Effect of radiation therapy after radical prostatectomy on serum prostate-specific antigen measured by an ultrasensitive assay

ADULT

UROLOGY

EFFECTOF RADIATION THERAPY AFTER RADICAL PROSTATECTOMY ON SERUM PROSTATE-SPECIFIC ANTIGEN MEASURED BY AN ULTRASENSITIVE ASSAY FRANCOIS HAAB, M.D. ALAIN MEULEMANS, M.D. LILIANE BOCCON-GIBOD, M.D. MARIE CHRISTINE DAUGE, M.D.

VINCENT DELMAS, M.D. C. HENNEQUIN, M.D. D. BENBUNAN, M.D. LAURENT BOCCON-GIBOD, M.D.

From the Departments of Urology, Pathology, and Nuclear Medicine, Bichat Hospital, the Department of Pathology, Trousseau Hospital, and the Departments of Radiotherapy, Saint Louis Hospital and Hartman Hospital, Paris, France

ABSTRACT-Objectives. To study prospectively the impact of adjuvant radiation therapy on the serum level of prostate-specific antigen (PSA), as measured by an ultrasensitive Yang Proscheck assay in patients with detectable serum PSA and a negative metastatic survey after radical prostatectomy for Tl or T2 prostate cancer. Methods. Seventeen patients had a detectable serum PSA (2.40 f 2.1 ng/mL; range, 0.5 to 10) by the Yang polyclonal assay 2 to 7 1 months after radical prostatectomy for P2NO (2 patients) or P3NO (15 patients) prostate cancer. Metastatic workup (bone and computed tomography scan) was negative; 9 of 17 patients had a local recurrence documented by a positive biopsy of the vesicourethral anastomosis. All patients were treated by external radiotherapy, receiving 65 Gy on the prostate fossa over 5 weeks for an assumed low volume residual disease. Patients were followed up by determination of serum PSA every 3 months, using the Yang ultrasensitive assay for a mean duration of 14.4 months. Results. In 17.6% of the patients (3 of 17) PSA became undetectable (less than 0.05 ng/mL] after radiotherapy. Radiotherapy had no impact on PSA in 35.3% (6 of 17). PSA decreased after radiation therapy within 6 months in 47.1% (8 of 17) and for up to 12 months in 2 patients, with a nadir of 0.28 ng/mL. All patients in this group experienced a secondary rise in PSA a mean of 10.6 months (range, 6 to 18 months) after radiotherapy. Conclusions. External radiotherapy has a limited impact on residual disease after radical prostatectomy, as assessed by its impact on PSA.

Serum prostate-specific antigen (PSA) is recognized as the best tumor marker with which to monitor the response to therapy for prostate cancer.l Radical prostatectomy is accepted today as an effective treatment for localized (Tl or T2) prostate cancer, and an undetectable postoperative PSA is the hallmark of therapeutic efficacy2 However, the tumor extends beyond the prostate capsule in approximately 40% of the patients, and PSA remains detectable or reappears in the serum Submitted: August December 21, 1994

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29, 1994, accepted

(with

revisions):

sometime after surgery, identifying a biologic failure that may predict clinical failure.3 Several investigators have recommended adjuvant radiation therapy for patients with extracapsular disease or detectable PSA after radical prostatectomy. However, its efficacy is still controversial.4-6 We have therefore carried out a prospective study to evaluate the impact of adjuvant radiotherapy after radical prostatectomy in patients with detectable serum PSA and no clinical evidence of disseminated disease. Post-treatment serum PSA was assessed using an ultrasensitive assay. UROLOGY@ /JUNE 1995 I VOLUME 45, NLMBER 6

MATERIAL

AND

METHODS

PSA

(ng/mL)

A total of 22 patients were enrolled between 1989 and 1991 in a prospective study to assess the impact of radiation therapy after radical prostatectomy in the presence of elevated PSA. Four patients were excluded because they were given simultaneous hormone suppressive treatment, and 1 was lost to follow-up. Radical prostatectomy was performed according to Walsh et a1.7 Pathologic specimens were analyzed according to McNea18 Fifteen patients were P3NO and 2 were P2NO. The median preoperative Gleason score was 7 (range, 6 to 9). PSA MEASUREMENTS

