Enrollment Criteria Controversies for Active Surveillance and Triggers for Conversion to Treatment in Prostate Cancer

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  • 1 From H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.

In the era of widespread prostate-specific antigen screening, low-risk and very-low-risk prostate cancers are commonly identified, many of which will be of clinical insignificance. This has led to overtreatment and undue exposure to treatment-related morbidity in men harboring indolent tumors. Over the past 10 years, active surveillance (AS) has been evolving as a management strategy for these cancers. With continual reevaluation, the intent is to definitively treat tumors that are clearly progressive before the window of opportunity for cure has closed. To date, many of the surveillance parameters are without validation of utility, variably used, and without a standardized schedule. However, new instruments for characterizing prostate cancer offer the potential to better distinguish which men are best managed definitively at the outset from those who would be better served with observation. The findings of currently available AS cohorts suggest that initial expectant management of early prostate cancer is reasonable, showing that only approximately 30% of observed tumors are reclassified to ones of intermediate risk with short-term follow-up. Prostate cancer survival for men undergoing AS is close to 100% in all available studies, but long-term data remain scarce for those requiring delayed curative therapy.

The year 2012 marks the 10th anniversary of the initial reporting of active surveillance (AS) as a management strategy for low-risk prostate cancer.1,2

Since the widespread use of prostate-specific antigen (PSA) beginning in the early 1990s, a downward risk migration of newly diagnosed prostate cancer3 has occurred, along with the revelation that low-risk tumors are often of clinical insignificance.48 Despite the fact that these low-risk cancers have a slow growth rate and a low probability of metastasis and death within the first 10 years after diagnosis,9 91% of patients with tumors fulfilling Epstein’s criteria for low risk or very low risk still undergo treatment.10 This occurs amidst recent reporting that, at a median follow-up of 11 years, 37 cancers, spanning all risk categories, must be treated to prevent 1 prostate cancer–specific mortality.11 In 2011, the United States Preventative Services Task Force cautioned that the use of PSA to screen for prostate cancer in asymptomatic men leads to overdiagnosis and overtreatment in most men diagnosed with prostate cancer,12 supporting AS as a reasonable management option for well-selected patients.

Critical uncertainties still surround the AS algorithm. Specifically, a need remains to optimize the criteria that qualify a man as either low risk or very low risk, and to establish standardized criteria defining disease progression. Further, there is a paucity of reports on the long-term outcomes of men electing to delay or forgo definitive treatment.

This article reviews the most recent literature regarding these clinical questions and provides a practical algorithm that may assist practitioners when counseling men undergoing AS. This algorithm may be modified and expanded as new knowledge develops.

Risk Stratification and Eligibility Criteria

The D’Amico et al13 and Epstein et al4 criteria are the most commonly used risk stratification systems. Low-risk cancers14 are those presenting with a PSA of less than 10 ng/mL and a Gleason sum of 6 or lower, and very-low-risk tumors4 are those that meet the low-risk criteria and also show tumor involvement of less than 50% of any biopsy core, involve fewer than 3 biopsy cores, are nonpalpable, and are associated with a PSA density of 0.15 ng/mL/g or less. Tumors of very low risk have been associated with tumor volume of less than 0.5 cm3 at prostatectomy. Both sets of criteria require the findings of either a normal prostate or the presence of only a small nodule (cT1, cT2a) on digital rectal examination (DRE) and have been incorporated into the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Prostate Cancer (to view the most recent version of these guidelines, visit NCCN.org). Current NCCN Guidelines define low-risk tumors as clinical T1 through T2a tumors with a Gleason sum of 6 or lower and are associated with a PSA of less than 10 ng/mL. Very-low-risk tumors are clinically T1 tumors, have a Gleason sum of 6 or lower, involve fewer than 3 cores and 50% or less of any individual core, and are associated with a PSA density of less than 0.15 ng/mL/g.15 Patients with these characteristics have been found to harbor clinically insignificant tumors with a tumor volume of less than 0.5 cm3, have a Gleason sum of 6 or lower, have no extraprostatic extension, and have negative margins, seminal vesicles, and lymph nodes at the time of radical prostatectomy (RP).4 These men also have a very low prostate cancer–specific mortality even at long-term follow-up.16

A review of reported AS series1724 reveals significant lack of standardization with respect to inclusion criteria (Table 1). Although PSA, Gleason grade, and clinical stage are generally accepted selection criteria, the additional parameters of PSA density, percent-free PSA, and extent to which biopsy cores are involved by tumor are variably considered.

