eMedicine Specialties > Urology > Cancer, Prostate
Prostate Cancer - Brachytherapy (Radioactive Seed Implantation Therapy)
Updated: Apr 27, 2009
Introduction
Brachytherapy (the term derived from the Greek word brachys, which means brief or short) refers to cancer treatment with electromagnetic radiation delivered via radioactive material placed a short distance from, or within, the tumor. In prostate cancer, brachytherapy involves the ultrasound- and template-guided insertion of radioactive seeds into the gland. Along with radical prostatectomy, cryotherapy, and external beam radiation therapy (EBRT; most recently termed intensity-modulated radiation therapy [IMRT]), interstitial brachytherapy is a potentially curative treatment for localized prostate cancer. For appropriately selected patients, brachytherapy appears to offer cancer control comparable to these other techniques. However, although proponents of brachytherapy claim better quality-of-life results, the evidence supportingthis claim is mixed. This article outlines both the technique and outcomes, with respect to cancer control and quality of life.
History of the Procedure
In the 1970s, several centers used brachytherapy to treat prostate cancer. Implants were placed into the prostate under direct vision following open pelvic lymphadenectomy. Unfortunately, long-term follow-up revealed less-than-satisfactory results in terms of cancer control. Currently, these less-than-optimal results are thought to have resulted from (1) a technical inability to accurately implant the sources and (2) the relative paucity of objective dosimetric criteria by which to analyze the radiation dose in that era. Interest in brachytherapy waned in the early 1980s because of these results, the advent of more advanced EBRT equipment, and the development of the nerve-sparing radical prostatectomy.
In the late 1980s and early 1990s, the emergence of transrectal ultrasonography (TRUS) and the development of template guidance led to the introduction of percutaneous brachytherapy for the treatment of localized prostate cancer. This technique was supported by improved dosimetry and offered the potential advantage of delivering a higher radiation dose to the prostate than would be possible with EBRT. This latter consideration was particularly important in view of the high rate of positive prostate biopsy findings following conventional EBRT.
Problem
Ionizing radiation delivered by either an external or interstitial source generates free radicals such as superoxide or hydrogen peroxide, which damage cellular DNA. The resultant cytotoxicity depends on cell division; therefore, the more rapid the cell turnover, the higher the cell death per unit of time. Thus, although lethally irradiated, in most cases, a tumor cell does not die until it attempts cell division.
Frequency
Prostate cancer is currently the most frequently diagnosed malignancy among men and the second leading cancer cause of death. With the advent of prostate-specific antigen (PSA) screening, a greater number of men require education about prostate cancer and how it is diagnosed, staged, and treated in order to select the most appropriate treatment.
Despite the apparent survival advantage of early diagnosis conferred by PSA screening, a recent U.S. Preventive Services Task Force statement recommends against screening for prostate cancer in men aged 75 years or older. The statement also concludes that, currently, the balance of benefits versus drawbacks of prostate cancer screening in men younger than age 75 years cannot be assessed because of insufficient evidence.1
Approximately 1 in 6 men older than 50 years will be diagnosed with prostate cancer. Prostate cancer is rarely diagnosed in men younger than 40 years and is uncommon in men younger than 50 years. The prevalence of prostate cancer remains significantly higher in African American men than in white men.
Between 1989 and 1992, prostate cancer incidence rates increased dramatically. This rise was probably due to earlier diagnoses in asymptomatic men due to the increased use of serum PSA testing. In 1994, Catalona et al showed that the incidence of organ-confined disease at diagnosis was increased by evaluating PSA values in addition to performing the standard digital rectal examination (DRE). Prostate cancer incidence rates are continuing to decline; rates in white men peaked in 1992, and they peaked in African American men in 1993.
From 1992-1996, prostate cancer mortality rates declined significantly (by 2.5% per year). Although mortality rates are continuing to decline among white and African American men, mortality rates in African American men remain more than twice as high as rates in white men.
Prostate cancer is also found during autopsies performed following other causes of death. The rate of latent cancer or cancer found at autopsy is much greater than the rate of clinical cancer, possibly reaching as high as 80% by age 80 years.