The polyclonal Yang Proscheck-R-PSA was used for all sera in the classic range. The detection limit was 0.5 ng/mL with the normal range below 2.5 ng/mL. The kit was modified to give the ultrasensitive radioimmunoassay described by Graves et a1.9 and used for all sera below 0.5 ng/mL. In our hands, its detection limit was 0.05 ng/mL. Interassay and intra-assay variations were below 20% over the range studied (0.05 to 0.5 ng/mL). Preoperative serum PSA was 29 * 21.9 ng/mL (range, 1.2 to 70). All patients had a detectable serum PSA 2 months after surgery, or increased levels of PSA during follow-up (range, 6 to 71 months). The mean PSA at inclusion was 2.40 f 2.1 ng/mL (range, 0.6 to 10). No patient showed evidence of systemic disease, as assessed by physical examination, serum prostatic acid phosphatase, pelvic computed tomography, or bone scan. Nine of 17 (53%) of the patients had local disease, as was evident from transrectal ultrasound (TRUS)-guided (Bruel and Kjaers) random needle biopsies of the urethrovesical anastomosis. STUDY

PROTOCOL

Radiation therapy was administered at only two institutions, and 65 Gy was delivered to the prostate fossa, including the urethrovesical anastomosis, over a period of 6 weeks. Serum PSA was measured every 3 months for 1 year after radiotherapy, and then every 6 months. The mean follow-up after radiotherapy was 18.2 months. Patients were divided into three groups according to their biologic response to radiation therapy Group 1: complete response, defined by an undetectable PSA after radiation therapy; group 2: partial response, defined by an initial decrease in PSA that remained detectable; group 3: no response, radiation therapy had no impact on serum PSA.

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0

10

20

30

T (months) FIGURE 1. Group 1 (complete responders): 3/l 7 patients (17.6%). Prostate-specific antigen (PSA) was below 0.1 ng/mL. Follow-up was 12.6 months. RESULTS

Three of the 17 patients (17.6%) were considered to be complete responders to radiation therapy (group l), since they had an undetectable serum PSA, even with the ultrasensitive assay (PSA ~0.1 ng/mL). They were disease-free with an undetectable serum PSA after a mean follow-up of 12.6 months. All patients in group 1 had local disease, as indicated by TRUS-guided random needle biopsies of the urethrovesical anastomosis. Two patients were PZNO, and one was P3N0, with a microcapsular effraction (Fig. 1; Table I). Eight of the 17 patients (47.1%) were considered to be partial responders to radiation therapy (group 2). Their serum PSA dropped within 6 months after treatment and remained low for up to 12 months for 2 patients. The nadir was 0.28 ng/mL. All patients in group 2 showed a mean rise in serum PSA of 10.6 months (range, 6 to 18) after radiotherapy. PSA velocity after radiation therapy was 0.95 f 0.5 ng/mL per year (Fig. 2; Table II). Six of the 17 patients (35.3%) did not respond to radiation therapy (group 3), since there was no significant decrease in serum PSA. Serum PSA velocity after radiotherapy treatment was 1.22 * 0.92 ng/mL per year (Fig. 3; Table III). All 3 patients who had an undetectable PSA after radiotherapy had documented local disease, with positive biopsies of the urethrovesical anastomosis, compared with 50% (4 of 8) in the group of patients who showed a later rise in serum PSA after radiotherapy and 33% (2 of 6) in the group of nonresponders. 1023

TABLE I. PSA Level Before RP (ng/mLl 22 20 8

Pt. No. 1 2 3

PSA Level 1 Month After RP WmL) Undetectable Undetectable 0.9

Group I patients

Biochemical Failure to Radiation Therapy (mo) 24 18 16

(complete

RP to Radiation Therapy (mo) 60 71 16

responders)

PSA Level Before Radiation Therapy (ng/mL) 1.4 0.9 2.4

*

Pathologic Stage p-f2 pT2 pT3

Extension to sv Negative Negative Negative

Biopsy of UVA Positive Positive Positive

KEY: PSA = prostate-specijic antigen; RP = radical prostatectomy; SV = seminal vesicles; WA = urethrovesical anastomosis. *PSA levels and histopathologic data. Postoperative PSA was measured with the standard Yang Proscheck assay, with a detection limit ofO.5 ng/mL

TABLE II. PSA Level Before RP hW-) 12 61 15 24 9.1 50 58 66

Pt. No. 4 5 6 7 8 9 10 11

PSA Level 1 Month Post RP hz/mL) Undetectable 1 Undetectable Undetectable 0.7 Undetectable 0.7 2.5