PSA Density

A PSA density of 0.08 ng/mL/g or greater25 is identified as a significant predictor of future disease progression in those with low-risk prostate cancer initially managed expectantly.26 However, this is not a consistent finding,17,23 because other clinicians use a level of 0.15 ng/mL/g as a threshold.4

Percent Free/Total PSA

Shariat et al27 indentified percent-free PSA to be a significant predictor of organ-confined disease, seminal vesicle invasion, lymphovascular invasion, and Gleason sum on multivariate analysis of 402 patients presenting with a PSA of less than 10 ng/mL who were managed with RP and pelvic lymph node dissection. Other reports confirm this observation.17,23,28 Inspection of whole-mount prostatectomy specimens has previously shown a significant indirect correlation between percent-free PSA and prostate cancer volume.29 In 376 patients on AS, a multivariate analysis accounting for age, PSA, PSA density, and number of cores positive for prostate cancer found that a percent-free PSA of 15 or less was predictive of future tumor reclassification.25 Nevertheless, this parameter is not widely accepted as a predictor of cancer extent.3033

Number of Cores and Volume of Involvement

All but one of the evaluated AS studies lists the number of positive cores and the extent to which each core is involved as part of the enrollment criteria. Reports are consistent in showing the predictive value of the number of positive cores,34,35 but limited data support optimal cutoff points,35,36 and this finding remains controversial regarding outcomes in AS cohorts.17,23

Cheng et al34 investigated the significance of the extent to which a single biopsy core was involved. They found a significant correlation with prostate cancer volume in univariable analysis, and provided a graphical representation showing that the probability of finding only low-volume disease at RP in patients with greater than 30% of any one core was less than 5%.

Accounting for both the number of positive cores and the extent to which each core was involved by tumor, Ploussard et al37 prospectively found that obtaining 21 cores, compared with 12, provided a more accurate prediction of those with truly indolent prostate cancer based on RP specimens. However, Eggener et al19 found that the total number of positive cores after 2 standard biopsies (but not the total number of cores) identified before assignment to AS correlated with progression-free interval.

Surveillance Protocols

Frequency of PSA/DRE

No standardized protocol exists for the frequency of PSA or DRE. Current guidelines vary, with recommendations to obtain a PSA every 3 to 6 months and perform a DRE every 3 to 6 months, or 12 months in men with a life expectancy of 10 years or more. Most surveillance protocols include a PSA every 3 to 4 months and a DRE every 6 months, especially within the first 2 years (Table 2).

Table 1

Inclusion Criteria

Table 1

Frequency of Prostate Biopsies

The frequency at which prostatic biopsies are indicated is also variable. Recommended intervals range from once a year to every 3 years, with most investigators in favor of obtaining an initial repeat biopsy 1 year after the original diagnostic biopsy. Some authors advocate performing an immediate restaging biopsy,19,38 because 27% of tumors may either be upgraded or upstaged on repeat biopsy.38 Others suggest performing a more extensive transperineal biopsy at the second biopsy39 to sample the transition zone where approximately 20% of prostate cancer tumors occur,40 and at the midline peripheral zone, which is traditionally not sampled at the time of transrectal biopsy. Using a transperineal template biopsy at restaging, Ayres et al39 found that 32% of men were upstaged or upgraded.

A compromise of the 2 aforementioned biopsy strategies is the transrectal acquisition of the standard sextet templated biopsies plus an additional 3 posterolateral biopsies from both the right and left lobe directed at an approximately 30° angle.41 This technique is intended to minimize undersampling of the anterior and posterior/posterolateral regions previously shown to harbor approximately 90% of the dominant malignant nodules at RP after a period of AS.42

Serial prostatic biopsies are not without consequence, because rectal bleeding, hematuria, and hematospermia commonly manifest postprocedurally. The proven practice of using periprocedural prophylactic antibiotics has led to more than 90% of urologists within the United States providing patients with a fluoroquinolone before performing transrectal ultrasound-guided biopsies of the prostate.4345 However, the incidence of infectious complications and those specifically attributed to fluoroquinolone-resistant microbes is increasing,46,47 with Escherichia coli the most common pathogen.48 Previous exposure to fluoroquinolones within 6 months significantly increases the risk of prostatitis from prostatic biopsy48 and should be considered at repeat prostatic biopsy. Recent studies explored the potential benefit of obtaining cultures from rectal swabs and adjusting prophylactic antibiotics accordingly.49 Erectile dysfunction has also been associated with serial biopsies.50