The prevalence of clinical cancer varies by region. In northern Europe and North America, the rate is high. In southern Europe and Central and South America, the rate is intermediate. In Eastern Europe and Asia, the rate is low. These differences may be due to genetic, hormonal, and/or dietary factors. Interestingly, the prevalence of the latent or autopsy form of the disease is similar worldwide. This, together with migration studies, suggests that environmental factors such as diet may play a significant role in the development of clinical cancer from a latent precursor.
Etiology
Genetics
Alteration of genes on chromosome 1 and the X chromosome have been found in some patients with a family history of prostate cancer. In addition, genetic studies suggest that a strong familial predisposition may be responsible for as many as 10% of prostate cancer cases. Recently, several reports have suggested a shared familial risk (inherited or environmental) for prostate and breast cancer.
Race
Prostate cancer is more prevalent and aggressive in African Americans than in white men. The prevalence of prostate cancer is even lower in men of Asian origin. Studies have found that testosterone levels are 15% higher in young African American men than in young white men. Furthermore, evidence indicates that 5-alpha reductase may be more active in African Americans than in whites, implying that hormonal differences may play a role. Others argue that barriers to health care, not biological factors, lead to more advanced disease in African Americans.
Diet
A high-fat diet may lead to increased risk, while a diet rich in soy may be protective. These observations have been proposed as reasons for the low prevalence of prostate cancer in Asia. Cell culture work has shown that omega-6 fatty acids are positive stimulants of prostate-cancer cell growth, while omega-3 fatty acids are negative stimuli. These fats may exert their effects by altering sex hormones or growth factors or affecting 5-alpha reductase.
Soy seems to decrease the growth of prostate cancer cells in mouse models, but, apart from epidemiologic factors, no direct evidence has supported a beneficial effect in humans. The low-fat diet has some support based on the cell culture work mentioned above. Vitamin E may have some protective effects because it is an antioxidant. Decreased levels of vitamin A may be a risk factor because this can promote cell differentiation and stimulate the immune system. Vitamin D deficiency was suggested as a risk factor, and studies show an inverse relationship between ultraviolet exposure and mortality rates for prostate cancer. However, specific correlation between 1,25-dihydroxyvitamin D levels and palpable disease, well-differentiated tumors, or mortality is inconclusive.
Selenium may have a protective effect based on epidemiologic studies and is also believed to extend its effect via its antioxidant properties. The Selenium and Vitamin E Cancer Prevention Trial (SELECT) is an ongoing intergroup, phase 3, randomized, controlled trial designed to test the efficacy of selenium and vitamin E alone and in combination in the prevention of prostate cancer.
Hormones
Hormonal causes have also been postulated. Androgen ablation causes a regression of prostate cancer. In addition, as indirect evidence of hormonal causes, eunuchs do not develop adenocarcinoma of the prostate.
Hsing and Comstock performed a large study comparing patients with prostate cancer with controls and found no difference in levels of testosterone, dehydrotestosterone, prolactin, follicle-stimulating hormone, or estrone.2
The effects of blocking the conversion of testosterone to dihydrotestosterone were examined in the Prostate Cancer Prevention Trial (PCPT). This trial studied the prevalence of prostate cancer between a control group and a cohort given a 5-alpha reductase inhibitor, finasteride. While the 5-alpha reductase inhibitor appeared to decrease the prevalence of tumors, those that did arise appeared histologically more aggressive. Whether these are biologically more aggressive remains as yet undetermined.
Pathophysiology
Prostate cancer develops when the rates of cell division and cell death are no longer equal, leading to uncontrolled tumor growth.
Following the initial transformation event, further mutations of a multitude of genes, including TP53 and RB1, can lead to tumor progression and metastasis. Most prostate cancers (95%) are adenocarcinomas. Approximately 4% have transitional cell morphology and are thought to arise from the lining of the prostatic urethra. Few have neuroendocrine morphology. When present, they are believed to arise from the neuroendocrine stem cells normally present in the prostate or from aberrant differentiation programs during cell transformation.
Seventy percent of prostate cancers arise in the peripheral zone, 25-30% in the transitional zone, and less than 5% in the central zone. These zones can often be identified using TRUS. Most prostate cancers are multifocal, with synchronous involvement of multiple zones of the prostate, which may be due to clonal and nonclonal tumors. Multifocality may indicate a more aggressive tumor biology.
