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EDITORIAL COMMENT

The authors are to be congratulated for their study examining PSA response to hormonal therapy manipulations in black and white men to determine potential racial differences in the behavior of androgen independent prostate cancer. They found no racial difference in PSA nadir after gonadal androgen withdrawal, time to PSA relapse or PSA doubling time during relapse. Furthermore, the PSA response to deferred flutamide treatment and flutamide withdrawal was the same in black and white patients. Based on these data the authors concluded that the biology of androgen independent prostate cancer was similar for white and black patients.

Although the article is well written and timely, provides new information and addresses an important problem, there are several concerns. Most importantly, the study represents an older patient population (mean ages 72.8 and 71.5 years) and may not be repre- sentative of younger black and white patients. Powell et al recently

demonstrated an ethnic survival crossover based on age. African American men had a worse survival than American white men younger than 65 years but a better survival a t older ages.' The cause of this phenomenon is as yet unknown but the present study must be duplicated in younger black and white men.

Another concern is that this cohort (and other cohorts) of African American men may not be representative of this population in gen- eral. The definition of race, defined as African American, is unclear and there is clearly phenotypic heterogeneity. A proposed common denominator of this group is a diet high in fat that may contribute to prostate cancer progression.2 I t is possible that this cohort of older, lower socioeconomic black patients may have a different diet and, therefore, different prostate cancer behavior. Further studies must be performed comparing diet, socioeconomic status and prostate cancer. Could it be that as African Americans increase the socioeco- nomic status and diet, a diet change to increased fat has potentiated prostate cancer risk and behavior? The age crossover effect reported by Powell et a1 must be studied in this context' and the current study needs confirmation in other cohorts.

Finally, there is now concern that PSA may not mirror the biolog- ical behavior of metastatic prostate cancer as previously assumed. In the National Cancer Instituk 0105 Intergroup Study of orchiectomy and flutamide versus orchiectomy and placebo in more than 1,300 men with metastatic prostate cancer the PSA response did not cor- relate with survival. Although the flutamide group had a superior PSA response compared to the placebo group, the survival in the 2 groups was the same (D. Crawford, personal communication). These data throw into question the value of PSA as a surrogate end point for survival in advanced prostate cancer. Similarly, to use PSA derivatives to make conclusions regarding the behavior of androgen independent prostate cancer, as does the current study, may be somewhat naive. Despite these concerns, it was reassuring to see that in this cohort the African American patients derived similar benefit from hormonal therapy and again the authors should be congratulated for their continued important contributions.

Judd W. M o d Department of Surgery Uniformed Services University of the Health Sciences Bethesda, Maryland

1. Powell, I. J., Schwartz, K. and Hussain, M.: Removal of the financial barrier to health care: does it impact on prostate cancer a t presentation and survival? A comparative study between black and white men in a Veteran Affairs system. Urology, 146 825, 1995.

2. Gao, X., Grignon, D. J., Chbihi, T., Zacharek, A,, Chen, Y. Q., Sakr, W., Porter, A. T., Crissman, J. D., Pontes, J. E., Powell, I. J. and Hohn, K V.: Elevated 12-lipoxygenase mRNA expres- sion correlates with advanced stage and poor differentiation of human prostate cancer. Urology, 46: 227, 1996.

REPLY BY AUTHOR

We do not believe that the preliminary results of the National Cancer Institute 0105 Intergroup Study, in which we participate, are relevant to our observations. More specifically, the findings have no bearing on the considerable body of evidence that PSA nadir and time to PSA elevation after hormonal therapies are important prog- nostic variables or that PSA doubling time correlates with clinical measures of tumor growth.