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Journal of Clinical Oncology, Vol 19, Issue 1 (January), 2001: 54-61
© 2001 American Society for Clinical Oncology

Equivalent Racial Outcome After Conformal Radiotherapy for Prostate Cancer: A Single Departmental Experience

By Philip P. Connell, Lani Ignacio, Daniel Haraf, Azhar M. Awan, Howard Halpern, Ibrahim Abdalla, Jaishanker Nautiyal, Ashesh B. Jani, Ralph R. Weichselbaum, Srinivasan Vijayakumar

From the Department of Radiation and Cellular Oncology, University of Chicago/University of Illinois/Micheal Reese Center for Radiation Therapy, University of Chicago, Chicago, IL.

Address reprint requests to Srinivasan Vijayakumar, MD, University of Illinois at Chicago, 1801 West Taylor St, OCC-C400, Chicago, IL 60612; email: vijay{at}jasmine.rado.uic.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
PURPOSE: African-American (AA) men with prostate cancer present with advanced disease, relative to white (W) men. This report summarizes our clinical and biochemical control (bNED) rates after conformal radiotherapy (RT). In particular, we aim to characterize any race-based outcome differences seen after comparable treatment.

PATIENTS AND METHODS: We reviewed 893 patients (418 AA and 475 W) with clinically localized prostate cancer treated between 1988 and 1997. Neoadjuvant hormonal blockade was used in 22.5% of cases, and all patients received conformal RT to a median dose of 68 Gy (range, 60 to 74.8 Gy). Biochemical failure was defined according to the American Society of Therapeutic Radiology and Oncology consensus definition. Median follow-up was 24 months (range, 1 to 114 months).

RESULTS: The 5-year actuarial survival, disease-free survival, and bNED rates for the entire population were 80.5%, 70.0%, and 57.6%, respectively. When classified by prognostic risk category, the 5-year actuarial bNED rates were 78.7% for favorable, 57.7% for intermediate, and 39.8% for unfavorable category patients. AA men presented at younger ages and with more advanced disease. Controlled for prognostic risk category, AA and W men had similar 5-year actuarial bNED rates in favorable (78% v 79%, P = .91), intermediate (52% v 62%, P = .44), and unfavorable categories (36% v 45%, P = .09). Race was not an independent prognostic factor (P = .36).

CONCLUSION: Conformal RT is equally effective for AA and W patients. More research is needed in order to understand and correct the advanced presentations in AA men. These data suggest a need for early screening in AA populations.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
FOR AMERICAN MEN, prostate cancer remains the second most common malignancy (after skin cancer) and the second most common cause of cancer-related death. The Surveillance, Epidemiology, and End Results program has consistently shown especially high rates of prostate cancer mortality among African-American (AA) men. In fact, AA men are approximately twice as likely to die from prostate cancer (53.7 per 100,000) compared with white (W) men (24.1 per 100,000).1-3

Most investigators agree that AA patients present with more advanced disease.4-6 However, it remains unclear whether prostate cancers are biologically more virulent in AA men or whether the mortality rates simply reflect differential access to early screening and treatment. Most population-based studies demonstrate worse outcomes for AA patients after diagnosis and treatment,5,7 particularly for AA men younger than age 70.8,9 In contrast, smaller reports from single institutions and cooperative groups typically show equivalent outcomes after radiotherapy (RT)10-12 or radical prostatectomy.13

At the University of Chicago, we care for a mixed racial population. Once in our system, patients are staged and treated in a uniform manner. This communication summarizes our experience with conformal RT for prostate cancer and focuses on race-based differences. Our report has several unique strengths, including analyses controlled for treatment details and prognostic risk categories. Outcome data are presented in terms of overall survival, disease-free survival, and biochemical control. Finally, this report includes a large patient population, with a well-balanced (46.8% AA) racial distribution.


   PATIENTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Nine hundred thirty-seven patients with prostate cancer were treated at the University of Chicago and affiliated hospitals with conformal external-beam RT between 1988 and 1997. For the purpose of this analysis, patients were excluded if clinic chart records were incomplete or unavailable (44 patients). The remaining 893 patients (475 W and 418 AA) form the basis of this report.

