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© 2003 American Society for Clinical Oncology Indium-111–Capromab Pendetide Radioimmunoscintigraphy and Prognosis for Durable Biochemical Response to Salvage Radiation Therapy in Men After Failed Prostatectomy
From the Division of Radiation Oncology, University of Cincinnati, Barrett Center for Cancer Prevention, Treatment and Research, Cincinnati, OH; Center for Epidemiology and Biostatistics, University of Texas Health Science Center at San Antonio, San Antonio; Department of Biomathematics, M.D. Anderson Cancer Center, Houston, TX; Department of Urology, University of Michigan Health Systems; Department of Biostatistics, University of Michigan; Department of Radiation Oncology, University of Michigan Health Systems, Ann Arbor, MI; and the Division of Nuclear Medicine, Department of Radiology, The Johns Hopkins Medical Institutions, Baltimore, MD. Address reprint requests to Richard L. Wahl, MD, Department of Radiology, The Johns Hopkins Medical Institutions, The Johns Hopkins Outpatient Center, 601 North Caroline St, Room 3231A, Baltimore, MD 21287-0817; email: RWahl{at}jhmi.edu or Cherry.Thomas{at}uc.edu.
Purpose: We evaluated the prognostic significance of indium-111 (111In)–capromab pendetide imaging for patients with prostate cancer who underwent salvage radiotherapy (RT) for recurrent disease after prostatectomy. Patients and Methods: Records were reviewed for all men who underwent 111In–capromab pendetide imaging at a single institution from February 1997 through December 1999. We identified 30 eligible men who were radiographically negative for metastatic disease, who had increasing serum prostate-specific antigen (PSA) after primary radical prostatectomy, and who received salvage RT. Clinical interpretations of indium monoclonal antibody (In-mab) scan results were compared with postsalvage RT PSA response. Results: Using an American Society of Therapeutic Radiation and Oncology definition of PSA failure, in men with a positive scan in at least one location (n = 14), the cumulative 2-year PSA control after salvage RT was 0.38 ± 0.13 (± SE) compared with 0.31 ± 0.13 for men with a normal antibody scan in and outside the prostate fossa (n = 15; proportional hazard ratio [PHR] = 1.32; 95% confidence interval [CI], 0.52 to 3.36). For men with a positive antibody scan limited to the prostate fossa (n = 9), PSA control at 2 years was 0.13 ± 0.12 (PHR 1.77; 95% CI, 0.65 to 4.85). The 2-year probability of PSA control after salvage RT for men with positive scan results outside the prostate bed irrespective of In-mab findings in the prostate fossa (n = 5) was 0.60 ± 0.22 (PHR 0.81; 95% CI, 0.17 to 3.78). Conclusion: In contrast to previous reports, for patients with postprostatectomy biochemical relapse who received salvage RT, presalvage RT In-mab scan findings outside the prostate fossa were not predictive of biochemical control after RT.
RECENT STUDIES have identified the indium-111 (111In)–capromab pendetide scan (ProstaScint, Cytogen Corporation, Princeton, NJ) as one of multiple significant variables with prognostic value in determining nodal or metastatic disease in men with increasing serum prostate-specific antigen (PSA) after primary treatment for prostate cancer.1–5 Radioimmunoscintigraphy with 111In–capromab pendetide is an imaging modality indicated for postprostatectomy patients who have increasing PSA, a negative or equivocal metastatic evaluation, and a high clinical suspicion of occult metastatic disease.6 111In–capromab pendetide makes use of a murine immunoglobulin G (IgG1k) monoclonal antibody designated, in its radiolabeled form, 7E11-C5.3. Developed by Horoszewicz et al,7 the antibody recognizes the intracellular epitope of prostate-specific membrane antigen (PSMA), a 100-kd transmembrane glycoprotein almost entirely specific to human prostate epithelial cells.8,9 111In–capromab pendetide imaging has been reported as prognostic for candidates for salvage radiation therapy after a failed radical prostatectomy.10,11 Kahn et al10,12 showed that patients who underwent salvage radiation