Croup 2 patients (partial responders) *

Biochemical Failure to Radiation Therapy (mo) 28 18 21 12 6 6 6 16

RP to Radiation Therapy [mo) 50 18 48 24 6 12 6 16

PSA Level Before Radiation Therapy (ng/mL) 1 2.3 6 0.6 0.6 2.2 1.2 3.6

Pathologic Stage pT3 pT3 pT3 pT3 pT3 pT3 pT3 pT3

Extension to sv Negative Positive Positive Negative Negative Positive Negative Positive

Biopsy of UVA Positive Positive Negative Negative Positive Negative Negative Positive

KEY: PSA = prostate-spai& antigen; RP = radical prostatectomy; SV = seminal vesicles; UVA = urethrovesical anastomosis. *PSA levels and histopathological data. Postoperative PSA was measured with the standard Yang Proscheck assay, with a detection limit ofO.5 ng/mL

PSA

PSA (ng/mL)

(ng/mL)

100

1 0.5

10

20

-I 30

T (months) FIGURE 2. Group 2: 8/l 7 patients (47.1%) significant decrease in serum prosate-specific antigen [PSA) with secondary rise. Nadir was 0.28 ng/mL. Secondary rise occurred 10.6 months after radiotherapy.

Seven patients would have been considered as complete responders after radiation therapy using a standard PSA radioimmunoassay, with a serum PSA nadir below 0.5 ng/mL, but their PSA actually remained detectable by the ultrasensitive assay (PSA >0.05 ng/mL). All 7 of these patients 1024

T (months) FIGURE3. Group 3: 6/l 7 patients (35.3%) no significant decrease in serum prostate-specific antigen (PSA) after radiation treatment.

had a further PSA above 0.5 ng/mL with a mean follow-up of 12.6 months (Table IV). Although it was not significant, the preradiation serum PSA in group 1 (1.5 * 0.6 ng/mL) was lower than those of groups 2 (2.17 f 1.7 ng/mL) and 3 (3.5 f 1.4 ng/mL). The seminal vesicles were not involved in group 1 patients, whereas the cancer extended to the

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TABLE III. PSA Pt. No. 12 13 14 15 16 17

Level Before RP WmLl 17 22 70 10 1.2 28

PSA Level 1 Month Post RP (w/W Undetectable 1.5 1.8 2.5 0.9 0.6

Group 3 patients

Biochemical Failure to Radiation Therapy (mo) 6 2 20 21 24 6

RP to Radiation Therapy (mo) 12 2 20 21 24 6

(nonresponders)* PSA Level Before Radiation Therapy (nglml) 0.8 1.5 5.3 10 2.6 1

Pathologic Stage pT3 pT3 pT3 pT3 pT3 pT3

Extension to sv Positive Positive Positive Positive Negative Negative

Biopsy of UVA Positive Negative Positive Negative Negative Negative

KEY: PSA = prostate-specific antigen; RF’ = radical prostatectomy; SV = seminal vesicles; LJVA = urethrovesical anastomosis. *PSA levels and histopathological data. Postoperative PSA was measured with the standard Yang Proscheck assay, with a detection limit ofO.5 ng/mL

TABLE IV.

PSA ~0.1 0.1 < PSA ~0.5

Comparison between standard ultrasensitive assay No. of Pts 3 7

No. Disease Free (%) 3 (100%) 0 (0%)

and

Follow-up 0-W 14.6 12.6

seminal vesicles in 62.5% of the cases in group 2 and in 66.6% of group 3 patients. Elapsed time between radical prostatectomy and biochemical failure had no impact on treatment efficacy Also, time interval between the first elevation in serum PSA and the initiation of radiotherapy was not statistically different among the three groups, with, respectively, 19.3 f 3.4, 14.1 f 7.6, and 13.1 + 8.6 months in groups 1, 2, and 3 (P >0.05). The morbidity of adjuvant radiation therapy was widespread but not severe: 70.5% of the patients (12 of 17) complained of mild to moderate symptoms of diarrhea and urinary urgency or pollakiuria during and up to 6 months after radiation treatments. No patient exhibited loss of sphincter control. No hospitalization was required for the side effects of radiation therapy COMMENT Most of the published studies of radical prostatectomy for prostate cancer report that nearly 50% of the patients believed to have clinically localized disease have in fact a pathologic T3 tumor.‘O However, a review of reports of surgery alone for pathologic T3 lesions reveals a local recurrence rate of 8% to 43%,l” with tumor-free survival ranging from 25% to 92% at 5 to 10 years. When radiotherapy was used to treat patients with clinical T3 disease without radical prostatectomy, only 21% to 32% of the patients appeared to be cured at 5 years.ll The use of postoperative adjuvant radiation therapy for pT3 cancers was initially reported by George et al. UROLOGY@ /JUNE ~~~~IVOLUME~~,N~BER~