Table 2

Surveillance Protocols

Table 2

New Potential Tools in the Management of Men Undergoing AS

PCA3 Urinary Marker

A noncoding portion of mRNA mapped to chromosome 9q21–22 is known as prostate cancer gene 3 (PCA3). Using a urine sample collected after performing a prostate massage, an assay is performed to quantify the copies of PCA3 and PSA mRNA. Using the copy number of PSA mRNA as the denominator, a ratio (PCA3 copies/PSA mRNA copy) is calculated to provide a PCA3 score. The ratio allows the PSA mRNA to serve as a positive control (assuring the sample has adequate material for evaluation) and accounts for background or baseline expression that can be found in normal and hypertrophic prostatic tissue. Currently, a PCA3 score of 35 or greater is considered suggestive of the presence of malignancy. Since its discovery, PCA3 scores have been found to be prostate cancer–specific51,52 and unaffected by the presence of prostatitis or prostatic volume/benign prostatic hyperplasia,53 which historically have been confounders associated with an elevated serum PSA. Further, PCA3 scores have been found to correlate with tumor volumes.54,55

To validate previous reports regarding the application of the PCA3 score, 1140 patients within the REDUCE chemoprevention trial were evaluated. These men were in the placebo arm and had provided PCA3 samples before repeat prostatic biopsies at years 2 and/or 4.56 PCA3 score was independent of prostate volume. The median PCA3 score was significantly different for those found to have prostate cancer (33.8) versus those found to have benign biopsies (16.7). The sensitivity and specificity for prostate cancer detection were 48.4% and 78.6%, respectively, using the standard cutoff value of 35; with those having a PCA3 score of 35 being 3.5 times more likely to have a positive prostatic biopsy. This is consistent with prior studies.57,58 The results showed a direct correlation between PCA3 scores and the rate of positive biopsies (ie, the positive predictive value [PPV]). Using a cutoff of 100, a PPV of 57.1% was noted. Further, in those with a PCA3 score of less than 5, the chance of prostate cancer detection was only 6% and, thus, a low value may provide more comfort in prolonging the interval between biopsies.

PCA3 scores were also found to correlate with Gleason scores. Of those with a Gleason sum of 6 or lower, the median PCA3 score was 31.8 compared with a median of 49.8 for those with a Gleason sum greater than 6. Lastly, a multivariable analysis accounting for age, family history, PCA3 score, PSA, percent-free PSA, and prostate volume found that all factors had a significant influence on the outcomes of prostatic biopsy.

Despite potential clinical utility when applied to AS protocols, the prognostic capability of baseline PCA3 levels to distinguish those who will experience progression from those who will not while on AS remains unproven. In a series inclusive of 294 men on AS, PCA3 levels obtained at diagnosis were not predictive of progression on short-term follow-up.59

Table 3

Reclassification Parameters

Table 3

Endorectal Multiparametric MRI

Recently, a single-armed prospective trial60 examined the efficacy of multiparametric T2-weighted endorectal MRI of the prostate with and without intravenous contrast. The accuracy of the MRI assessment was evaluated through prostatic biopsy within 1 year of initial biopsy or immediately in those with a suspicious lesion of greater than 1 cm in any one dimension, because the spherical volume of such a lesion would represent a significant lesion of 0.5 cm3.36 Of those initially classified as low-risk, 38% and 40% of patients, respectively, had either no radiographic evidence of prostate cancer or insignificant lesions smaller than 1 cm identified at MRI, leaving only 22% of the patients showing clinically significant lesions larger than 1 cm on MRI despite initial classification. Patients with positive radiographic lesions were significantly more likely to be reclassified at confirmatory biopsy than those with radiographically insignificant or absent lesions. The positive and negative predictive values for MRI findings were 83% and 81%, respectively, based on the associated confirmatory biopsies.60

Table 4

Examination of Oncologic Outcomes With Respect to All Patients Placed on Active Surveillance

Table 4
Table 5

Examination of Oncologic Outcomes in Patients Managed With Delayed Curative Treatment

Table 5
Figure 1
Figure 1

An active surveillance strategy for those with low-risk and very-low-risk prostate cancer.

Abbreviations: AS, active surveillance; DRE, digital rectal examination; PCA3, prostate cancer gene 3; PSA, prostate-specific antigen; PSAd, prostate-specific antigen density; PSAdt, prostate-specific antigen doubling time; PSAv, prostate-specific antigen velocity.