Presentation
Brachytherapy is an accepted treatment option for early-stage prostate cancer. The various institutions that offer brachytherapy have subtle differences in technique. Most of the techniques discussed in this article are generic in description, but some modifications are unique to the implant procedure performed at the University of Virginia.
Indications
Primary treatment - Risk-dependent protocols
Evidence-based protocols for brachytherapy have been developed, although data are limited. A 2008 research summary by the Agency for Healthcare Research and Quality (AHRQ) noted that no randomized controlled trials had compared brachytherapy alone with other major treatment options for clinically localized prostate cancer.3 The American Brachytherapy Society (ABS) formed a committee of experts in prostate brachytherapy to develop consensus guidelines through a critical analysis of published data supplemented by the experts' clinical experience.4 The recommendations of the panel were reviewed and approved by the board of directors of the ABS. They published a review of their recommendations concerning permanent (low-dose rate) implants in 2007.
- Patients with a high probability of organ-confined disease are appropriately treated with brachytherapy alone. Most practitioners include patients with stage T1-T2a (according to the American Joint Committee on Cancer/International Union Against Cancer 1997 staging), PSA level of 10 ng/mL or less, and Gleason score of 6 or lower in this category. The recommended prescription doses for monotherapy are 145 Gy for iodine (I)–125 and 120-125 Gy for palladium (Pd)–103.
- Brachytherapy candidates with a significant risk of extraprostatic extension should be treated with supplemental IMRT. A high risk of extraprostatic extension is defined as the presence of 2 or more of the following risk factors: a Gleason score greater than or equal to 7, a PSA level greater than 10 ng/mL, and a stage higher than T2b. The IMRT dose is 40-50 Gy with a boost of 110 Gy or 100 Gy, depending on which IMRT dose was administered.
- Intermediate-risk patients have only one of the aforementioned risk factors. Brachytherapy monotherapy appears to demonstrate good results in several studies. The combination of IMRT and brachytherapy has not uniformly produced better cancer-control results. Length of follow-up time is critical for discerning treatment differences.
A patterns-of-care study conducted by Frank et al found that a subset of intermediate-risk patients are treated with brachytherapy monotherapy.5 Specifically, monotherapy is used to treat T1c disease characterized by absent perineural invasion, positive results in less than 30% of core samples, and a Gleason score of 7 or a PSA level of 10-20 ng/mL. Even select T2a and T2b cases were treated with monotherapy.
A current Radiation Therapy Oncology Group (RTOG) trial, RTOG 0232, is assessing the role of IMRT plus brachytherapy boost versus brachytherapy alone in the treatment of intermediate-risk prostate cancer in a prospective randomized setting. Until results of this study are available, individual radiation oncologists typically assess risk across the wide range included within the intermediate-risk category to base treatment recommendations.
While clinical evidence to guide selection of the radionuclide (Pd-103 or I-125) is lacking, many practitioners use Pd-103 (in combination with IMRT) as the isotope of choice in the treatment of locally advanced disease because of its higher dose rate.
A prospective randomized multicenter trial examined long-term morbidity associated with I-125 compared with that of Pd-103 in the treatment of low-risk prostate cancer. The study found that patients who received I-125 were more likely to develop proctitis, while patients who received Pd-103 were more likely to develop prostatitis.6 Careful treatment planning should mitigate the adverse effects associated with I-125. A study by Niehaus et al evaluated International Prostate Symptom Scores (IPSSs) in 976 patients treated with brachytherapy and demonstrated that neither isotope was favorable in terms of IPSS resolution, catheter dependence, or need for postbrachytherapy surgical intervention.7
Studies of cesium (Cs)–131 in permanent prostate brachytherapy have been increasing. Cs-131 is an attractive alternative, as its average energy is similar to that of I-125 and it has a half-life of only 9.7 days.
The modern technique of prostate brachytherapy requires 3 components: (1) dosimetric planning, (2) placement of sources, and (3) evaluation of implant quality.
- Dosimetric planning of the implant should be performed in all patients before or during seed insertion. Debate persists as to whether intraoperative planning or preplanning is preferred. A modified peripheral loading plan is preferred when the sources are placed. The ABS also recommends that, for optimal patient care, postimplant dosimetry should be performed in all patients undergoing permanent prostate brachytherapy. At present, CT-based dosimetry is recommended, based on availability, cost, and the ability to image the prostate and the seeds. Additional plain radiographs should be obtained to verify the seed count.
