Journal of Clinical Oncology, Vol 15, 2928-2938, Copyright © 1997 by American Society of Clinical Oncology
Bicalutamide for advanced prostate cancer: the natural versus treated history of disease
HI Scher, C Liebertz, WK Kelly, M Mazumdar, C Brett, L Schwartz, G Kolvenbag, L Shapiro and M Schwartz
Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA. scherh@mskcc.org
PURPOSE: To determine the therapeutic effects of bicalutamide 200 mg in
patients with prostate cancers of different hormone sensitivities. METHODS:
Patients with progressive prostate cancer were treated with bicalutamide
200 mg daily. Before treatment, patients' tumors were classified on the
basis of prior hormone exposure and by serum testosterone levels into
androgen-dependent and androgen-independent groups. Prior exposure to
flutamide and response to flutamide withdrawal was also considered.
Outcomes were reported independently on the basis of posttherapy changes in
prostate-specific antigen (PSA), measurable disease, and radionuclide bone
scans. RESULTS: Outcomes varied by prior hormone exposure as a higher
proportion of patients with progression of androgen-dependent tumors showed
posttherapy PSA decreases of more than 50% or more than 80%, measurable
disease regression, and improvement on radionuclide bone scans than did
patients with androgen-independent progression. Within the category of
androgen-independent progression, clinical benefit was observed in patients
who had previously progressed on flutamide, independent of the response to
flutamide withdrawal. Patients who had progressed on a
gonadotropin-releasing hormone (GnRH) analog alone had a low response
proportion, whereas those who progressed after two or more hormone
therapies did not respond. Overall, the drug was well tolerated. After
progression on bicalutamide monotherapy, one third of patients with
androgen-dependent progression responded to medical castration with a GnRH
analog. CONCLUSION: Classifying patient tumors on the basis of prior
hormone exposure permits a more precise estimate of the potential benefit
of a specific hormone therapy for the individual patient. The precision is
further increased by reporting the effects of a drug on each parameter of
disease independently. The difference in outcomes for patients with
androgen-independent progression suggests that the specific hormone therapy
administered and the response to that therapy can influence the biology of
the relapsing tumor and the sensitivity to subsequent therapies. The
sensitivity to bicalutamide after progression on flutamide deserves further
study.
This article has been cited by other articles:
|
|
|
|
 
X. Yuan, T. Li, H. Wang, T. Zhang, M. Barua, R. A. Borgesi, G. J. Bubley, M. L. Lu, and S. P. Balk
Androgen Receptor Remains Critical for Cell-Cycle Progression in Androgen-Independent CWR22 Prostate Cancer Cells
Am. J. Pathol.,
August 1, 2006;
169(2):
682 - 696.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. I. Scher and C. L. Sawyers
Biology of Progressive, Castration-Resistant Prostate Cancer: Directed Therapies Targeting the Androgen-Receptor Signaling Axis
J. Clin. Oncol.,
November 10, 2005;
23(32):
8253 - 8261.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
O. Smaletz, H. I. Scher, E. J. Small, D. A. Verbel, A. McMillan, K. Regan, W. K. Kelly, and M. W. Kattan
Nomogram for Overall Survival of Patients With Progressive Metastatic Prostate Cancer After Castration
J. Clin. Oncol.,
October 1, 2002;
20(19):
3972 - 3982.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Masiello, S. Cheng, G. J. Bubley, M. L. Lu, and S. P. Balk
Bicalutamide Functions as an Androgen Receptor Antagonist by Assembly of a Transcriptionally Inactive Receptor
J. Biol. Chem.,
July 12, 2002;
277(29):
26321 - 26326.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C.-Y. Chang, P. J. Walther, and D. P. McDonnell
Glucocorticoids Manifest Androgenic Activity in a Cell Line Derived from a Metastatic Prostate Cancer
Cancer Res.,
December 1, 2001;
61(24):
8712 - 8717.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. E. Taplin and S.-M. Ho
The Endocrinology of Prostate Cancer
J. Clin. Endocrinol. Metab.,
August 1, 2001;
86(8):
3467 - 3477.
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. McDonald, L. Brive, D. B. Agus, H. I. Scher, and K. R. Ely
Ligand Responsiveness in Human Prostate Cancer: Structural Analysis of Mutant Androgen Receptors from LNCaP and CWR22 Tumors
Cancer Res.,
May 1, 2000;
60(9):
2317 - 2322.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
M.-E. Taplin, G. J. Bubley, Y.-J. Ko, E. J. Small, M. Upton, B. Rajeshkumar, and S. P. Balk
Selection for Androgen Receptor Mutations in Prostate Cancers Treated with Androgen Antagonist
Cancer Res.,
June 1, 1999;
59(11):
2511 - 2515.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