Citation: Journal of the National Comprehensive Cancer Network J Natl Compr Canc Netw 10, 9; 10.6004/jnccn.2012.0116

Characteristics of Cancer Progression/Reclassification

Value of PSA Kinetics

Although most current large AS trials include PSA kinetics as part of the reclassification criteria (Table 3), in 2009, Vickers et al61 performed a systematic review of studies examining the clinical utility of calculating a PSA velocity or PSA doubling time to aid decision-making regarding prostate cancer treatment. They concluded that there was “a near complete lack of evidence” supporting the value of pretreatment PSA kinetics for early-stage prostate cancer.61 Subsequent studies comprising more than 500 patients failed to show utility of PSA velocity62,63 or PSA doubling time62 to predict prostate cancer progression specifically in patients within AS cohorts. However, the implications of serial PSA surveillance remain controversial.64,65

Long-Term Outcomes With AS

Most AS series report that approximately 30% of men will be reclassified in the short term (Table 4). The median time of surveillance free of curative intervention has been reported to be 6.5 years23 and, of those undergoing definitive treatment with RP or radiotherapy, the median time to treatment ranged between 1.3 and 2.3 years, with only very limited follow-up available (Table 5). Two studies have sought to compare the RP pathologic features of men with low-risk prostate cancer who were initially managed definitively versus those men undergoing RP after an interval of AS.66,67 Substantial selection bias confounded the comparisons. Early outcomes in patients managed with delayed RP and radiotherapy have been reported (Table 5), with one study finding no significant difference between modality-specific outcomes21 and another finding a lower cumulative rate of biochemical recurrence in the cohort undergoing RP as opposed to radiotherapy.23 Those receiving radiotherapy had a longer median follow-up. At the time of delayed RP, the rate of positive surgical margins has been reported to be 18.2% to 24.5%.66,68 Fewer than 1% of all men enrolled in AS have shown histologic nodal involvement. The cumulative prostate cancer–specific survival is close to 100%.

Discussion

Standard inclusion criteria are lacking; the efficacy of PSA density and percent-free PSA, and the extent to which biopsy cores are involved by the tumor remain controversial. The potential merit of performing a restaging biopsy is evident when noting that the percentage of tumors that are either upgraded or upstaged after restaging biopsy38 nearly mirrors the percentage of tumors that are reclassified while on AS.21,23,24 More extensive restaging biopsy strategies have been investigated39 but have not shown a grossly evident benefit. Because prostatic biopsies are not without potential for significant morbidity, such as urosepsis6971 and decline in erectile function when performed serially,50 optimization is needed for both restaging and surveillance protocols. PCA3 testing and endorectal MRI represent novel prostate cancer tools that may aid in clinical decision-making. PSA kinetics (PSA velocity and PSA doubling time) have no clear role in AS monitoring, and no optimal surrogate for pathology exists. When counseling men with early prostate cancer, all treatment options, risks, and complications should be discussed. For men electing AS, a diagnostic and follow-up strategy is outlined in Figure 1.

Conclusions

AS is a reasonable management strategy for low-risk and very-low-risk prostate cancer. It obviates exposure to the morbidity that can be associated with definitive management in men with truly indolent lesions, while allowing for continual reassessment and identification of progressive tumors.

The authors have disclosed that they have no financial interests, arrangements, or affiliations with the manufacturers of any products discussed in this article or their competitors.

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    Ross AE, Loeb S, Landis P. Prostate-specific antigen kinetics during follow-up are an unreliable trigger for intervention in a prostate cancer surveillance program. J Clin Oncol 2010;28:28102816.

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    • Export Citation
  • 63

    Whitson JM, Porten SP, Hilton JF. The relationship between prostate specific antigen change and biopsy progression in patients on active surveillance for prostate cancer. J Urol 2011;185:16561660.

    • Search Google Scholar
    • Export Citation
  • 64

    Carvalhal GF, Daudi SN, Kan D. Correlation between serum prostate-specific antigen and cancer volume in prostate glands of different sizes. Urology 2010;76:10721076.

    • Search Google Scholar
    • Export Citation
  • 65

    Loeb S, Metter EJ, Kan D. Prostate-specific antigen velocity (PSAV) risk count improves the specificity of screening for clinically significant prostate cancer. BJU Int 2012;109:508513; discussion 513–514.

    • Search Google Scholar
    • Export Citation
  • 66

    Dall’Era MA, Cowan JE, Simko J. Surgical management after active surveillance for low-risk prostate cancer: pathological outcomes compared with men undergoing immediate treatment. BJU Int 2011;107:12321237.

    • Search Google Scholar
    • Export Citation
  • 67

    van den Bergh RC, Steyerberg EW, Khatami A. Is delayed radical prostatectomy in men with low-risk screen-detected prostate cancer associated with a higher risk of unfavorable outcomes? Cancer 2010;116:12811290.