therapy for failed prostatectomy were more likely to sustain a durable complete PSA response if they had a negative 111In–capromab pendetide scan outside the pelvis compared with men with a positive extraprostatic scan. Levesque et al11 corroborated the results. These studies indicate that the indium monoclonal antibody (In-mab) scan incrementally adds to other predictors of decline in increasing PSA after salvage radiation therapy. Other prognostic factors include, but are not limited to, the PSA level at the time of salvage radiation therapy,13–15 radiation dose,14 and undetectable postoperative PSA nadir.16 However, analysis of a subset of patients by Seltzer et al17 supports the premise that helical computed tomography (CT) or positron emission tomography detects metastatic disease more accurately than 111In–monoclonal antibody scanning. Data that support the use of 111In–capromab pendetide to select patients for salvage radiation therapy after failed prostatectomy have been described as promising but still preliminary.18 We hypothesized that extrapelvic findings in the 111In–capromab pendetide scan would predict PSA outcome after salvage radiation therapy. To test this hypothesis, we assessed a group of patients from a single institution who underwent 111In–capromab pendetide imaging as part of their evaluation for increasing PSA after radical prostatectomy. All of these patients received salvage radiotherapy followed by regular PSA testing. We compared PSA outcome with clinical In-mab scan interpretations. With a median follow-up time of 34.5 months, our results were discordant with prior reports that indicated that the In-mab scan accurately identifies men who will respond biochemically to salvage radiation therapy.
We identified the medical records of all patients (N = 194) who underwent 111In–capromab pendetide imaging at the University of Michigan Health System (UMHS) from February 1997 through December 1999. One hundred sixty-five patients had increasing serum PSA levels after primary treatment for prostate cancer, 147 of whom underwent primary radical prostatectomy. Eighty-five of the 147 patients were imaged on referral from outside hospitals; because their records were incomplete, these patients were excluded. Sixty-two of the 147 were UMHS patients. One of the 62 UMHS patients was excluded from this analysis because he underwent primary brachytherapy and was imaged with 111–capromab pendetide before salvage prostatectomy. The remaining 61 patients underwent In-mab imaging as part of an evaluation for postprostatectomy PSA relapse. They were men who underwent primary radical prostatectomy, salvage radiation therapy, salvage hormone ablation, or chemotherapy in the UMHS and who were observed regularly by UMHS physicians. All In-mab scans were interpreted and reported by UMHS nuclear medicine physicians, and clinical reports were used for this study. After In-mab imaging, 17 of the 61 UMHS patients who had primary prostatectomy elected observation only (n = 5), palliative androgen ablation (n = 8), or chemotherapy for metastatic disease (n = 4). Of these 61 patients, 44 received salvage radiation therapy. From this group of 44 men, those who received neoadjuvant salvage androgen deprivation with radiation therapy salvage (n = 11), had a PSA measuring less than 0.2 ng/mL before the In-mab scan (n = 2), or had a more than a 7-month interval between In-mab imaging and completion of radiation therapy (n = 1) were excluded from study, leaving 30 study patients. Four study patients had a positive digital rectal examination (DRE) at the time of evaluation for biochemical relapse. Only one of the four patients underwent biopsy of the prostate fossa, the results of which diagnosed poorly differentiated adenocarcinoma, consistent with the pathology identified on radical prostatectomy. None of the 30 patients had radiographic evidence of metastatic disease by CT imaging or bone scan at the time of postprostatectomy PSA relapse, but before salvage radiation therapy. We compared diagnostic PSA and Gleason sums for men included and excluded from our analytic cohort.