Initial work-up included digital rectal examination, serum prostate-specific antigen (PSA) assay (in the majority of patients), and pathologic sampling of the prostate via transrectal biopsy (92.2%) or transurethral resection (7.8%). Bone scans were performed in most patients and in all patients with PSA levels greater than 15 ng/mL. All patients received pelvic computed tomography scans (for RT planning purposes), none of which showed gross evidence of lymphadenopathy. The median pretreatment PSA level was 12.3 ng/mL (range, 0.7 to 418 ng/mL). The American Joint Committee on Cancer tumor stage was T1 in 219 patients (32.6%), T2 in 459 patients (51.4%), and T3 or T4 in 143 patients (16.0%). The breakdown by Gleason score showed 147 patients (16.5%) with a score of 2 to 4, 676 (75.7%) with a score of 5 to 7, and 70 (7.8%) with a score of 8 to 10.

Patients were evaluated and managed by a common academic faculty using similar treatment policies. Treatment consisted of conformal external-beam RT, performed at one of four affiliated hospitals. RT planning techniques included computed tomography–based methods, previously described in detail,14 and more recently three-dimensional dosimetry planning software (Planning at UNC; University of North Carolina, Chapel Hill, NC). Radiation treatments (10- to 24-MV photon irradiation) were typically delivered in 1.8- to 2.0-Gy daily fractions via four or six field techniques. Over the past decade, our department has gradually escalated radiation doses from 66 Gy to 74.8 Gy (minimum organ dose). The median radiation dose in this analysis was 68 Gy (range, 60 to 74.8 Gy) delivered over a median of 48 days. Neoadjuvant and/or concurrent therapy with androgen deprivation medications was administered to 201 patients (22.5%).

PSA assays were typically repeated several weeks after the completion of treatment, and patients returned for follow-up visits every 3 to 6 months thereafter. According to the American Society of Therapeutic Radiology and Oncology consensus definition, biochemical failure was defined as three consecutive increases in the PSA level.15 The date of failure was defined as the midpoint between the posttreatment PSA nadir and the first PSA increase. This definition was modified to also include cases wherein large, rapid increases in PSA levels prompted salvage androgen deprivation, before three consecutive increases. In such cases, the date of failure was recorded as the midpoint between the PSA nadir and the initiation of hormonal therapy. Local recurrence (determined by physical examination and/or biopsy) and distant metastases were considered as events for disease-free survival (DFS) analyses.

This analysis includes some patients treated in the late 1980s; therefore, our review of charts revealed cases with incomplete PSA data or pathologic tumor grading via the earlier Broder system. For the purpose of biochemical control (bNED) analyses, we excluded any patient with unknown pretreatment PSA levels (135 patients), grading via the Broder scoring system (105 patients), or a PSA-based follow-up interval of less than 6 months (96 patients). The remaining 557 patients fulfilling these biochemical analysis criteria formed the basis of all PSA-based results.

Since combinations of pretreatment factors have been shown to be of prognostic importance, patients were grouped according to prognostic risk categories.16,17 Favorable prognosis was defined as a PSA level <= 10 ng/mL, tumor stage less than T3, and Gleason score less than 7. An increase in one of the aforementioned factors would classify a patient into the intermediate prognosis group, and an increase in two or more of these factors would classify a patient as having an unfavorable prognosis.

The {chi}2 test was used to analyze the distribution of prognostic factors among different groups. Actuarial survival, DFS, and bNED curves were calculated using the method of Kaplan and Meier18 and compared by the log-rank test.19 All intervals were calculated from the initiation of RT. The median follow-up interval was 24 months (range, 1 to 114 months) for the entire study population and 26 months (range, 6 to 96 months) for patients fulfilling the biochemical analysis criteria. A total of 120 patients were followed for at least 5 years. There was no difference (P = .98) in follow-up length between AA and W patients.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
The 5-year actuarial survival, DFS, and bNED rates for the entire population were 80.5%, 70.0%, and 57.6%, respectively (Fig 1). When classified by prognostic risk category, the 5-year actuarial bNED rates were 78.7% for favorable, 57.7% for intermediate-risk, and 39.8% for unfavorable category disease (Fig 2). Patients achieved a median PSA nadir of 0.8 ng/mL (range, 0 to 240 ng/mL) at a median time interval of 1.0 year (range, 0 to 6.2 years) after the initiation of RT.