Brachytherapy for prostate cancer. Abdominal radiograph following the procedure.
- Until the ideal postoperative interval for CT scanning has been determined, each center should perform dosimetric evaluation of prostate implants at a consistent postoperative interval. This interval should be reported. Isodose displays should be obtained at 50%, 80%, 90%, 100%, 150%, and 200% of the prescription dose and displayed on multiple cross-sectional images of the prostate. Dose-volume histography of the prostate should be performed, and all centers should report the D90 (dose to 90% of the prostate gland). Additionally, the D80; D100; the fractional V80, V90, V100, V150, and V200 (ie, the percentage of prostate volume receiving 80%, 90%, 100%, 150%, and 200% of the prescribed dose, respectively); and the rectal and urethral doses should be reported and ultimately correlated with clinical outcome in the research environment. Urbanic et al recently reported that a review of 4 series confirms that freedom from recurrence depends on adequate dosimetry.8
Temporary isotopes
In addition to permanent brachytherapy (discussed above), high dose rate brachytherapy has also been used. In this technique, the dose is delivered at a higher dose rate than is provided by a permanent implant. This delivers radiation to the prostate using temporary high dose rate radioactive implants. The most common isotope used for temporary brachytherapy is iridium (Ir)–192, which provides a higher dose of radiation than the I-125 or Pd-103 permanent implants. As such, the Ir-192 implants are not left in the prostate gland.
Using an imaging modality such as ultrasonography, MRI, or CT, temporary catheters that contain the implants are positioned in the prostate. Patients require hospitalization while the implants remain in place but may go home once the implants are removed. IMRT is usually used with this technique. The optimal patient population has not yet been determined. High dose rate brachytherapy is commonly delivered in 2 or more fractions of 810 Gy or more. Most series reported are from single centers.
Most brachytherapy for prostate cancer is performed using the permanent technique, which is the focus of the remainder of this article.
Relevant Anatomy
The prostate lies below the bladder and encompasses the prostatic urethra. It is surrounded by a capsule and is separated from the rectum by a layer of fascia termed the Denonvilliers aponeurosis. The blood supply to the base of the bladder and prostate is from the inferior vesicle, which is derived from the internal iliac. The capsular branches of the inferior vesicle artery help identify the pelvic plexus arising from the S2-4 and T10-12 nerve roots. The neurovascular bundle lies on either side of the prostate on the rectum. It is derived from the pelvic plexus and is important for erectile function.
Contraindications
Brachytherapy has several relative contraindications, as follows:
- Transurethral resection of the prostate: Initially, prior transurethral resection of the prostate was associated with increased symptoms and urinary incontinence rates as high as 50%, but more recent studies have reported incontinence rates of less than 10%.
- Pubic arch interference: Interference may occur because of a large prostate (a gland >40 g), and this interference may preclude adequate placement of seeds. Hormonal ablation, exaggerated lithotomy, horizontal probe position, and CT-guided placement are all potential solutions.
- Obstructive symptoms: Significant preoperative obstructive symptoms increase the likelihood of postoperative urinary retention. While glands larger than 40 g are more likely to have obstructive symptoms, symptoms can occur in anyone. Glands between 50 g and 60 g require downsizing. Hormone ablation has been reported to downsize the prostate gland by 25-40% and is used to facilitate brachytherapy in patients with large glands. One study randomized prostates of comparable size to brachytherapy alone or brachytherapy after hormone ablation.9 They found that the acute side effects of urinary retention and dysuria were actually greater in the hormone ablation group. Clinicians often compromise and use a 5-alpha reductase inhibitor rather than true androgen ablation for downsizing. Nonetheless, brachytherapy is not advisable in patients with glands larger than 60 g.
- Morbid obesity: Focusing on the target is feasible, but the equipment often cannot sustain the weight or is not long enough to reach the prostate.