Imaging Protocol Immediate imaging began within 30 minutes after a single dose injection of 5 or 6 mCi 111In–capromab pendetide monoclonal antibody on day 0. Delayed imaging was performed 5 and 6 days after injection. Whole-body scanning was performed with autocontouring and a scanning speed of 20 cm/min. Acquisition parameters for the 111In–capromab pendetide scan included step-and-shoot detector motion, a 128 x 128 acquisition matrix without zoom, 180° rotation per head, and 60 stops at 3° each. Single photon emission computed tomography (SPECT) imaging was performed for pelvis and abdomen views. Parameters included a 64 x 64 matrix, 32 projections for each detector, and 30 seconds per projection. On days 5 and 6, whole-body imaging was obtained with a scanning speed of 8 cm/min with autocontouring. Static views were obtained as they were on day 0. SPECT imaging was also obtained in the same manner as in day 0, save projection time, which was 40 seconds. Following initial SPECT scanning, three planar views of the head and chest, chest and abdomen, and abdomen and pelvis were obtained using a 256 x 256 matrix. These views were acquired for 10 minutes each. To remove fecal radioactivity from the bowel, patients were generally prescribed bisacodyl, 10 mg daily, with instructions to start the medication 48 hours before imaging on days 5 and 6 and to continue taking the medication until completion of imaging. Tomographic data were attenuation corrected and processed using three-dimensional postfiltering algorithms. Images were reconstructed in transverse planes. Coronal and sagittal planes were derived from the transverse images.
Primary and Salvage Therapy At UMHS treatments were delivered to the prostate bed plus a 1-cm margin with four fields, two of which were off axial beams (right anterior inferior oblique, left anterior inferior oblique). Patients received 64.8, 68.4, or 70.2 Gy in 1.8-Gy fractions prescribed to the 100% isodose line and delivered with 15- to 18-MV photons. Some patients received 45 Gy in 1.8-Gy fractions to the pelvis, followed by 19.8 Gy in 1.8-Gy fractions to the prostate bed plus a 1-cm margin. Radiation treatment from known outside hospitals delivered 64 to 70 Gy to the prostate fossa using CT-based treatment planning. Target volume included 15- to 20-mm margins and was determined using CT to identify the prostate fossa or, in one patient, using a three-dimensional CT reconstruction of the preoperative prostate and seminal vesicles. Physicians based their decision to offer salvage radiation therapy on standard clinical criteria, including patterns of PSA increase, physical examination (with DRE), radiological imaging such as bone scintigraphy or CT, and patient risk factors. No patient was deprived of salvage radiation therapy because of In-mab scan results alone. For the 29 patients with available information concerning technique, radiation treatment was planned without consideration of 111In–capromab pendetide scans.
Postsalvage Follow-Up Care
Image Interpretation
Determination of Biochemical Failure
Statistical Analysis
Approval of the Study Protocol
Characteristics of the Patients Thirty men met eligibility criteria. The median diagnostic PSA value was 10.0 ng/mL (n = 28), compared with the same 10.0 ng/mL (n = 43) for excluded patients who underwent primary radical prostatectomy. Median Gleason sums for study patients and excluded subjects were 7 for both groups. Differences between these groups by diagnostic PSA and Gleason sum were not statistically significant (two-sided t test, P = .15 and .49, respectively). Ages at the time of In-mab imaging ranged from 53 to 79 years (median, 64 years). Patients underwent 111In–capromab pendetide scintigraphy at the time of evaluation for postprostatectomy increasing PSA; therefore, the months from radical prostatectomy to the date of In-mab imaging was a surrogate for time to postoperative failure (Table 1  ). Table 2 shows the pathologic stage distribution (1997 American Joint Committee Cancer system22) and the surgical margins at the time of radical prostatectomy.
Follow-Up The median follow-up since completion of radiation therapy was 34.5 months (Table 1  ). PSA testing averaged 15.1 tests per patient over the entire follow-up period, with an average of 5.2 tests per year. Twenty-eight patients continue to receive follow-up care. One patient died of metastatic prostate cancer after 49 months of follow-up. Sixteen months after completing salvage radiation therapy, a second patient died of a vascular event not associated with prostate cancer.
In-Mab Scan Results Compared With PSA Control After Salvage Radiation Therapy
We also performed the time-to-failure analysis using three alternative PSA threshold cut points: PSA more than 0.2 ng/mL, more than 0.3 ng/mL, and more than 0.4 ng/mL. All 30 patients had sufficient PSA follow-up to make these assessments. There were no statistically significant associations between 111In–capromab pendetide imaging results and PSA outcome. These results were invariant to choice of cut points.