in 1965.12 In 1975, the Stanford group recommended routine postoperative radiotherapy for residual or recurrent tumor after radical prostatectomy l3 However, there is still controversy over the use of radiation therapy as adjuvant treatment after radical prostatectomy.4-6,14-18 The rationale for extending the role of adjuvant radiation therapy after radical prostatectomy depends on the demonstration of cancer control with an acceptable morbidity Although PSA has been shown to have limited value as a screening or staging tool for prostate cancer, it is remarkably sensitive for detecting the presence of prostatic tissue, either benign or malignant, local or metastatic. Because of this property, PSA seems to be an ideal marker for monitoring patients for recurrent or residual disease after therapy that is intended to eradicate completely all traces of prostatic tissue.18 Serum PSA is an independent pretherapeutic and posttherapeutic predictor of outcome; with a median follow-up of 25 months, delayed PSA failures are associated with localized or metastatic recurrence. Detectable PSA after radical prostatectomy indicates local or systemic residual or recurrent disease.2T3 According to Kaplan et al.,lg the interval between biochemical and clinical relapse is 156 * 46 days. It has been reported that patients with T3 lesions treated by adjuvant radiation therapy after radical retropubic prostatectomy for an elevated postoperative serum PSA showed a decrease in PSA levels, which was significantly different from those left untreated. However, the effect of adjuvant radiotherapy on serum PSA was only temporary in the small number of patients with a longer follow-up, and serum PSA was measured using a standard Tandem kit, which is not ultrasensitive.18 The Johns Hopkins group recently reported fewer than 30% of the patients with undetectable PSA 2 years after adjuvant radiation therapy for an elevated postprostatectomy serum PSA.21 Eisbruch 1025

et aL5 reported that adjuvant radiation therapy after radical prostatectomy did not affect the survival of patients with positive surgical margins or seminal vesicle invasion. They also found no significant difference in the outcomes of patients given treatment to the whole pelvis and those given irradiation to the pelvic bed only It has been demonstrated that the measurement of serum PSA by an ultrasensitive assay allows earlier detection of residual prostate cancer after radical prostatectomy. 2o When it was used in patients after radiotherapy for residual disease after radical prostatectomy, the serum PSA assessed by an ultrasensitive assay allowed a more accurate evaluation of the efficacy of the adjuvant treatment. Hudson and Catalona4 used a standard assay to show that adjuvant radiation therapy is responsible for a drop in serum PSA to undetectable levels in approximately 43% of the patients with detectable PSA after radical prostatectomy. In our study, when PSA was assessed using the standard assay, 58.8% (10 of 17) of the patients were considered to have undetectable levels. Seven patients in group 2 still had detectable PSA by the ultrasensitive assay. All 7 patients exhibited increasing levels of PSA, with PSA below 0.5 ng/mL with a mean follow-up of 12.6 months. PSA velocity in these patients indicated that this secondary rise was due to prostate cancer and not to a residual secretion by benign tissue or periurethral glands, since an average annual rate of change of 0.75 ng/mL corresponded to a 90% specificity for PSA in differentiating prostate cancer from benign prostatic hyperplasia.‘g,22 These patients could be considered as false-negative results of the standard assay in predicting the efficacy of the adjuvant radiotherapy Only 3 patients had undetectable levels with the ultrasensitive assay All had a low PSA at entry and proven local disease with positive biopsies of the urethrovesical anastomosis. Two were P2NO and 1 was P3NO with a microcapsular effraction and none had seminal vesicle involvement. However, because of the short follow-up, it cannot be actually stated that these 3 patients are definitively cured. The rationale for adjuvant radiation therapy in patients with P3NO prostate cancer is the belief that residual tumor is confined to the pelvis postoperatively and can serve as a source of local and distant failure if it remains untreated.23 However, most of the cancers that have penetrated the capsule have already produced metastases that will often be manifested and fatal before a local recurrence becomes a problem.6 It has been reported that postoperative radiation therapy is associated with a lower pelvic recurrence rate.24 Montie2* 1026