    • Search Google Scholar
    • Export Citation
  • 68

    Bul M, Zhu X, Rannikko A. Radical prostatectomy for low-risk prostate cancer following initial active surveillance: results from a prospective observational study. Eur Urol 2012;62:195200.

    • Search Google Scholar
    • Export Citation
  • 69

    Zaytoun OM, Vargo EH, Rajan R. Emergence of fluoroquinolone-resistant Escherichia coli as cause of postprostate biopsy infection: implications for prophylaxis and treatment. Urology 2011;77:10351041.

    • Search Google Scholar
    • Export Citation
  • 70

    Patel U, Dasgupta P, Amoroso P. Infection after transrectal ultrasonography-guided prostate biopsy: increased relative risks after recent international travel or antibiotic use. BJU Int 2012;109:17811785.

    • Search Google Scholar
    • Export Citation
  • 71

    Mosharafa AA, Torky MH, Said WM. Rising incidence of acute prostatitis following prostate biopsy: fluoroquinolone resistance and exposure is a significant risk factor. Urology 2011;78:511514.

    • Search Google Scholar
    • Export Citation

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Correspondence: Julio Pow-Sang, MD, Genitourinary Oncology Program, H. Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Drive, Tampa, FL 33612-9416. E-mail: Julio.Powsang@moffitt.org
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    An active surveillance strategy for those with low-risk and very-low-risk prostate cancer.

    Abbreviations: AS, active surveillance; DRE, digital rectal examination; PCA3, prostate cancer gene 3; PSA, prostate-specific antigen; PSAd, prostate-specific antigen density; PSAdt, prostate-specific antigen doubling time; PSAv, prostate-specific antigen velocity.

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    Margel D, Yap SA, Lawrentschuk N. Impact of multiparametric endorectal coil prostate magnetic resonance imaging on disease reclassification among active surveillance candidates: a prospective cohort study. J Urol 2012;187:12471252.

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    Ross AE, Loeb S, Landis P. Prostate-specific antigen kinetics during follow-up are an unreliable trigger for intervention in a prostate cancer surveillance program. J Clin Oncol 2010;28:28102816.

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    • Export Citation
  • 63

    Whitson JM, Porten SP, Hilton JF. The relationship between prostate specific antigen change and biopsy progression in patients on active surveillance for prostate cancer. J Urol 2011;185:16561660.

    • Search Google Scholar
    • Export Citation
  • 64

    Carvalhal GF, Daudi SN, Kan D. Correlation between serum prostate-specific antigen and cancer volume in prostate glands of different sizes. Urology 2010;76:10721076.

    • Search Google Scholar
    • Export Citation
  • 65

    Loeb S, Metter EJ, Kan D. Prostate-specific antigen velocity (PSAV) risk count improves the specificity of screening for clinically significant prostate cancer. BJU Int 2012;109:508513; discussion 513–514.

    • Search Google Scholar
    • Export Citation
  • 66

    Dall’Era MA, Cowan JE, Simko J. Surgical management after active surveillance for low-risk prostate cancer: pathological outcomes compared with men undergoing immediate treatment. BJU Int 2011;107:12321237.

    • Search Google Scholar
    • Export Citation
  • 67

    van den Bergh RC, Steyerberg EW, Khatami A. Is delayed radical prostatectomy in men with low-risk screen-detected prostate cancer associated with a higher risk of unfavorable outcomes? Cancer 2010;116:12811290.

    • Search Google Scholar
    • Export Citation
  • 68

    Bul M, Zhu X, Rannikko A. Radical prostatectomy for low-risk prostate cancer following initial active surveillance: results from a prospective observational study. Eur Urol 2012;62:195200.

    • Search Google Scholar
    • Export Citation
  • 69

    Zaytoun OM, Vargo EH, Rajan R. Emergence of fluoroquinolone-resistant Escherichia coli as cause of postprostate biopsy infection: implications for prophylaxis and treatment. Urology 2011;77:10351041.

    • Search Google Scholar
    • Export Citation
  • 70

    Patel U, Dasgupta P, Amoroso P. Infection after transrectal ultrasonography-guided prostate biopsy: increased relative risks after recent international travel or antibiotic use. BJU Int 2012;109:17811785.

    • Search Google Scholar
    • Export Citation
  • 71

    Mosharafa AA, Torky MH, Said WM. Rising incidence of acute prostatitis following prostate biopsy: fluoroquinolone resistance and exposure is a significant risk factor. Urology 2011;78:511514.

    • Search Google Scholar
    • Export Citation
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