results: 18 pts fit the inclusion criteria, of which 11 were chemotherapy-naïve, and 7 had received prior docetaxel. None had received P or D monotherapy previously. 8 pts (44%) achieved a > 50% PSA reduction with AA+P (PSA50), and 3 pts (17%) had a > 30% PSA response (PSA30). In 6 pts (33%) we found PSA stabilization (PSA-SD) as best response, whereas 1 pt (6%) biochemically progressed on AA+P. Mean (±SD) AA+P treatment duration was 213.44 (±151.24) days. Upon switch to AA+D, 5 pts (28%) achieved a PSA50, 1 pt (6%) a PSA30, PSA remained stable in 11 pts (61%), and 1 pt (6%) progressed biochemically. 6 pts are still continuing on AA+D after a median follow-up of 278 days. Amongst 11 AA+P responders (ie PSA50 or PSA30), 4 pts also achieved a sustained PSA50 on AA+D (202, 251, 399+, 587+ days), and 1 pt a PSA30 (274+). By contrast, only 1 of the 7 AA+P non-responders (14%) achieved a PSA response. Prior docetaxel did not affect the response to steroid switching. No unexpected adverse events were observed. Further data is being collected prospectively. Conclusions: In these mostly chemotherapy-naïve CRPC pts undergoing AA therapy, switching from P to D resulted in sustained PSA50 or PSA30 in 33% of pts. Whereas responses were seen in 5 of 11 pts (45%) with prior response to AA+P, the benefit of a P to D switch seems to be very limited in pts without prior response to AA+P.

About this research paper

What this paper is about

e16568 Background: Abiraterone plus prednisone (AA+P) delays symptomatic progression, palliates symptoms, and improves survival of pts with castration-resistant prostate cancer (CRPC). While inherent or acquired therapeutic resistance limits the benefit of AA+P, emerging data suggest that a switch from prednisone to dexamethasone (D) may achieve durable biochemical responses in CRPC pts progressing on AA+P. Methods: To better understand who may benefit from a steroid switch, we analyzed the outcome of pts switched to AA+D upon biochemical progression on AA+P, among CRPC pts treated at Sunnybrook Odette Cancer Centre, Toronto, Canada. Pts were included if they had undergone AA+D therapy (D 0.5 or 1.0 mg po daily) for at least 12 weeks. Results: 18 pts fit the inclusion criteria, of which 11 were chemotherapy-naïve, and 7 had received prior docetaxel. None had received P or D monotherapy previously. 8 pts (44%) achieved a > 50% PSA reduction with AA+P (PSA50), and 3 pts (17%) had a > 30% PSA response (PSA30). In 6 pts (33%) we found PSA stabilization (PSA-SD) as best response, whereas 1 pt (6%) biochemically progressed on AA+P. Mean (±SD) AA+P treatment duration was 213.44 (±151.24) days. Upon switch to AA+D, 5 pts (28%) achieved a PSA50, 1 pt (6%) a PSA30, PSA remained stable in 11 pts (61%), and 1 pt (6%) progressed biochemically. 6 pts are still continuing on AA+D after a median follow-up of 278 days. Amongst 11 AA+P responders (ie PSA50 or PSA30), 4 pts also achieved a sustained PSA50 on AA+D (202, 251, 399+, 587+ days), and 1 pt a PSA30 (274+). By contrast, only 1 of the 7 AA+P non-responders (14%) achieved a PSA response. Prior docetaxel did not affect the response to steroid switching. No unexpected adverse events were observed. Further data is being collected prospectively. Conclusions: In these mostly chemotherapy-naïve CRPC pts undergoing AA therapy, switching from P to D resulted in sustained PSA50 or PSA30 in 33% of pts. Whereas responses were seen in 5 of 11 pts (45%) with prior response to AA+P, the benefit of a P to D switch seems to be very limited in pts without prior response to AA+P.

Why it matters

OpenAlex reports 1 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

e16568 Background: Abiraterone plus prednisone (AA+P) delays symptomatic progression, palliates symptoms, and improves survival of pts with castration-resistant prostate cancer (CRPC). While inherent or acquired therapeutic resistance limits the benefit of AA+P, emerging data suggest that a switch from prednisone to dexamethasone (D) may achieve durable biochemical responses in CRPC pts progressing on AA+P. Methods: To better understand who may benefit from a steroid switch, we analyzed the outcome of pts switched to AA+D upon biochemical progression on AA+P, among CRPC pts treated at Sunnybrook Odette Cancer Centre, Toronto, Canada. Pts were included if they had undergone AA+D therapy (D 0.5 or 1.0 mg po daily) for at least 12 weeks. Results: 18 pts fit the inclusion criteria, of which 11 were chemotherapy-naïve, and 7 had received prior docetaxel. None had received P or D monotherapy previously. 8 pts (44%) achieved a > 50% PSA reduction with AA+P (PSA50), and 3 pts (17%) had a > 30% PSA response (PSA30). In 6 pts (33%) we found PSA stabilization (PSA-SD) as best response, whereas 1 pt (6%) biochemically progressed on AA+P. Mean (±SD) AA+P treatment duration was 213.44 (±151.24) days. Upon switch to AA+D, 5 pts (28%) achieved a PSA50, 1 pt (6%) a PSA30, PSA remained stable in 11 pts (61%), and 1 pt (6%) progressed biochemically. 6 pts are still continuing on AA+D after a median follow-up of 278 days. Amongst 11 AA+P responders (ie PSA50 or PSA30), 4 pts also achieved a sustained PSA50 on AA+D (202, 251, 399+, 587+ days), and 1 pt a PSA30 (274+). By contrast, only 1 of the 7 AA+P non-responders (14%) achieved a PSA response. Prior docetaxel did not affect the response to steroid switching. No unexpected adverse events were observed. Further data is being collected prospectively. Conclusions: In these mostly chemotherapy-naïve CRPC pts undergoing AA therapy, switching from P to D resulted in sustained PSA50 or PSA30 in 33% of pts. Whereas responses were seen in 5 of 11 pts (45%) with prior response to AA+P, the benefit of a P to D switch seems to be very limited in pts without prior response to AA+P.

Key concepts: Medicine, Prednisone, Prostate cancer, Docetaxel, Dexamethasone, Internal medicine, Abiraterone acetate, Cancer

Related papers

Back to paper searchBrowse research topicsOriginal source
Identifying candidates for prednisone to dexamethasone switch amongst patients with castration-resistant prostate cancer undergoing abiraterone therapy. — Research Paper | ScholarLens