More on Prostate Cancer - Brachytherapy (Radioactive Seed Implantation Therapy) |
 Overview: Prostate Cancer - Brachytherapy (Radioactive Seed Implantation Therapy) |
| Workup: Prostate Cancer - Brachytherapy (Radioactive Seed Implantation Therapy) |
| Treatment: Prostate Cancer - Brachytherapy (Radioactive Seed Implantation Therapy) |
| Follow-up: Prostate Cancer - Brachytherapy (Radioactive Seed Implantation Therapy) |
| Multimedia: Prostate Cancer - Brachytherapy (Radioactive Seed Implantation Therapy) |
| References |
| Further Reading |
| Next Page » |
References
U.S. Preventive Services Task Force. Screening for prostate cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. Aug 5 2008;149(3):185-91. [Medline].
Hsing AW, Comstock GW. Serological precursors of cancer: serum hormones and risk of subsequent prostate cancer. Cancer Epidemiol Biomarkers Prev. Jan-Feb 1993;2(1):27-32. [Medline].
Agency for Healthcare Research and Quality. Comparative Effectiveness of Therapies for Clinically Localized Prostate Cancer. AHRQ: Agency for Healthcare Research and Quality. Available at http://effectivehealthcare.ahrq.gov/healthInfo.cfm?infotype=rr&ProcessID=9&DocID=79. Accessed January 15, 2009.
Nag S. Brachytherapy for prostate cancer: summary of American Brachytherapy Society recommendations. Semin Urol Oncol. May 2000;18(2):133-6. [Medline].
Frank SJ, Grimm PD, Sylvester JE, Merrick GS, Davis BJ, Zietman A, et al. Interstitial implant alone or in combination with external beam radiation therapy for intermediate-risk prostate cancer: a survey of practice patterns in the United States. Brachytherapy. Jan-Mar 2007;6(1):2-8. [Medline].
Herstein A, Wallner K, Merrick G, Mitsuyama H, Armstrong J, True L, et al. I-125 versus Pd-103 for low-risk prostate cancer: long-term morbidity outcomes from a prospective randomized multicenter controlled trial. Cancer J. Sep-Oct 2005;11(5):385-9. [Medline].
Niehaus A, Merrick GS, Butler WM, Wallner KE, Allen ZA, Galbreath RW, et al. The influence of isotope and prostate volume on urinary morbidity after prostate brachytherapy. Int J Radiat Oncol Biol Phys. Jan 1 2006;64(1):136-43. [Medline].
Urbanic JJ, Lee WR. Update on brachytherapy in localized prostate cancer: the importance of dosimetry. Curr Opin Urol. May 2006;16(3):157-61. [Medline].
Petit JH, Gluck C, Kiger WS 3rd, Laury Henry D, Karasiewicz C, Talcott JA, et al. Androgen deprivation-mediated cytoreduction before interstitial brachytherapy for prostate cancer does not abrogate the elevated risk of urinary morbidity associated with larger initial prostate volume. Brachytherapy. Oct-Dec 2007;6(4):267-71. [Medline].
Pilepich MV, Caplan R, Byhardt RW, Lawton CA, Gallagher MJ, Mesic JB, et al. Phase III trial of androgen suppression using goserelin in unfavorable-prognosis carcinoma of the prostate treated with definitive radiotherapy: report of Radiation Therapy Oncology Group Protocol 85-31. J Clin Oncol. Mar 1997;15(3):1013-21. [Medline].
Bolla M, Gonzalez D, Warde P, Dubois JB, Mirimanoff RO, Storme G, et al. Improved survival in patients with locally advanced prostate cancer treated with radiotherapy and goserelin. N Engl J Med. Jul 31 1997;337(5):295-300. [Medline].
Koutrouvelis P, Hendricks F, Lailas N, Gil-Montero G, Sehn J, Khawand N, et al. Salvage reimplantation in patient with local recurrent prostate carcinoma after brachytherapy with three dimensional computed tomography-guided permanent pararectal implant. Technol Cancer Res Treat. Aug 2003;2(4):339-44. [Medline].
de la Taille A, Hayek O, Benson MC, Bagiella E, Olsson CA, Fatal M, et al. Salvage cryotherapy for recurrent prostate cancer after radiation therapy: the Columbia experience. Urology. Jan 2000;55(1):79-84. [Medline].
Perrotte P, Litwin MS, McGuire EJ, Scott SM, von Eschenbach AC, Pisters LL. Quality of life after salvage cryotherapy: the impact of treatment parameters. J Urol. Aug 1999;162(2):398-402. [Medline].