emphasized that local recurrence is only delayed, but not eliminated. However, the larger locally extensive lesions with gross residual disease may well cause further local symptoms and a prevention of local recurrence in these cases is justifiable. Patients who should benefit from adjuvant radiotherapy are clearly those with a low tumor volume. It has been demonstrated that radiotherapy is not able to cure T3 prostate cancer.ll In agreement with Freeman et al.1° we found that extension to the seminal vesicles is a factor of poor prognosis. Consequently, the probable best indications of adjuvant radiotherapy for postradical prostatectomy are patients with minimal extracapsular disease, no seminal vesicle involvement, and documented local failure. There were no major complications after radiation therapy in our patients. Doses of 60 to 65 Gy were well tolerated. Limitation of the radiation field to the prostatic fossa and bladder neck could reduce the incidence of lymphedema of the genitalia or lower extremities.25 However, it has been reported that radiation therapy can aggravate postoperative complications from radical prostatectomy, especially continence or anastomotic stricture.26 We have not done in this series a specific evaluation of potency before and after radiotherapy. However, Freeman et al.1° have observed that radiotherapy diminished potency rates following nerve-sparing procedures. The low morbidity of radiation treatment in this series is possibly related to the limited follow-up. Radiation therapy should be delayed until postoperative recovery is complete to limit these complications.27 CONCLUSION The use of an ultrasensitive PSA assay indicates that adjuvant radiotherapy is rarely a curative treatment for residual disease after radical prostatectomy. Patients who could benefit from this treatment are those with an initial low volume disease with no seminal vesicle involvement, a low postsurgery PSA value, and documented residual disease on TRUS-guided biopsies. Laurent Boccon-Gibod, M.D. Service d’Urologie Hopi&l Bichat 48 rue Henri Huchard 75018 Paris, France REFERENCES 1. Oesterling JE: Prostate specific antigen: a critical assessment of the most useful tumor marker for adenocarcinoma of the prostate. J Urol 145: 907-923, 1991.

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2. Oesterling JE, Chan DW, Epstein JI, Kimball AW Jr, Bruzek DJ, Rock RC, Brendler CB, and Walsh PC: Prostate specific antigen in the preoperative and postoperative evaluation of localized prostatic cancer treated with radical prostatectomy. J Urol 139: 766-772, 1988. 3. Stamey TA, Kabalin JN, McNeal JE, Johnstone IM, Freiha F, Redwine EA, and Yang N: Prostate specific antigen in the diagnosis and treatment of adenocarcinoma of the prostate. II. Radical prostatectomy treated patients. J Urol 161: 1076-1083, 1989. 4. Hudson MA, and Catalona WJ: Effect of adjuvant radiation therapy on prostate specific antigen following radical prostatectomy. J Urol 143: 1174-1177, 1990. 5. Eisbruch A, Perez CA, Roessler EH, and Lockett MA: Adjuvant irradiation after prostatectomy for carcinoma of the prostate with positive surgical margins. Cancer 73: 384-388, 1994. 6. Walsh PC: Adjuvant radiotherapy after radical prostatectomy: is it indicated? J Urol 138: 1427-1428, 1987. 7. Walsh PC, Lepor H, and Eggleston JD: Radical prostatectomy with preservation of sexual function: anatomical and pathological considerations. Prostate 4: 473-485, 1983. 8. McNeal JE: Regional morphology and pathology of the prostate. Am J Clin Path01 49: 347-357, 1968. 9. Graves HC, Wehner N, and Stamey TA: Ultrasensitive radioimmunoassay of prostate-specific antigen. Clin Chem 38: 735-742, 1992. 10. Freeman JA, Lieskovsky G, Cook DW, Petrovich Z, Chen C, Groshen S, and Skinner DG: Radical retropubic prostatectomy and post operative adjuvant radiation for pathological stage C (PcNO) prostate cancer from 1976 to 1989: intermediate findings. J Urol 149: 1029-1034, 1993. 11. Stamey TA, Ferrari MK, and Schmid HP: The value of serial prostate specific antigen determinations 5 years after radiotherapy: steeply increasing values characterize 80% of patients. J Urol 150: 1856-1859, 1993. 12. George FW, Carlton CE Jr, Dykhuizen RF, and Dillon JR: Cobalt 60 telecurietherapy in the definitive treatment of carcinoma of the prostate: a preliminary report. J Urol 93: 102-109, 1965. 13. Ray GR, Cassady JR, and Bagshaw MA: External beam megavoltage radiation therapy in the treatment of post-radical prostatectomy residual or recurrent tumor: preliminary results. J Uroll14: 98-101, 1975. 14. Hanks GE, and Dawson AK: The role of external beam radiation therapy after prostatectomy for prostate cancer. Cancer 58: 2406-2410, 1986. 15. Link P, Freiha FS, and Stamey TA: Adjuvant radiation therapy in patients with detectable prostate specific antigen following radical prostatectomy. J Urol 145: 532-534, 1991. 16. Zincke H, Utz DC, and Taylor WF: Bilateral pelvic lymphadenectomy and radical prostatectomy for clinical stage C prostate cancer: role of adjuvant treatment for residual cancer and in disease progression. J Urol 135: 1199-1205, 1986. 17. Lange PH, Lightner DJ, Medini E, Reddy PK, and Vessella RL: The effect of radiation therapy after radical prostatectomy in patients with elevated prostate specific antigen levels. J Urol 144: 927-932, 1990. 18. Morgan WR, Zincke H, Rainwater LM, Myers RP, and Klee GG: Prostate specific antigen values after radical retropubic prostatectomy for adenocarcinoma of the prostate. Impact of adjuvant treatment (hormonal and radiation). J Urol 145: 319-323, 1991. 19. Kaplan ID, Cox RS, and Bagshaw MA: Prostate specific antigen after external beam radiotherapy for prostatic cancer: followup. J Urol 149: 519-522, 1993.

