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[Cancer Research 59, 2511-2515, June 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 2511-2515, June 1, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Selection for Androgen Receptor Mutations in Prostate Cancers Treated with Androgen Antagonist1

Mary-Ellen Taplin, Glenn J. Bubley, Yoo-Joung Ko, Eric J. Small, Melissa Upton, Barur Rajeshkumar and Steven P. Balk2

University of Massachusetts Cancer Center, Worcester, Massachusetts 01655 [M-E. T., B. R.]; Cancer Biology Program-Hematology/Oncology Division [G. J. B., S. P. B.], Clinical Investigator Training Program, Beth Israel Deaconess Medical Center-Harvard/Massachusetts Institute of Technology Health Sciences and Technology, in collaboration with Pfizer, Inc. [Y-J. K.], and Pathology Department [M. U.], Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215; and Urologic Oncology Program, University of California at San Francisco-Mount Zion Cancer Center, San Francisco, California 94120 [E. J. S.]

The role of androgen receptor (AR) mutations in androgen-independent prostate cancer (PCa) was determined by examining AR transcripts and genes from a large series of bone marrow metastases. Mutations were found in 5 of 16 patients who received combined androgen blockade with the AR antagonist flutamide, and these mutant ARs were strongly stimulated by flutamide. In contrast, the single mutant AR found among 17 patients treated with androgen ablation monotherapy was not flutamide stimulated. Patients with flutamide-stimulated AR mutations responded to subsequent treatment with bicalutamide, an AR antagonist that blocks the mutant ARs. These findings demonstrate that AR mutations occur in response to strong selective pressure from flutamide treatment.




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