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  		Fig 1. Outcome of the 893 treated patients.

 


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  		Fig 2. Biochemical control of the 557 patients fulfilling bNED analysis criteria.

 
Table 1 shows the breakdown of patient- and treatment-related factors by racial group. In general, the AA men presented at younger ages with more advanced disease. The tumor stages, Gleason scores, pretreatment PSA levels, and prognostic risk categories were significantly higher among AA men. Because of these poor prognostic factors, AA patients were treated with more aggressive therapies, consisting of more frequent administration of neoadjuvant androgen deprivation and higher radiation doses. Despite this, AA patients achieved PSA nadirs below 1.0 ng/mL less frequently than did W patients, according to univariate analysis (P = .05). No race-based differences were noted in the time intervals between treatment and PSA nadir.


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  		Table 1. Patient and Treatment Characteristics
 
The results of univariate analyses for potential prognostic factors are detailed in Table 2. Worse survival rates were observed for patients who experienced short intervals (<= 1 year) between treatment and PSA nadir. Also, a trend toward worse survival was observed for patients with higher tumor grades (P = .09). None of the other variables had an impact on overall survival. Clinical recurrences were more prevalent in the patients with higher tumor stages (P = .0002), higher Gleason scores (P = .003), and higher PSA levels (P = .001). Posttreatment factors associated with improved clinical control included low PSA nadir (<= 1.0 ng/mL) and long interval to PSA nadir (P < .0001 for both). AA race became a significant adverse factor (P = .0002) when the definition of clinical recurrence was broadened to include the administration of salvage hormonal therapy. On multivariate analysis for clinical control (using this broadened definition), only PSA level, Gleason score, tumor stage, PSA nadir, and interval to PSA nadir were independent prognostic factors.


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  		Table 2. Treatment Outcome: Univariate Analysis
 
In terms of bNED rates on univariate analysis, significantly worse outcomes were observed in patients with higher tumor stages (P < .0001), higher Gleason scores (P = .0001), and higher PSA levels (P < .0001). To a lesser degree, AA race and age <= 70 years were unfavorable prognostic factors. After RT, low PSA nadir and long interval to PSA nadir were strong predictors of biochemical control (P < .0001 for both). Multivariate analysis for bNED showed that PSA level, PSA nadir, Gleason score, and the interval to PSA nadir were the only independent predictors of biochemical control (Table 3).


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  		Table 3. Multivariate Analysis for Biochemical Control
 
To better illustrate the impact of race on biochemical outcome, patients were classified by prognostic risk category (Table 4). Based on race, no significant differences in bNED rates were seen in patients with favorable (P = .91), intermediate (P = .44), or unfavorable (P = .09) category disease. Although RT doses were comparable between the racial groups, AA patients received neoadjuvant hormonal deprivation therapy somewhat more frequently.


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  		Table 4. Impact of Race on Biochemical Control Rates: Based on Prognostic Risk Category and Treatment
 
No benefit was seen with escalated RT doses (60 to 66 Gy v 66.1 to 69.9 Gy v 70 to 74.8 Gy) in terms of bNED or clinical DFS. Furthermore, no RT dose response could be demonstrated in any of the three prognostic risk categories, when analyzed separately. Additionally, no long-term benefit could be demonstrated from the use of neoadjuvant hormonal deprivation therapy.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
This large single-department report demonstrates that race is not an independent prognostic factor after conformal RT for prostate cancer. Like other investigators,4-6,20-22 we noted that AA men present with relatively advanced stages, PSA levels, and grades. After known prognostic factors were controlled for, however, treatment efficacy seemed comparable for AA and W patients.

Our data support the theory that high mortality rates for AA men result from late diagnoses and the associated advanced nature of these tumors. This is likely related to imbalances in socioeconomic factors, including availability of health care.22,23 Several studies have even documented that AA men receive less aggressive therapies for prostate cancer on average.24,25 After comparable treatment, however, the stage-specific control rates seem equivalent between AA and W patients.26 Investigators from single institutions10,12 and cooperative groups11 have shown this to be true after RT. Likewise, Islelin et al13 reported that race was not an independent prognostic factor after radical prostatectomy at Duke University (Durham, NC).

