eISSN: 2081-2841
ISSN: 1689-832X
Journal of Contemporary Brachytherapy
Current Issue Archive Supplements Articles in Press Journal Information Aims and Scope Editorial Office Editorial Board Register as Author Register as Reviewer Instructions for Authors Abstracting and indexing Subscription Advertising Information Links
SCImago Journal & Country Rank

Interview with Professor Janusz Skowronek
ABS 2015
vol. 10
Original paper

Five-year effectiveness of low-dose-rate brachytherapy: comparisons with nomogram predictions in patients with non-metastatic prostate cancer presenting significant control of intra- and periprostatic disease

Jörg S Zimmermann, Rudolf Osieka, Thorsten Bruns, Helge Hollberg, Bastian Wiechmann, Olaf Netzbandt, Jörg Sablotny, Michael Malade, Matthias Heitz, Fritz Bernhardt, Jörg Tiemann, Marc Wilkens, Tom Brüske, Utz Welker, Volker Heinemann, Petra Zimmermann, Salvador Fernandez de la Maza, Dietrich Pfeiffer, Roland Tauber, Dorothea Thomas, Christos Moustakis

J Contemp Brachytherapy 2018; 10, 4: 297–305
Online publish date: 2018/08/31
Article file
- five-year.pdf  [0.25 MB]
Get citation
JabRef, Mendeley
Papers, Reference Manager, RefWorks, Zotero


Low-dose-rate (LDR) brachytherapy, controlled by trans­rectal ultrasound, is an established treatment option for non-metastatic prostate cancer of various stages. LDR brachytherapy has been known for almost 30 years [1,2,3, 4,5,6], and is recognized as an appropriate treatment option in many relevant guidelines worldwide [7,8,9,10]. For early tumor stages (low-risk), LDR brachytherapy as monotherapy is the recommended therapeutic option. At favorable intermediate-risk of progression, LDR brachytherapy may be carried out as monotherapy, while at advanced intermediate-risk or at high-risk, it is typically combined with external beam radiation therapy (EBRT) and/or androgen deprivation therapy (ADT). Such multimodal therapy in locally advanced stages of prostate cancer has been recommended in several guidelines such as the European ESTRO/EAU/EORTC guidelines from 2000 [11], the European EAU-ESTRO-SIOG guidelines from 2017 [10] as well as those of the American Brachy­therapy Society [7] and the National Comprehensive Cancer Network (NCCN) [9]. Efficacy of multimodal therapy at high-risk of progression has been evidenced in a recent randomized trial (ASCENDE RT) [12] and in a meta-analysis comparing different treatment options [2].
In spite of this evidence, long-term experience with LDR brachytherapy in non-metastatic prostate cancer has been sparse for a long time, in particular when applied in patients at higher risk of progression. In the current German S3 guidelines, multimodal treatment with LDR brachytherapy is not included as an established treatment option [8]. This calls for large-scale observational studies, because long-term evaluation of radiotherapeutic methods (such as LDR brachytherapy) is not easily amenable to randomized clinical trials [13]. A planned large-scale prospective randomized trial to compare four treatment options (including LDR brachytherapy) in low- and early intermediate-risk prostate cancer in Germany (PREFERE, clinicaltrials.gov: NCT01717677) had to be discontinued due to poor acceptance and recruitment.
The purpose of this retrospective observational cohort study was (a) to evaluate the long-term effectiveness of LDR brachytherapy as monotherapy, and in combination with EBRT and/or ADT, (b) to compare the outcome to Kattan nomogram predictions for 5-year outcome, and (c) to evaluate destruction of periprostatic tumor invasion by LDR brachytherapy. Control of periprostatic disease is known to be pivotal, at least after radical surgery. Pathologic specimens after radical prostatectomy show that already at intermediate-risk, the tumor penetrates and grows through the prostatic capsule in 30-50% of patients [14,15,16]. This tumor invasion is the most frequent reason for clinical relapse after radical surgery [17].