111In–Capromab Pendetide Scintigraphy Imaging
We investigated whether 111In–capromab pendetide immunoscintigraphy in men with prostate cancer who underwent evaluation for biochemical relapse after radical prostatectomy would predict a durable PSA response to salvage radiation therapy. By four different measures of biochemical progression after postprostatectomy salvage radiation therapy, we found no statistically significant association between 111In–capromab pendetide immunoscintigraphy and discrimination between men who would or would not achieve biochemical control. A negative scan outside the pelvis was no more prognostic of postsalvage radiation therapy PSA control than a positive scan. In the pelvis, scan results for PSA control showed a small, but statistically insignificant difference. Therefore, this surveillance method is of limited use for medical decision making for an individual patient. Our findings are discordant with previous reports that show a capacity for 111In–capromab pendetide to discriminate between patients who will or will not achieve a durable complete PSA response after salvage radiation therapy.10–12 One study of patients with postprostatectomy biochemical relapse and a negative In-mab scan outside the pelvis demonstrated, after 13 and 35 months median follow-up, a statistically higher likelihood for durable complete PSA response to salvage radiotherapy compared with similar patients with positive findings outside the pelvis.10,12 Durable complete response was defined as a PSA value of 0.3 ng/mL or less for longer than 6 months at the time of last follow-up. A contemporaneous analysis of 13 men who underwent In-mab imaging for increasing PSA after primary prostatectomy found, with 14 months mean follow-up after salvage radiation therapy, PSA failure in four of six patients with extrapelvic positivity. The authors reported a good response (PSA levels 0.2 ng/mL or less after 17 months mean follow-up) in five of seven men with a negative In-mab scan beyond the salvage radiation therapy field.11 Compared with previous reports,10,12 our study patients had a similar distribution of pathologic stage of prostate cancer, median follow-up time,12 and Gleason sums. Similarly, our study patients received salvage radiation therapy alone without combined salvage androgen deprivation. Because postsalvage PSA values were unaffected by androgen deprivation, biochemical successes were more likely to have resulted from local radiation therapy. Our patients received a range of radiation doses considered to be the standard of care and shown to control biochemical relapse in 64% of patients after 36 months follow-up.23 Unlike previous reports, our study patients underwent uniform 111In–capromab pendetide imaging at a single institution. Twenty-six of 30 study patients underwent salvage radiation therapy at a single institution. In addition, we excluded from analysis one patient who completed radiation therapy 28 months after In-mab imaging. The long-time duration between In-mab imaging and completion of salvage treatment suggested that the scan was not part of the patient’s evaluation for salvage radiotherapy. We excluded two patients whose increasing PSA values were 0.1 ng/mL, because these men may have received androgen deprivation therapy or may have received salvage radiation therapy on the basis of criteria different from those of study cohorts. Although these factors lead to a more homogeneous study population, they are small differences and are unlikely to explain the discordant study results. With respect to outcome assessment, because there is no consensus for biochemical relapse after salvage radiotherapy, we chose generalized definitions currently used for postprimary treatment biochemical failure that would most likely be used in a clinical setting by most urologists or radiation oncologists. A recent analysis of definitions for PSA progression after radical prostatectomy recommended PSA 0.4 ng/mL as an appropriate cut point because a significant number of patients with lower PSA do not have a continued increase in PSA.24 Other studies have used ranges from 0.2 to 0.5 ng/mL as representative measurable values above the level of detection for the PSA assay.25–28 The ASTRO consensus guidelines define biochemical failure in the context of mitotically inactive but residual surviving cancer cells after radiation therapy.29 Radiation-treated cells have the potential to produce PSA but eventually undergo mitotic cell death, which may likely account for the wide range in PSA tumor marker half-life after radiation therapy.30 In accordance with these considerations, we tested three commonly used cut point definitions of PSA failure after primary treatment and the ASTRO consensus for the same. 111In–capromab pendetide imaging results were not prognostic of postsalvage radiation therapy PSA outcome by any of the four measures of PSA progression. Our study did not provide histologic confirmation of positive findings in the 111In–capromab pendetide scan. Similar shortcomings in histologic validation are well documented for MRI imaging.31 Although histologic confirmation is a valuable means of determining imaging accuracy, it can be problematic for some new