On the other hand, there is evidence to support the competing theory that prostate cancer is more virulent in AA men, even after controlling for stage and other prognostic factors. Several reports have demonstrated relatively poor outcomes for AA patients, despite equivalent access to health care.7,8,27 Among patients undergoing radical prostatectomy at Walter Reed Army Medical Center (Washington, DC), AA race remained a significant adverse factor after multivariate analysis.27 Robbins et al recently analyzed cancer registry data from the San Francisco Bay area, which included many patients covered by the Kaiser Permanente Medical Care Program. Despite equivalent coverage by health maintenance organizations, the AA men had relatively poor survival rates for all stages of prostate cancer.7

It remains unclear why AA men present with more advanced stages and grades. The age-specific incidence of prostate cancer is approximately 50% higher for AA men,3 and the median age at presentation is relatively young.13,26,28 Therefore, inadequate screening measures and delays in diagnosis cannot completely explain these advanced presentations. Other proposed explanations include racial differences in diet29,30 and basal androgen levels.31,32 More recently, investigators have linked prostate cancer to familial inheritance patterns33,34 and a hereditary prostate cancer gene (HPC1).35 Furthermore, certain genetic variations seem to be risk factors for the prostate carcinogenesis, including CAG repeats in androgen receptor genes,36,37 alterations of vitamin D receptor genes,38 and missense substitutions in the 5-alfa reductase gene.39 These genetic findings are associated with high-grade cancers,36,40 and early evidence suggests that they are relatively common in AA men.37-39,41

Early screening in AA populations seems crucial, given the young/advanced presentations together with the efficacy of treatment for early cases. Powell et al42 initiated the community-based Detroit Education and Early Detection Study in 1993. This screening measure resulted in more effective treatments (fewer positive surgical margins) and lower recurrence rates (7% v 25%, P = .033) among the AA population compared with the nonenrolled clinic population.

Our study also confirmed the prognostic significance of pretreatment PSA level, Gleason score, and tumor stage. Additionally, we found low PSA nadir (<= 1.0 ng/mL) to be a favorable prognostic factor. Other investigators have similarly reported improved control rates after low nadirs.43-46 However, it remains unclear how low the PSA level must fall after external-beam RT or radiation implantation.15 An interesting finding in our study relates to the time interval between treatment and PSA nadir. Short intervals (<= 1 year) were associated with significantly worse outcomes, even in terms of overall survival (P = .005). Similar observations have been reported from investigators at Stanford University (Palo Alto, CA) and Fox Chase Cancer Center (Philadelphia, PA).15 However PSA profiles during and after treatment depend on dynamic interactions between multiple factors.47-49 Therefore, more research is necessary to completely understand this observation.

We were unable to detect any improvement in control rates using higher RT doses; however, this may have been due to the narrow range of doses reviewed. Our treatment philosophy over the past decade has been relatively conservative, with a slow escalation of RT doses over time. However, several other groups have reported benefits from considerably higher RT doses in certain select groups.50-52 For example, Zelefsky et al reported improved bNED rates in patients with intermediate and unfavorable prognoses who were receiving RT doses >= 75.6 Gy.51 A problem common to many dose escalation protocols, however, is that patients treated with the higher dose levels tend to have shorter follow-up intervals. We previously reported that bNED rates, based on commonly used definitions, are highly dependent on length of follow-up interval.53 More recently, M.D. Anderson Cancer Center (Houston, TX) reported a randomized comparison of 70 Gy and 78 Gy (dose defined at the center of the prostate). No significant difference was detected when pretreatment PSA levels were below 10 ng/mL; however, 78 Gy was superior in patients with a PSA level of 10 ng/mL.54

One limitation of this report that should be noted is the relatively short follow-up length. Although the length of follow-up was equivalent between the racial groups, our ability to detect differences may have been somewhat limited.

