Background. Prostate cancer is often understaged following 12-core transrectal ultrasound- (TRUS-) guided biopsies. Our goal is to understand where cancers are typically missed by this method. Methods. Transperineal 3-dimensional mapping biopsy (3DMB) provides a more accurate depiction of disease status than transrectal ultrasound- (TRUS-) guided biopsy. We compared 3DMB findings in men with prior TRUS-guided biopsies to determine grade and location of missed cancer. Results were evaluated for 161 men with low-risk organ confined prostate cancer. Results. The number of cancer-positive biopsy zones per patient with TRUS was 1.38 ± 1.21 compared to 3.33 ± 4.06 with 3DMB, with most newly discovered cancers originating from the middle lobe and apex. Approximately half of all newly discovered cancerous zones resulted from anterior 3DMB sampling. Gleason upgrade was recognized in 56 patients using 3DMB. When both biopsy methods found positive cores in a given zone, Gleason upgrades occurred most frequently in the middle left and right zones. TRUS cancer-positive zones not confirmed by 3DMB were most often the basal zones. Conclusion. Most cancer upgrades and cancers missed from TRUS biopsy originated in the middle left zone of the prostate, specifically in anterior regions. Anterior sampling may lead to more accurate diagnosis and appropriate followup. 1. Introduction An increasing proportion of prostate cancer is being diagnosed at clinically insignificant stages, raising controversy surrounding overdiagnosis and overtreatment of a growing number of patients with potentially nonmortal yet psychologically morbid disease [1]. Data seem to suggest that Watchful Waiting (WW) or Active Surveillance protocols (AS) should be the method of choice in many or even most low-risk situations due to the long natural history of prostate cancer and the generally favorable prognosis for clinically localized noninvasive disease [2–4]. There now exists substantial evidence that an observational approach would be a practical, cost saving, and quality-of-life preserving option for many [5]. The proportion of men with clinically localized prostate cancer (LPC) who could potentially benefit from AS has risen from approximately 25% in the early 1990s to almost 50% as of 2007 [6]; however the proportion of men on AS has remained largely unchanged for over a decade. Only 6.8% of men with prostate cancer opt for AS according to the CaPSURE database. This level has fluctuated somewhat over the years but has changed only slightly since 2000 when it was at 6.2% [6, 7]. The vast majority
References
[1]
A. B. Barqawi, K. Krughoff, and K. Eid, “Current challenges in prostate cancer management and the rationale behind targeted focal therapy,” Advances in Urology, vol. 2012, Article ID 862639, 7 pages, 2012.
[2]
P. C. Albertsen, “Is screening for prostate cancer with prostate specific antigen an appropriate public health measure?” Acta Oncologica, vol. 44, no. 3, pp. 255–264, 2005.
[3]
P. C. Albertsen, J. A. Hanley, and J. Fine, “20-Year outcomes following conservative management of clinically localized prostate cancer,” Journal of the American Medical Association, vol. 293, no. 17, pp. 2095–2101, 2005.
[4]
L. Klotz, L. Zhang, A. Lam, R. Nam, A. Mamedov, and A. Loblaw, “Clinical results of long-term follow-up of a large, active surveillance cohort with localized prostate cancer,” Journal of Clinical Oncology, vol. 28, no. 1, pp. 126–131, 2010.
[5]
N. Lawrentschuk and L. Klotz, “Active surveillance for low-risk prostate cancer: an update,” Nature Reviews Urology, vol. 8, no. 6, pp. 312–320, 2011.
[6]
M. R. Cooperberg, J. M. Broering, P. W. Kantoff, and P. R. Carroll, “Contemporary trends in low risk prostate cancer: risk assessment and treatment,” Journal of Urology, vol. 178, no. 3, pp. S14–S19, 2007.
[7]
M. R. Cooperberg, J. M. Broering, and P. R. Carroll, “Time trends and local variation in primary treatment of localized prostate cancer,” Journal of Clinical Oncology, vol. 28, no. 7, pp. 1117–1123, 2010.
[8]
R. Chou, J. M. Croswell, T. Dana et al., “Screening for prostate cancer: a review of the evidence for the U.S. preventive services task force,” Annals of Internal Medicine, vol. 155, no. 11, pp. 762–771, 2011.
[9]
V. Iremashvili, M. Manoharan, D. L. Rosenberg, and M. S. Soloway, “Biopsy features associated with prostate cancer progression in active surveillance patients: comparison of three statistical models,” British Journal of Urology, vol. 111, no. 4, pp. 574–579, 2013.
[10]
M. C. Large and S. E. Eggener, “Active surveillance for low-risk localized prostate cancer,” Oncology, vol. 23, no. 11, pp. 974–979, 2009.
[11]
A. S. Duffield, T. K. Lee, H. Miyamoto, H. B. Carter, and J. I. Epstein, “Radical prostatectomy findings in patients in whom active surveillance of prostate cancer fails,” Journal of Urology, vol. 182, no. 5, pp. 2274–2279, 2009.
[12]
K. Lees, M. Durve, and C. Parker, “Active surveillance in prostate cancer: patient selection and triggers for intervention,” Current Opinion in Urology, vol. 22, no. 3, pp. 210–215, 2012.
[13]
A. B. Barqawi, K. O. Rove, S. Gholizadeh, C. I. O'Donnell, H. Koul, and E. D. Crawford, “The role of 3-dimensional mapping biopsy in decision making for treatment of apparent early stage prostate cancer,” Journal of Urology, vol. 186, no. 1, pp. 80–85, 2011.
[14]
J. L. Dominguez-Escrig, S. R. C. McCracken, and D. Greene, “Beyond diagnosis: evolving prostate biopsy in the era of focal therapy,” Prostate Cancer, vol. 2011, Article ID 386207, 11 pages, 2011.
[15]
A. R. Patel and J. S. Jones, “Optimal biopsy strategies for the diagnosis and staging of prostate cancer,” Current Opinion in Urology, vol. 19, no. 3, pp. 232–237, 2009.
[16]
A. S. Duffield, T. K. Lee, H. Miyamoto, H. B. Carter, and J. I. Epstein, “Radical prostatectomy findings in patients in whom active surveillance of prostate cancer fails,” Journal of Urology, vol. 182, no. 5, pp. 2274–2279, 2009.
[17]
S. R. J. Bott, M. P. A. Young, M. J. Kellett, and M. C. Parkinson, “Anterior prostate cancer: is it more difficult to diagnose?” British Journal of Urology, vol. 89, no. 9, pp. 886–889, 2002.
[18]
M. A. Haider, T. H. Van Der Kwast, J. Tanguay et al., “Combined T2-weighted and diffusion-weighted MRI for localization of prostate cancer,” American Journal of Roentgenology, vol. 189, no. 2, pp. 323–328, 2007.
[19]
P. Puech, N. Betrouni, N. Makni, A.-S. Dewalle, A. Villers, and L. Lemaitre, “Computer-assisted diagnosis of prostate cancer using DCE-MRI data: design, implementation and preliminary results,” International Journal of Computer Assisted Radiology and Surgery, vol. 4, no. 1, pp. 1–10, 2009.
[20]
E. K. Vos, G. J. S. Litjens, T. Kobus, et al., “Assessment of prostate cancer aggressiveness using dynamic contrast-enhanced magnetic resonance imaging at 3T,” European Urology, vol. 64, no. 3, pp. 448–455, 2013.
[21]
R. J. Hamilton and S. J. Freedland, “5-α reductase inhibitors and prostate cancer prevention: where do we turn now?” BMC Medicine, vol. 9, article 105, 2011.