Material and methods

Patient characteristics

This was a retrospective observational cohort study involving 1,187 patients, with non-metastatic prostate cancer (TXN0M0). The patients were treated with LDR brachytherapy between June 2002 and June 2010 at a specialized radiation oncology institution in Hamburg (Germany), in cooperation with numerous urological partner centers and hospitals.
Patient characteristics are displayed in Figure 1. In total, 1,187 patients with non-metastatic prostate cancer were accrued and treated with LDR brachytherapy. One hundred and twenty-three patients were lost to follow-up or died of other causes than prostate cancer in the course of 60 months. Six patients died due to systemic prostate cancer progression. Hence, 1,064 patients (1,058 patients alive plus 6 patients who died of prostate cancer) could be evaluated at 60 months after seed implantation (analysis set).
Patients were only included in the study if they received LDR brachytherapy with curative intent, i.e., within the first 180 days after initial histologic assessment of the tumor. Patients after active surveillance or watchful waiting were excluded. Each patient was treated with the best care option at the physician’s discretion, according to guidelines [7,8,9,10,11]: either LDR brachytherapy alone or LDR brachytherapy in combination with EBRT, and/or ADT. In some cases, LDR brachytherapy was applied as monotherapy based on the patient’s request, even though combination therapy was indicated.
LDR brachytherapy was performed with iodine-125 seeds as strands (S06 EZAG; 6711, Oncura) rather than loose seeds [18]. A transperineal procedure monitored by transrectal ultrasound was used, under continuous control of the z-axis by fluoroscopy until December 2005, exclusively ultrasound-based as real-time planning after December 2005. The D90 target dose was set to 160-180 Gy in patients with LDR brachytherapy as monotherapy, and 130 Gy in patients with multimodal therapy (reference dose: 145 Gy and 108 Gy, respectively). From 2007, the clinical target volume (CTV) was defined as the prostate contour surrounded by a clinical margin, according to the GEC/ESTRO/EAU recommendations from 2007 [19]. In multimodal therapy, EBRT was applied at doses between 45 and 50.4 Gy (1.8 Gy per day) to the prostate region, including the seminal vesicles, three months after implantation of the LDR brachytherapy seeds to avoid overdosage. Some patients received anti-hormonal therapy in neoadjuvant or adjuvant setting, with patient-individual medication and duration, here collectively reported as “ADT”. Duration of ADT was typically 2-6 months in the neoadjuvant, and 6-12 months in the adjuvant setting; no patient was treated with ADT for more than 2 years.
At baseline (prior to seed implantation), each patient was evaluated with respect to clinical and pathologic tumor stage, initial prostate-specific antigen (PSA) level, and Gleason score, and was classified into a prognostic risk group according to d’Amico [20], the risk definition commonly applied in Germany [8]. For further analysis, patients were also classified according to alternative definitions: Mt. Sinai [21], Seattle/Memorial Sloan-Kettering Cancer Center (MSKCC) [22], and NCCN criteria (clinical and biopsy-based/ histopathologic) [9].
For counselling of each patient, the preoperative Kattan nomogram [15] was employed to predict the likelihood that a patient remains free of PSA progression within 5 years. In addition, both the Kattan [15] and the Partin nomogram [16] were used to determine the patient-individual likelihood of organ-confined disease at the time of seed implantation.
The oncological remission status of each patient was determined 60 (± 3) months after starting LDR brachytherapy, to match the 5-year time frame of the Kattan nomogram predictions. Biochemical progression-free survival (bPFS) was determined using the Phoenix definition (PSA cut-off = nadir + 2 ng/ml, [23]).
Patients who underwent any type of salvage therapy within the first 60 months were also considered relapsed. To allow for the comparison of patient outcomes and 5-year nomogram predictions, the analysis comprised only patients who were alive 60 months after seed implantation, and who were not lost to follow-up (analysis set).

Statistical analyses

As this study is observational, the statistical analysis is descriptive without corrections or modelling. Fisher’s exact test (two-sided) was employed to assess whether the observed bPFS rates differed significantly from the mean probability of bPFS or organ-confined disease, as predicted with nomograms in the respective patients. Analysis was conducted with R, version 3.4.1, and was done in a hierarchical manner (for the entire cohort, then for each risk group, then for the treatment modality subgroups within each risk group). P values below 0.05 were considered statistically significant.