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20. Stamey TA, Graves HC, Wehner N, Ferrari M, and Freiha FS: Early detection of residual prostate cancer after radical prostatectomy by an ultrasensitive assay for prostate specific antigen. J Urol 149: 787-792, 1993. 21. Partin AW, Pound CR, Clemens JQ, Epstein JI, and Walsh PC: Serum PSA after anatomic radical prostatectomy. The Johns Hopkins experience after 10 years. Urol Clin North Am 20: 713-725, 1993. 22. Crawford ED, and DeAntoni EP: PSA as a screening test for prostate cancer. Urol Clin North Am 20: 637-646, 1993. 23. Frazier HA, Robertson JE, Humphrey PA, and Paulson DF: Is prostate specific antigen of clinical importance in evaluating outcome after radical prostatectomy? J Urol 149: 516-518, 1993. 24. Gibbons RP, Cole BS, Richardson RG, Correa RJ Jr, Brannen GE, Mason JT, Taylor WJ, and Hafermann MD: Adjuvant radiotherapy following radical prostatectomy: results and complications. J Urol 135: 65-68, 1986. 25. Montie JE: Significance and treatment of positive margins or seminal vesicle invasion after radical prostatectomy. Urol Clin North Am 17: 803-812, 1990. 26. Kaufman JJ, Smith RB, and Raz S: Radiation therapy in carcinoma of the prostate: a contributing cause of urinary incontinence. J Urol 132: 998-999, 1984. 27. Lange PH, Moon TD, Narayan P, and Medini E: Radiation therapy as adjuvant treatment after radical prostatectomy: patient tolerance and preliminary results. J Urol 136: 45-49, 1986. EDITORIAL COMMENT A measurable serum prostate-specific antigen (PSA) following radical prostatectomy usually signifies the failure to eradicate the cancer. Although PSA values of 1 ng/mL or less that remain level over several months may represent benign elements, a steep rise of more than 0.8 ng/mUyear indicates the presence of cancer. The authors have presented a series of 17 patients who had external beam radiation to the prostatic bed following a persistent PSA, a steep rise in PSA, or biopsy-proven residual disease after radical prostatectomy. In this series the vast majority of the authors’ patients failed radiation therapy, including 6 patients who had no seminal vesicle disease (only 2 of these 6 had biopsies that yielded cancer). Radiation therapy eradicated detectable PSA in 3 of 5 patients whose seminal vesicles also had shown no cancer, but who had biopsies that showed cancer at the anastomosis. The authors’ series supports the contention that radiation therapy is unlikely to benefit patients who had cancer involving the seminal vesicles; however, the dilemma facing most urologists occurs in the setting of a rising PSA in a postsurgical patient whose metastatic evaluation is negative and who had no seminal vesicle involvement. The authors’ results underscore the question of whether postsurgical biopsy of the anastomosis is warranted at all. A negative biopsy does not guarantee that the recurrence is not local. Recent advancements using monoclonal antibody-assisted imaging of prostate cancer metastases may help define which patients are good candidates for the limited benefits of radiation therapy.

JonathanFleischmann, M.D. Department of Urology 1825 Eastchester Road Bronx, NY 10461

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