Greene GF, Pisters LL, Scott SM, Von Eschenbach AC. Predictive value of prostate specific antigen nadir after salvage cryotherapy. J Urol. Jul 1998;160(1):86-90. [Medline].
Pisters LL, Perrotte P, Scott SM, Greene GF, von Eschenbach AC. Patient selection for salvage cryotherapy for locally recurrent prostate cancer after radiation therapy. J Clin Oncol. Aug 1999;17(8):2514-20. [Medline].
Lee WR, McQuellon RP, Case LD, deGuzman AF, McCullough DL. Early quality of life assessment in men treated with permanent source interstitial brachytherapy for clinically localized prostate cancer. J Urol. Aug 1999;162(2):403-6. [Medline].
Beyer DC. Permanent brachytherapy as salvage treatment for recurrent prostate cancer. Urology. Nov 1999;54(5):880-3. [Medline].
Grado GL, Collins JM, Kriegshauser JS, Balch CS, Grado MM, Swanson GP, et al. Salvage brachytherapy for localized prostate cancer after radiotherapy failure. Urology. Jan 1999;53(1):2-10. [Medline].
Ragde H, Korb LJ, Elgamal AA, Grado GL, Nadir BS. Modern prostate brachytherapy. Prostate specific antigen results in 219 patients with up to 12 years of observed follow-up. Cancer. Jul 1 2000;89(1):135-41. [Medline].
Kuban DA, el-Mahdi AM, Schellhammer P. The significance of post-irradiation prostate biopsy with long-term follow-up. Int J Radiat Oncol Biol Phys. 1992;24(3):409-14. [Medline].
Polascik TJ, Pound CR, DeWeese TL, Walsh PC. Comparison of radical prostatectomy and iodine 125 interstitial radiotherapy for the treatment of clinically localized prostate cancer: a 7-year biochemical (PSA) progression analysis. Urology. Jun 1998;51(6):884-9; discussion 889-90. [Medline].
Bittner N, Merrick GS, Wallner KE, Lief JH, Butler WM, Galbreath RW. The impact of acute urinary morbidity on late urinary function after permanent prostate brachytherapy. Brachytherapy. Oct-Dec 2007;6(4):258-66. [Medline].
Blasko JC. Low-dose-rate brachytherapy for prostate cancer: preplanning vs. intraoperative planning-preplanning is best. Brachytherapy. Jul-Sep 2006;5(3):139-42; discussion 145. [Medline].
Blasko JC, Grimm PD, Sylsvester JE, Cavanagh W. The role of external beam radiotherapy with I-125/Pd-103 brachytherapy for prostate carcinoma. Radiother Oncol. Dec 2000;57(3):273-8. [Medline].
Blasko JC, Ragde H, Luse RW, Sylvester JE, Cavanagh W, Grimm PD. Should brachytherapy be considered a therapeutic option in localized prostate cancer?. Urol Clin North Am. Nov 1996;23(4):633-50. [Medline].
Borghede G, Hedelin H, Holmang S, Johansson KA, Sernbo G, Mercke C, et al. Irradiation of localized prostatic carcinoma with a combination of high dose rate iridium-192 brachytherapy and external beam radiotherapy with three target definitions and dose levels inside the prostate gland. Radiother Oncol. Sep 1997;44(3):245-50. [Medline].
Caputo G. Devita VT, Hellman S, Rosenberg SA, eds. Cancer: Principles and Practice of Oncology. 5th ed. Philadelphia, Pa: Lippincott Williams and Wilkins; 1997.
Cox JD. Moss' Radiation Oncology. In: Rationale, Technique, Results. 7th ed. St. Louis, Mo: Mosby-Year Book; 1994.
Critz FA, Williams WH, Holladay CT, Levinson AK, Benton JB, Holladay DA, et al. Post-treatment PSA < or = 0.2 ng/mL defines disease freedom after radiotherapy for prostate cancer using modern techniques. Urology. Dec 1999;54(6):968-71. [Medline].
Dinges S, Deger S, Koswig S, Boehmer D, Schnorr D, Wiegel T, et al. High-dose rate interstitial with external beam irradiation for localized prostate cancer--results of a prospective trial. Radiother Oncol. Aug 1998;48(2):197-202. [Medline].