In total, 93.3% of patients in the analysis set (993/1,064) remained free of biochemical progression within 5 years (Table 1). While the patients treated between 2002 and 2005 had a bPFS rate of 91.9%, the bPFS rate was clearly higher (94.4%) in the patients treated after 2005, demonstrating either improvements due to intraoperative online planning [24] or a learning curve of the institution.
A wide variety of patients was included in this study, ranging from low- to high-risk of progression with initial PSA levels between 0.155 and 85.5 ng/ml, tumor stages between T1a and T3a, and Gleason scores between 4 and 10. Patients were grouped according to risk factors in Table 1.
This analysis shows that bPFS rates did not markedly differ between clinical tumor stages (Table 1). In particular, bPFS rates were very similar for the stages cT2a, cT2b, and cT2c (93.9%, 89.4%, and 91.1%, respectively) even though the cT2c stage in the d’Amico classification defines a high-risk situation also when the other parameters are favorable [20]. Overall, similar results were obtained when patients were stratified according to their biopsy-based histopathological tumor stage (Table 1). When outcomes were analyzed by initial PSA levels, bPFS was around or above 90% in patient subgroups with initial PSA below 20 ng/ml, but below 80% when initial PSA was ≥ 20 ng/ml (Table 1). Additionally, patients were grouped according to their
Gleason score before brachytherapy (Table 1). While Gleason scores up to 7a (3 + 4) were associated with 5-year bPFS rates above 90%, bPFS was 78.3% in the patients with Gleason score 7b (4 + 3). This lower rate of bPFS was predominantly resulting from tumor metastases in the spine and the pelvic bones, not local recurrence. In patients with Gleason scores ≥ 8, the bPFS rate was higher (83.3%), and all four patients with Gleason score 10 remained free of progression. None of the patients with a Gleason score of ≤ 6 have died of prostate cancer within 5 years, whereas systemic progress with death was seen in 6 patients with Gleason scores of 7a or higher.
When patients were classified in prognostic risk groups according to the d’Amico criteria [20], differences were evident with bPFS rates of 97.4%, 90.5%, and 87.4% for the patients at low-, intermediate-, and high-risk, respectively. Grouping the patients according to alternative prognostic models yielded very similar values (Table 2). This indicates that all the classification models are equally applicable to the patients in this study.

Five-year biochemical progression-free survival and comparison to Kattan nomogram predictions

To systematically evaluate the observed 5-year bPFS data, the outcome was compared to the probability of 5-year bPFS, as determined with established preoperative Kattan nomogram (Table 3). This nomogram represents an individualized assessment of a patient’s risk of biochemical progression [15]. For the patients in the analysis set, the average 5-year bPFS as predicted with the Kattan nomogram was 85% (range, 23-99%). Statistical analysis revealed that the observed outcome was significantly better than calculated from the Kattan nomogram (p < 0.001).
In 910 patients (85.5%), LDR brachytherapy was applied without additional EBRT, either as monotherapy or in combination with ADT. Of these patients, 94.6% (861/910) were free of biochemical progression after 5 years, a rate which was significantly higher than predicted (p < 0.001, average 5-year bPFS probability according to Kattan nomogram: 85%). One hundred fifty-four patients (14.5%) received LDR brachytherapy plus EBRT and had a 5-year bPFS of 85.7% (132/154 patients), which also exceeded the average Kattan nomogram-based probability of 5-year bPFS (79%), although not significantly (p = 0.09).
Next, the outcomes were compared to the respective Kattan nomogram predictions for each prognostic risk group (Table 3). Since bPFS rates were comparable between risk group classification models (as evidenced in Table 2), one of them, the biopsy-based histopathologic NCCN classification, was chosen for further analysis because it is independent of digital rectal examination (thus less error-prone), and because the NCCN classification distinguishes two separate levels of intermediate-risk (favorable and unfavorable intermediate-risk), providing higher selectivity. Five-year bPFS was 96.6%, 95.3%, 87.9%, and 82.4% at low-, favorable intermediate-, unfavorable intermediate-, and high-risk, respectively. For patients at low- and intermediate-risk, the outcomes were significantly better than predicted (p < 0.001), while for the patients at high-risk, the superiority of the outcomes (5-year bPFS in 82.4% of patients) compared to the Kattan nomogram prediction (average 5-year bPFS, 70% of patients) was just below the level of statistical significance (p = 0.091).