In conclusion, this large, single-department report confirms that conformal RT is equally effective for AA and W patients. However, AA men continue to present at younger ages and with relatively advanced cases of prostate cancer. More research is needed in order to completely understand and correct this racial disparity. Additionally, our data underscore the importance of early screening in AA populations.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
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2. Miller BA, Kolonel LN, Berstein L, et al: Racial/ethnic patterns of cancer in the United States, 1988-1992. Bethesda, MD, National Cancer Institute, 1996

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6. Powell IJ, Heilbrun LK, Sakr W, et al: The predictive value of race as a clinical prognostic factor among patients with clinically localized prostate cancer: A multivariate analysis of positive surgical margins. Urology 49: 726-731, 1997[Medline]

7. Robbins AS, Whittemore AS, Van Den Eeden SK: Race, prostate cancer survival, and membership in a large health maintenance organization. J Natl Cancer Inst 90: 986-990, 1998[Abstract/Free Full Text]

8. Powell IJ, Schwartz K, Hussain M: Removal of the financial barrier to health care: Does it impact on prostate cancer at presentation and survival? A comparative study between black and white men in a Veterans Affairs system. Urology 46: 825-830, 1995[Medline]

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10. Zagars GK, Pollack A, Pettaway CA: Prostate cancer in African-American men: Outcome following radiation therapy with or without adjuvant androgen ablation. Int J Radiat Oncol Biol Phys 42: 517-523, 1998[Medline]

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14. Vijayakumar S, Low N, Chen GT, et al: Beams eye view-based photon radiotherapy I . Int J Radiat Oncol Biol Phys 21: 1575-1586, 1991[Medline]

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16. Leibel SA, Zelefsky MJ, Kutcher GJ, et al: Three-dimensional conformal radiation therapy in localized carcinoma of the prostate: Interim report of a phase 1 dose-escalation study. J Urol 152: 1792-1798, 1994[Medline]

17. Shipley WU, Thames HD, Sandler HM, et al: Radiation therapy for clinically localized prostate cancer: A multi-institutional pooled analysis. JAMA 281: 1598-1604, 1999[Abstract/Free Full Text]

18. Kaplan EL, Meier P: Nonparametric estimation from incomplete observations. J Am Stat Assoc 53: 457-481, 1958

19. Mantel N: Evaluation of survival data and two new rank order statistics arising in its consideration. Cancer Chemother Rep 50: 163-170, 1966[Medline]

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22. Vijayakumar S, Weichselbaum R, Vaida F, et al: Prostate-specific antigen levels in African-Americans correlate with insurance status as an indicator of socioeconomic status. Cancer J Sci Am 2: 225-233, 1996[Medline]

23. Dale W, Vijayakumar S, Lawlor EF, et al: Prostate cancer, race, and socioeconomic status: Inadequate adjustment for social factors in assessing racial differences. Prostate 29: 271-281, 1996[Medline]

24. Harlan L, Brawley O, Pommerenke F, et al: Geographic, age, and racial variation in the treatment of local/regional carcinoma of the prostate. J Clin Oncol 13: 93-100, 1995[Abstract/Free Full Text]

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31. Ross R, Bernstein L, Judd H, et al: Serum testosterone levels in healthy young black and white men. J Natl Cancer Inst 76: 45-48, 1986

32. Ross RK, Bernstein L, Lobo RA, et al: 5-Alpha-reductase activity and risk of prostate cancer among Japanese and US white and black males. Lancet 339: 887-889, 1992[Medline]

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34. Carter BS, Bova GS, Beaty TH, et al: Hereditary prostate cancer: Epidemiologic and clinical features. J Urol 150: 797-802, 1993[Medline]

35. Smith JR, Freije D, Carpten JD, et al: Major susceptibility locus for prostate cancer on chromosome 1 suggested by a genome-wide search. Science 274: 1371-1374, 1996[Abstract/Free Full Text]

36. Giovannucci E, Stampfer MJ, Krithivas K, et al: The CAG repeat within the androgen receptor gene and its relationship to prostate cancer. Proc Natl Acad Sci U S A 94: 3320-3323, 1997 (published erratum appears in Proc Natl Acad Sci U S A 94: 8272, 1997)[Abstract/Free Full Text]

37. Irvine RA, Yu MC, Ross RK, et al: The CAG and GGC microsatellites of the androgen receptor gene are in linkage disequilibrium in men with prostate cancer. Cancer Res 55: 1937-1940, 1995[Abstract/Free Full Text]