Horwitz EM, Vicini FA, Ziaja EL, Dmuchowski CF, Stromberg JS, Martinez AA. The correlation between the ASTRO Consensus Panel definition of biochemical failure and clinical outcome for patients with prostate cancer treated with external beam irradiation. American Society of Therapeutic Radiology and Oncology. Int J Radiat Oncol Biol Phys. May 1 1998;41(2):267-72. [Medline].
Joly F, Brune D, Couette JE, Lesaunier F, Heron JF, Peny J, et al. Health-related quality of life and sequelae in patients treated with brachytherapy and external beam irradiation for localized prostate cancer. Ann Oncol. Jul 1998;9(7):751-7. [Medline].
Kabalin JN, Hodge KK, McNeal JE, Freiha FS, Stamey TA. Identification of residual cancer in the prostate following radiation therapy: role of transrectal ultrasound guided biopsy and prostate specific antigen. J Urol. Aug 1989;142(2 Pt 1):326-31. [Medline].
Koutrouvelis PG. Three-dimensional stereotactic posterior ischiorectal space computerized tomography guided brachytherapy of prostate cancer: a preliminary report. J Urol. Jan 1998;159(1):142-5. [Medline].
Krupski T, Petroni GR, Bissonette EA, Theodorescu D. Quality-of-life comparison of radical prostatectomy and interstitial brachytherapy in the treatment of clinically localized prostate cancer. Urology. May 2000;55(5):736-42. [Medline].
Laverdière J, Gomez JL, Cusan L, Suburu ER, Diamond P, Lemay M, et al. Beneficial effect of combination hormonal therapy administered prior and following external beam radiation therapy in localized prostate cancer. Int J Radiat Oncol Biol Phys. Jan 15 1997;37(2):247-52. [Medline].
Lee WR. The role of androgen deprivation therapy combined with prostate brachytherapy. Urology. Sep 2002;60(3 Suppl 1):39-44; discussion 44. [Medline].
Long JP, Bahn D, Lee F, Shinohara K, Chinn DO, Macaluso JN Jr. Five-year retrospective, multi-institutional pooled analysis of cancer-related outcomes after cryosurgical ablation of the prostate. Urology. Mar 2001;57(3):518-23. [Medline].
Mazeron JJ. Brachytherapy: a new era. Radiother Oncol. Mar 2005;74(3):223-5. [Medline].
McNeal J, Noldus J. Limitations of transition zone needle biopsy findings in the prediction of transition zone cancer and tissue composition of benign nodular hyperplasia. Urology. Nov 1996;48(5):751-6. [Medline].
Merrick GS, Butler WM, Galbreath RW, Lief JH, Adamovich E. Biochemical outcome for hormone-naive patients with Gleason score 3+4 versus 4+3 prostate cancer undergoing permanent prostate brachytherapy. Urology. Jul 2002;60(1):98-103. [Medline].
Merrill RM, Weed DL, Feuer EJ. The lifetime risk of developing prostate cancer in white and black men. Cancer Epidemiol Biomarkers Prev. Oct 1997;6(10):763-8. [Medline].
Miller DC, Sanda MG, Dunn RL, Montie JE, Pimentel H, Sandler HM, et al. Long-term outcomes among localized prostate cancer survivors: health-related quality-of-life changes after radical prostatectomy, external radiation, and brachytherapy. J Clin Oncol. Apr 20 2005;23(12):2772-80. [Medline].
Nag S, Beyer D, Friedland J, Grimm P, Nath R. American Brachytherapy Society (ABS) recommendations for transperineal permanent brachytherapy of prostate cancer. Int J Radiat Oncol Biol Phys. Jul 1 1999;44(4):789-99. [Medline].
Nag S, Bice W, DeWyngaert K, Prestidge B, Stock R, Yu Y. The American Brachytherapy Society recommendations for permanent prostate brachytherapy postimplant dosimetric analysis. Int J Radiat Oncol Biol Phys. Jan 1 2000;46(1):221-30. [Medline].
Nag S, Ciezki JP, Cormack R, Doggett S, DeWyngaert K, Edmundson GK, et al. Intraoperative planning and evaluation of permanent prostate brachytherapy: report of the American Brachytherapy Society. Int J Radiat Oncol Biol Phys. Dec 1 2001;51(5):1422-30. [Medline].