Five-year biochemical progression-free survival rates comparison to probability of organ-confined disease

Further, the observed 5-year bPFS outcomes were related to nomogram predictions that disease is confined within the prostate capsule. For the total patient cohort, the observed 5-year bPFS of 93.3% was significantly higher (p < 0.001) than the average likelihood of organ-confined disease as determined with the Kattan nomogram (50%) or the Partin nomogram (65%).
The observed bPFS rates were significantly higher than the predicted likelihood for organ-confined disease for nearly all subgroups (risk groups according to the NCCN classification, treatment modality), except for high-risk patients without EBRT. This superiority was more pronounced in the comparison of the observed outcomes with the Kattan nomogram predictions, which always yielded lower values than the Partin nomogram. For the total cohort and for some subgroups, the difference between the two nomogram predictions themselves was also statistically significant (Table 4).


This study demonstrates high long-term effectiveness of LDR brachytherapy as monotherapy and in the multimodal setting, under real-world conditions, in a large patient cohort (1,064 patients) ranging from low- to high-risk of progression, and thus representing large heterogeneity of non-metastatic prostate cancer patients in the clinical practice.
The data presented here are essentially in line with those of similar studies conducted elsewhere. A study at Mount Sinai Medical Center (USA) concluded that LDR brachytherapy is an effective treatment option for patients with non-metastatic prostate cancer of all risk groups, including high-risk patients [25]. Similarly, another large-scale study in the USA determined excellent long-term outcomes with modern LDR brachytherapy in patients at low-, intermediate-, and high-risk [26]. For LDR brachytherapy as monotherapy, long-term benefits comparable to those described here have been reported across all risk groups in various regions of the world including UK [27], USA [5,28], France [29], China [30], and Japan [31]. Similarly to the results of this study, superior bPFS rates of brachytherapy compared to those predicted with Kattan nomograms (pre and post-operative) have also been reported for a patient cohort in Israel, which was however smaller and mainly consisted of low-risk patients [32]. Overall, it can be concluded that international study results are transferrable to the standard of care in Germany.
The superiority of the observed 5-year bPFS rates compared to Kattan nomogram predictions was most significant in the monotherapy patients and those at lower risk. It is however remarkable that local control was also very good in advanced risk constellations, where relapse was typically due to systemic tumor spread rather than local progression. This may also argue in favor of PSA screening for early detection and early treatment of localized prostate cancer. We observed no death in patients with Gleason scores 5 or 6. At this stage, LDR brachytherapy as monotherapy is typically sufficient [7,8,9,10,33], which is also evidenced in this study.
The observed 5-year bPFS rates decreased gradually with increasing risk according to each of prognostic risk group definitions used. This indicates that the classification of patients into the risk groups was appropriate and accurate. Further, the usefulness of the two-separate intermediate-risk groups in the NCCN classification is highlighted by the observed 5-year bPFS rates, which differed considerably between the patients at favorable and unfavorable intermediate-risk (95.1% vs. 87.9%). Individual risk factors (tumor stages, PSA levels, Gleason scores) however correlated less well with the observed outcomes, and thus appear to be less valuable than prognostic risk groups in the context of brachytherapy, at least in the timeframe of 5 years [34]. In particular, the tumor stage cT2c (tumor covering both lobes) was not associated with lower 5-year bPFS than cT2a or cT2b (tumor confined to ≤ 50 or > 50% of one lobe, respectively). While the stage cT2c defines a high-risk in some risk group definitions in the context of radical prostatectomy [20], this elevated risk was not confirmed in this study for patients with cT2c disease treated with brachytherapy.
Both intra- and periprostatic disease appear to be controlled well with brachytherapy. This is evidenced in this study by significant superiority of the observed bPFS rates, compared to Kattan and Partin nomogram predictions for organ-confined disease. This significant advantage was seen across all risk strata and in most treatment modalities, with the exception of high-risk patients without EBRT.