technologies. There may be errors in registering the location of imaging foci with histologic slice specimens. More important, 111In–capromab pendetide targets the diagnosis of early prostate cancer recurrence that cannot be identified with existing laboratory or imaging technology. Appropriate reference standards simply do not exist. Nevertheless, our results indicate that the use of capromab pendetide imaging may not have clinical utility for assessment of salvage radiation therapy. Ultimately, the best validation of 111In–capromab pendetide imaging is how well it tracks with the natural history of the patient’s disease.32 111In–capromab pendetide scintigraphy targets a tissue-specific marker (PSMA) of neoplastic prostate cells, and it uses a stable in vivo immunoconjugate that produces a good target-to-background photon emission (tumor to blood) ratio.33–38 Despite these qualities, inaccuracy of 111In–capromab pendetide imaging has been reported. Levesque et al11 showed that 10 of 48 (21%) patients who had positive PSA results had scans that failed to localize any site of recurrence. In 21 patients who underwent 111In–capromab pendetide imaging for elevated serum PSA after primary treatment for prostate cancer, Seltzer et al17 found that the In-mab scan was true positive in one of six patients who underwent CT-guided fine-needle aspiration. False-positive radioimmunoscintigraphy with 111In–capromab pendetide has been attributed to areas of turbulence within vascular structures causing areas of radioactive material deposits,39 and to pooling of radiolabeled antibodies in tissues with high blood content.40,41 The question of whether circulating PSMA is measurably expressed in serum or sequestered from serum is under investigation, but serum levels appear to be low.42–44 Researchers have described the interpretation of 111In–capromab pendetide imaging as challenging,45 but have expected that increased experience with the imaging agent would improve image acquisition, quality, and interpretation.6 Yet observer variability in the interpretation of capromab pendetide imaging either between nuclear medicine physicians from different institutions or within nuclear medicine departments has not been studied. We did not scientifically test for interobserver variability. Until future studies qualify observer bias, we postulate that variability in image interpretation may be one potential cause for our discordant findings. In contrast to previous reports, we used actuarial statistics. Time-to-failure methods are more sensitive in that they account for varying lengths of follow-up for individuals in the cohort. However, with the relatively small sample size, our statistical power still may have been limited. Whether the In-mab scan should complement current medical management requires additional evaluation of the scan’s effect on clinical decision making, patient health outcome, and the cost for the benefit.46 These determinations should not be made on the basis of case series or imaging efficacy studies.47 A study design that evaluates both diagnostic accuracy and empirical outcome measures (specifically, how physicians actually use the test) would add relevance to rigor in the clinical investigation of such new technology.46 A future prospective cohort study or randomized trial of 111In-labeled capromab pendetide radioimmunoscintigraphy may more precisely determine the suitability of this technique for identifying postprostatectomy patients with biochemical relapse who should be spared salvage local therapy. However, our results indicate that 111In-labeled capromab pendetide radioimmunoscintigraphy may be of limited incremental value in selecting patients with local prostate cancer recurrence who may achieve PSA control after salvage radiation therapy.
We thank the General Clinical Research Center staff of the University of Michigan; Susan G. Hilsenbeck, PhD; Janna C. Lawrence, MLIS; Michael J. Lichtenstein, MD; Mark A. Rubin, MD; Martin G. Sanda, MD; Michael J. Welsh, PhD and John W. Wiley, MD whose invaluable support made this study possible.
Supported in part by U.S. Government Department of Health and Human Services Public Health Service grant no. M01-RR00042 awarded by the National Institutes of Health, National Center for Research Resources, and the National Cancer Institute, Bethesda, MD; and the University of Michigan Specialized Program of Research Excellence in Prostate Cancer grant no. SPORE-1-P50-CA69568.
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Copyright © 2003 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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ABSTRACT
INTRODUCTION
0.3 ng/mL were considered to have biochemical relapse. After salvage radiation therapy, biochemical relapse was defined using an application of the American Society of Therapeutic Radiation and Oncology (ASTRO) consensus definition of biochemical relapse after primary radiation therapy. The ASTRO guidelines for PSA define failure as three consecutive increases in PSA, and for clinical trials, the date of failure should be the midpoint between the postirradiation nadir PSA and the first of the three consecutive increases.
6 or > 6 ng/mL); Gleason sum (categorized as 