38. Ingles SA, Coetzee GA, Ross RK, et al: Association of prostate cancer with vitamin D receptor haplotypes in African-Americans. Cancer Res 58: 1620-1623, 1998[Abstract/Free Full Text]

39. Makridakis NM, Ross RK, Pike MC, et al: Association of mis-sense substitution in SRD5A2 gene with prostate cancer in African-American and Hispanic men in Los Angeles, USA. Lancet 354: 975-978, 1999[Medline]

40. Gronberg H, Isaacs SD, Smith JR, et al: Characteristics of prostate cancer in families potentially linked to the hereditary prostate cancer 1 (HPC1) locus. JAMA 278: 1251-1255, 1997[Abstract]

41. Cooney KA, McCarthy JD, Lange E, et al: Prostate cancer susceptibility locus on chromosome 1q: A confirmatory study. J Natl Cancer Inst 89: 955-959, 1997[Abstract/Free Full Text]

42. Powell IJ, Heilbrun L, Littrup PL, et al: Outcome of African American men screened for prostate cancer: The Detroit Education and Early Detection Study. J Urol 158: 146-149, 1997[Medline]

43. Critz FA, Levinson AK, Williams WH, et al: Prostate specific antigen nadir achieved by men apparently cured of prostate cancer by radiotherapy. J Urol 161: 1199-1203, 1999[Medline]

44. Zietman AL, Tibbs MK, Dallow KC, et al: Use of PSA nadir to predict subsequent biochemical outcome following external beam radiation therapy for T1-2 adenocarcinoma of the prostate. Radiother Oncol 40: 159-162, 1996[Medline]

45. Crook JM, Bahadur YA, Bociek RG, et al: Radiotherapy for localized prostate carcinoma: The correlation of pretreatment prostate specific antigen and nadir prostate specific antigen with outcome as assessed by systematic biopsy and serum prostate specific antigen. Cancer 79: 328-336, 1997[Medline]

46. Lee WR, Hanlon AL, Hanks GE: Prostate specific antigen nadir following external beam radiation therapy for clinically localized prostate cancer: The relationship between nadir level and disease-free survival. J Urol 156: 450-453, 1996[Medline]

47. Vijayakumar S, Karrison T, Quadri SF, et al: Localized prostate cancer: Use of serial prostate-specific antigen measurements during radiation therapy—An update. Onkologie 17: 578-585, 1994

48. Vijayakumar S, Quadri SF, Karrison TG, et al: Localized prostate cancer: Use of serial prostate-specific antigen measurements during radiation therapy. Radiology 184: 271-274, 1992[Abstract/Free Full Text]

49. Sutkowski DM, Goode RL, Baniel J, et al: Growth regulation of prostatic stromal cells by prostate-specific antigen. J Natl Cancer Inst 91: 1663-1669, 1999[Abstract/Free Full Text]

50. Hanks GE, Hanlon AL, Schultheiss TE, et al: Dose escalation with 3D conformal treatment: Five year outcomes, treatment optimization, and future directions. Int J Radiat Oncol Biol Phys 41: 501-510, 1998[Medline]

51. Zelefsky MJ, Leibel SA, Gaudin PB, et al: Dose escalation with three-dimensional conformal radiation therapy affects the outcome in prostate cancer. Int J Radiat Oncol Biol Phys 41: 491-500, 1998[Medline]

52. Michalaski JM, Purdy JA, Winter K, et al: Preliminary report of toxicity following 3D radiation therapy for prostate cancer on 3DOG/RTOG 9406. Int J Radiat Oncol Biol Phys 46: 391-402, 2000[Medline]

53. Connell PP, Ignacio L, McBride RB, et al: Caution in interpreting biochemical control rates after treatment of prostate cancer: Length of follow-up influences results. Urology 54: 875-879, 1999[Medline]

54. Pollack A, Zagars GK, Smith LG, et al: Preliminary results of a randomized dose-escalation study comparing 70 Gy to 78 Gy for the treatment of prostate cancer. Int J Radiat Oncol Biol Phys 45: 146, 1999 (abstr)

Submitted April 25, 2000; accepted August 3, 2000.




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Copyright © 2001 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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