To the authors’ knowledge, this is the first study, in which real-world data were assessed with respect to both the Kattan and the Partin nomogram and not just either of them. Interestingly, the Kattan nomogram values for the probability of organ-confined disease were consistently 10-15% below the respective Partin nomogram values, a difference that was statistically significant in the total cohort as well as in several subgroups. This possibly reflects differences in the characteristics of the patients used for establishment of the nomograms, and also differences in the extent of radical prostatectomy or histopathology performed at MSKCC in New York (Kattan nomogram) vs. Johns Hopkins University in Baltimore (Partin nomogram).
The nomogram predictions are derived from radical prostatectomy and describe the probability of organ-confined disease at the time of surgery. Hence, the finding that brachytherapy performed significantly better than in nomogram predictions can be interpreted as a potential advantage of brachytherapy over any kind of nerve-sparing radical prostatectomy [17]. This is consistent with a recent review that suggested better disease control with multimodal radiation therapy than surgery in high-risk patients, which implies that incomplete tumor resection after radical surgery may by itself be a cause for metastases [35]. Also, already a decade ago, small-scale randomized prospective trials showed that radical prostatectomy and LDR brachytherapy are similar in terms of long-term biochemical recurrence-free survival in low-risk prostate cancer [36,37]. Along similar lines, long-term follow-up data of the Surveillance, Epidemiology, and End Results (SEER) database including more than 240,000 patients with non-metastatic prostate cancer revealed that even in patients at highest risk, 8-year survival rates were comparable between radical prostatectomy (partially with adjuvant EBRT, 85.5%) and brachytherapy (85.1%), and much higher than with EBRT (78.8%) or no local treatment (50.2%) [38].
Especially in high-risk non-metastatic prostate cancer, achieving local control is paramount for long-term disease-free survival. In retrospective studies, there is evidence for a considerable long-term benefit when brachytherapy is combined with EBRT (with or without ADT) in men with high-risk prostate cancer, with benefits of multimodal brachytherapy compared to surgery alone or EBRT alone [2,35,39,40,41,42,43]. While several clinical trials have determined a bPFS benefit of EBRT + high-dose-rate brachytherapy over EBRT alone in patients at intermediate- and high-risk [44,45,46], only one large-scale prospective randomized trial has been conducted investigating LDR brachytherapy + EBRT vs. EBRT alone in patients with non-metastatic prostate cancer at elevated risk (“ASCENDE RT”, [12]). ASCENDE RT showed that patients at intermediate- and high-risk were twice as likely to remain free of biochemical recurrence when EBRT was combined with LDR brachytherapy, performed with iodine-125 seeds similar to those employed in this study. The results presented in this study basically confirm the high effectiveness of brachytherapy in the context of clinical practice, also in patients at elevated risk.
It has to be noted that bPFS rates cannot be compared directly between the treatment modalities, as there is an inherent imbalance between patients in this respect: multimodal therapy is more frequently applied in patients with less favorable prognosis. To account for such inherent differences, bPFS rates were compared to the respective patient-individualized nomogram predictions, which served as reference. The results show a trend towards more pronounced superiority of brachytherapy when performed as monotherapy. Consistent with this, a recent systematic review stated that patients treated with brachytherapy have excellent long-term disease outcomes and do not further benefit from addition of ADT to brachytherapy at low- or favorable intermediate-risk [47], while patients at higher risk appear to benefit from ADT in this setting [48]. This additional advantage of ADT in patients at higher risk was not seen in this study, possibly in part owing to patient-individual reasons, differences in disease severity, or low number of patients in the respective subgroups.
Since this study was an observational study, it has limitations like the lack of randomization of a control group. Further, PSA values may have fluctuated due to the antihormonal therapy in the first months or 2 years. Yet, such effects are negligible in the course of 60 months: influences of ADT (less than 2 years in each case) can be excluded, and “PSA bounces” after LDR brachytherapy are typically observed only within 6-24 months after seed insertion [49,50]; later rises in PSA indicate tumor progression rather than therapy-related alterations. Another limitation of this study is that patient-individual treatment choices might have confounded results. This potential source of bias was accounted for by using patient-individualized nomogram predictions as reference.


This study clearly demonstrates the benefit of LDR brachytherapy in terms of 5-year bPFS in one of the largest patient cohorts investigated so far in the context of clinical practice. The high effectiveness of LDR brachytherapy was observed across all risk groups. The outcomes of LDR brachytherapy were significantly better than expected on the basis of nomogram predictions for “organ-confined disease”, suggesting that LDR brachytherapy with stranded seeds effectively controls both intra- and periprostatic disease.


Dr. Bastian Thaa (co.medical, Berlin, Germany) and Dr. Ulrich Gauger (Berlin, Germany) are acknowledged for medical writing and statistical analyses, respectively.
The cooperating radiation oncology facilities are acknowledged for performing the external beam radiation (EBRT) in accordance with the predefined treatment protocols.


The authors report no conflict of interest.


1. Blasko JC, Grimm PD, Sylsvester JE et al. The role of external beam radiotherapy with I-125/Pd-103 brachytherapy for prostate carcinoma. Radiother Oncol 2000; 57: 273-278.
2. Grimm P, Billiet I, Bostwick D et al. Comparative analysis of prostate-specific antigen free survival outcomes for patients with low, intermediate and high risk prostate cancer treatment by radical therapy. Results from the Prostate Cancer Results Study Group. BJU Int 2012; 109 Suppl 1: 22-29.
3. Ragde H, Grado GL, Nadir B et al. Modern prostate brachytherapy. CA Cancer J Clin 2000; 50: 380-393.
4. Stone NN, Stock RG. 15-year cause specific and all-cause survival following brachytherapy for prostate cancer: negative impact of long-term hormonal therapy. J Urol 2014; 192: 754-759.
5. Sylvester JE, Grimm PD, Wong J et al. Fifteen-year biochemical relapse-free survival, cause-specific survival, and overall survival following I(125) prostate brachytherapy in clinically localized prostate cancer: Seattle experience. Int J Radiat Oncol Biol Phys 2011; 81: 376-381.
6. Zaorsky NG, Davis BJ, Nguyen PL et al. The evolution of brachytherapy for prostate cancer. Nat Rev Urol 2017; 14: 415-439.
7. Davis BJ, Horwitz EM, Lee WR et al. American Brachytherapy Society consensus guidelines for transrectal ultrasound-guided permanent prostate brachytherapy. Brachytherapy 2012; 11: 6-19.
8. Leitlinienprogramm Onkologie. Interdisziplinäre Leitlinie der Qualität S3 zur Früherkennung, Diagnose und Therapie der verschiedenen Stadien des Prostatakarzinoms, Langversion 4.0 (Interdisciplinary German guidelines for diagnosis and therapy of prostate cancer, version 4.0). Available at: http://leitlinienprogramm-onkologie.de/Prostatakarzinom.58.0.html. 2016.
9. National Comprehensive Cancer Network (NCCN). NCCN Clinical Practice Guidelines in Oncology: Prostate Cancer. Version 3.2016. Available at: nccn.org/professionals/physician_gls/pdf/prostate.pdf. 2016.
10. Mottet N, Bellmunt J, Bolla M et al. EAU-ESTRO-SIOG Guidelines on Prostate Cancer. Part 1: Screening, Diagnosis, and Local Treatment with Curative Intent. Eur Urol 2017; 71: 618-629.
11. Ash D, Flynn A, Battermann J et al. ESTRO/EAU/EORTC recommendations on permanent seed implantation for localized prostate cancer. Radiother Oncol 2000; 57: 315-321.
12. Morris WJ, Tyldesley S, Rodda S et al. Androgen Suppression Combined with Elective Nodal and Dose Escalated Radiation Therapy (the ASCENDE-RT Trial): An Analysis of Survival Endpoints for a Randomized Trial Comparing a Low-Dose-Rate Brachytherapy Boost to a Dose-Escalated External Beam Boost for High- and Intermediate-risk Prostate Cancer. Int J Radiat Oncol Biol Phys 2017; 98: 275-285.
13. Trone JC, Espenel S, Rehailia-Blanchard A et al. Navigating the highlights of phase III trials: a watchful eye on evidence-based radiotherapy. Ann Oncol 2017; 28: 2691-2697.
14. Davis BJ, Pisansky TM, Wilson TM et al. The radial distance of extraprostatic extension of prostate carcinoma: implications for prostate brachytherapy. Cancer 1999; 85: 2630-2637.
15. Kattan MW, Scardino PT. Prediction of progression: nomograms of clinical utility. Clin Prostate Cancer 2002; 1: 90-96.
16. Makarov DV, Trock BJ, Humphreys EB et al. Updated nomogram to predict pathologic stage of prostate cancer given prostate-specific antigen level, clinical stage, and biopsy Gleason score (Partin tables) based on cases from 2000 to 2005. Urology 2007; 69: 1095-1101.
17. Basiri A, de la Rosette JJ, Tabatabaei S et al. Comparison of retropubic, laparoscopic and robotic radical prostatectomy: who is the winner? World J Urol 2018; 36: 609-621.
18. Inada M, Yokokawa M, Minami T et al. Dosimetry advantages of intraoperatively built custom-linked seeds compared with loose seeds in permanent prostate brachytherapy. J Contemp Brachytherapy 2017; 9: 410-417.
19. Salembier C, Lavagnini P, Nickers P et al. Tumour and target volumes in permanent prostate brachytherapy: a supplement to the ESTRO/EAU/EORTC recommendations on prostate brachytherapy. Radiother Oncol 2007; 83: 3-10.
20. D’Amico AV, Whittington R, Malkowicz SB et al. Biochemical outcome after radical prostatectomy, external beam radiation therapy, or interstitial radiation therapy for clinically localized prostate cancer. JAMA 1998; 280: 969-974.
21. Lee LN, Stock RG, Stone NN. Role of hormonal therapy in the management of intermediate- to high-risk prostate cancer treated with permanent radioactive seed implantation. Int J Radiat Oncol Biol Phys 2002; 52: 444-452.
22. Sylvester JE, Grimm PD, Blasko JC et al. 15-Year biochemical relapse free survival in clinical Stage T1-T3 prostate cancer following combined external beam radiotherapy and brachytherapy; Seattle experience. Int J Radiat Oncol Biol Phys 2007; 67: 57-64.
23. Roach M 3rd, Hanks G, Thames H, Jr et al. Defining biochemical failure following radiotherapy with or without hormonal therapy in men with clinically localized prostate cancer: recommendations of the RTOG-ASTRO Phoenix Consensus Conference. Int J Radiat Oncol Biol Phys 2006; 65: 965-974.
24. Polo A, Salembier C, Venselaar J et al. Review of intraoperative imaging and planning techniques in permanent seed prostate brachytherapy. Radiother Oncol 2010; 94: 12-23.
25. Marshall RA, Buckstein M, Stone NN et al. Treatment outcomes and morbidity following definitive brachytherapy with or without external beam radiation for the treatment of localized prostate cancer: 20-year experience at Mount Sinai Medical Center. Urol Oncol 2014; 32: 38.e31-37.
26. Taira AV, Merrick GS, Butler WM et al. Long-term outcome for clinically localized prostate cancer treated with permanent interstitial brachytherapy. Int J Radiat Oncol Biol Phys 2011; 79: 1336-1342.
27. Langley SEM, Soares R, Uribe J et al. Long-term oncological outcomes and toxicity in 597 men aged  60 years at time of low-dose-rate brachytherapy for localised prostate cancer. BJU Int 2018; 121: 38-45.
28. Kittel JA, Reddy CA, Smith KL et al. Long-Term Efficacy and Toxicity of Low-Dose-Rate (125)I Prostate Brachytherapy as Monotherapy in Low-, Intermediate-, and High-Risk Prostate Cancer. Int J Radiat Oncol Biol Phys 2015; 92: 884-893.
29. Cosset JM, Flam T, Thiounn N et al. Selecting patients for exclusive permanent implant prostate brachytherapy: the experience of the Paris Institut Curie/Cochin Hospital/Necker Hospital group on 809 patients. Int J Radiat Oncol Biol Phys 2008; 71: 1042-1048.
30. Yan W, Chen J, Zhou Y et al. Long-term outcome of early stage prostate cancer treated with brachytherapy analysis after a mean follow-up of 7 years. Springerplus 2014; 3: 357.
31. Ito K, Saito S, Yorozu A et al. Nationwide Japanese Prostate Cancer Outcome Study of Permanent Iodine-125 Seed Implantation (J-POPS): first analysis on survival. Int J Clin Oncol 2018; DOI: 10.1007/s10147-10018-11309-10140.
32. Kaplan A, German L, Chen J et al. Validation and comparison of the two Kattan nomograms in patients with prostate cancer treated with (125) iodine brachytherapy. BJU Int 2012; 109: 1661-1665.
33. Shukla G, Sarkar A, Hanlon A et al. Biochemical control and toxicity for favorable- and intermediate-risk patients using real-time intraoperative inverse optimization prostate seed implant: Less is more! Brachytherapy 2017; 16: 490-496.
34. Okazaki E, Kuratsukuri K, Ishii K et al. Correlations of post-implant regional dosimetric parameters at 24 hours and one month, with clinical results of low-dose-rate brachytherapy for localized prostate cancer. J Contemp Brachytherapy 2017; 9: 499-507.
35. Spratt DE, Soni PD, McLaughlin PW et al. American Bra­chy­therapy Society Task Group Report: Combination of bra­chytherapy and external beam radiation for high-risk prostate cancer. Brachytherapy 2017; 16: 1-12.
36. Giberti C, Chiono L, Gallo F et al. Radical retropubic prostatectomy versus brachytherapy for low-risk prostatic cancer: a prospective study. World J Urol 2009; 27: 607-612.
37. Giberti C, Gallo F, Schenone M et al. Robotic prostatectomy versus brachytherapy for the treatment of low risk prostate cancer. Can J Urol 2017; 24: 8728-8733.
38. Pompe RS, Davis-Bondarenko H, Zaffuto E et al. Population-Based Validation of the 2014 ISUP Gleason Grade Groups in Patients Treated With Radical Prostatectomy, Brachytherapy, External Beam Radiation, or no Local Treatment. Prostate 2017; 77: 686-693.
39. Shilkrut M, Merrick GS, McLaughlin PW et al. The addition of low-dose-rate brachytherapy and androgen-deprivation therapy decreases biochemical failure and prostate cancer death compared with dose-escalated external-beam radiation therapy for high-risk prostate cancer. Cancer 2013; 119: 681-690.
40. Bittner N, Merrick GS, Galbreath RW et al. Treatment outcomes with permanent brachytherapy in high-risk prostate cancer patients stratified into prognostic categories. Brachytherapy 2015; 14: 766-772.
41. Carpenter TJ, Forsythe K, Kao J et al. Outcomes for patients with extraprostatic prostate cancer treated with trimodality therapy, including brachytherapy, external beam radiotherapy, and hormone therapy. Brachytherapy 2011; 10: 261-268.
42. Jackson MW, Amini A, Jones BL et al. Prostate brachytherapy, either alone or in combination with external beam radiation, is associated with longer overall survival in men with favorable pathologic Group 4 (Gleason score 8) prostate cancer. Brachytherapy 2017; 16: 790-796.
43. Okamoto K, Wada A, Kohno N. High biologically effective dose radiation therapy using brachytherapy in combination with external beam radiotherapy for high-risk prostate cancer. J Contemp Brachytherapy 2017; 9: 1-6.
44. Dayes IS, Parpia S, Gilbert J et al. Long-Term Results of a Randomized Trial Comparing Iridium Implant Plus External Beam Radiation Therapy With External Beam Radiation Therapy Alone in Node-Negative Locally Advanced Cancer of the Prostate. Int J Radiat Oncol Biol Phys 2017; 99: 90-93.
45. Sathya JR, Davis IR, Julian JA et al. Randomized trial comparing iridium implant plus external-beam radiation therapy with external-beam radiation therapy alone in node-negative locally advanced cancer of the prostate. J Clin Oncol 2005; 23: 1192-1199.
46. Hoskin PJ, Rojas AM, Bownes PJ et al. Randomised trial of external beam radiotherapy alone or combined with high-dose-rate brachytherapy boost for localised prostate cancer. Radiother Oncol 2012; 103: 217-222.
47. Pickles T, Morris WJ, Keyes M. High-intermediate prostate cancer treated with low-dose-rate brachytherapy with or without androgen deprivation therapy. Brachytherapy 2017; 16: 1101-1105.
48. Keyes M, Merrick G, Frank SJ et al. American Brachytherapy Society Task Group Report: Use of androgen deprivation therapy with prostate brachytherapy – a systematic literature review. Brachytherapy 2017; 16: 245-265.
49. Burchardt W, Skowronek J. Time to PSA rise differentiates the PSA bounce after HDR and LDR brachytherapy of prostate cancer. J Contemp Brachytherapy 2018; 10: 1-9.
50. Martell K, Meyer T, Sia M et al. Parameters predicting for prostate specific antigen response rates at one year post low-dose-rate intraoperative prostate brachytherapy. J Contemp Brachytherapy 2017; 9: 99-105.
Copyright: © 2018 Termedia Sp. z o. o. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
Quick links
© 2018 Termedia Sp. z o.o. All rights reserved.
Developed by Bentus.
PayU - płatności internetowe