Nag S, Ellis RJ, Merrick GS, Bahnson R, Wallner K, Stock R, et al. American Brachytherapy Society recommendations for reporting morbidity after prostate brachytherapy. Int J Radiat Oncol Biol Phys. Oct 1 2002;54(2):462-70. [Medline].
Neill M, Studer G, Le L, McLean M, Yeung I, Pond G. The nature and extent of urinary morbidity in relation to prostate brachytherapy urethral dosimetry. Brachytherapy. Jul-Sep 2007;6(3):173-9. [Medline].
Ragde H, Elgamal AA, Snow PB, Brandt J, Bartolucci AA, Nadir BS, et al. Ten-year disease free survival after transperineal sonography-guided iodine-125 brachytherapy with or without 45-gray external beam irradiation in the treatment of patients with clinically localized, low to high Gleason grade prostate carcinoma. Cancer. Sep 1 1998;83(5):989-1001. [Medline].
Ray ME, Thames HD, Levy LB, Horwitz EM, Kupelian PA, Martinez AA, et al. PSA nadir predicts biochemical and distant failures after external beam radiotherapy for prostate cancer: a multi-institutional analysis. Int J Radiat Oncol Biol Phys. Mar 15 2006;64(4):1140-50. [Medline].
Stamey TA, McNeal JE, Yemoto CM, Sigal BM, Johnstone IM. Biological determinants of cancer progression in men with prostate cancer. JAMA. Apr 21 1999;281(15):1395-400. [Medline].
Stock RG, Stone NN, Iannuzzi C. Sexual potency following interactive ultrasound-guided brachytherapy for prostate cancer. Int J Radiat Oncol Biol Phys. May 1 1996;35(2):267-72. [Medline].
Stromberg J, Martinez A, Gonzalez J, Edmundson G, Ohanian N, Vicini F, et al. Ultrasound-guided high dose rate conformal brachytherapy boost in prostate cancer: treatment description and preliminary results of a phase I/II clinical trial. Int J Radiat Oncol Biol Phys. Aug 30 1995;33(1):161-71. [Medline].
Theodorescu D, Gillenwater JY, Koutrouvelis PG. Prostatourethral-rectal fistula after prostate brachytherapy. Cancer. Nov 15 2000;89(10):2085-91. [Medline].
Vicini FA, Vargas C, Edmundson G, Kestin L, Martinez A. The role of high-dose rate brachytherapy in locally advanced prostate cancer. Semin Radiat Oncol. Apr 2003;13(2):98-108. [Medline].
Waller K, Blasko J, Dattoli MJ. Prostate Brachytherapy Made Complicated. ed. Seattle, Wash: SmartMedicine; 1997.
Wallner K, Lee H, Wasserman S, Dattoli M. Low risk of urinary incontinence following prostate brachytherapy in patients with a prior transurethral prostate resection. Int J Radiat Oncol Biol Phys. Feb 1 1997;37(3):565-9. [Medline].
Zelefsky MJ, Nedelka MA, Arican ZL, Yamada Y, Cohen GN, Shippy AM, et al. Combined brachytherapy with external beam radiotherapy for localized prostate cancer: Reduced morbidity with an intraoperative brachytherapy planning technique and supplemental intensity-modulated radiation therapy. Brachytherapy. Jan-Mar 2008;7(1):1-6. [Medline].
Zelefsky MJ, Wallner KE, Ling CC, Raben A, Hollister T, Wolfe T, et al. Comparison of the 5-year outcome and morbidity of three-dimensional conformal radiotherapy versus transperineal permanent iodine-125 implantation for early-stage prostatic cancer. J Clin Oncol. Feb 1999;17(2):517-22. [Medline].
Zelefsky MJ, Whitmore WF Jr. Long-term results of retropubic permanent 125iodine implantation of the prostate for clinically localized prostatic cancer. J Urol. Jul 1997;158(1):23-9; discussion 29-30. [Medline].
Zelefsky MJ, Zaider M. Low-dose-rate brachytherapy for prostate cancer: preplanning vs. intraoperative planning-intraoperative planning is best. Brachytherapy. Jul-Sep 2006;5(3):143-4; discussion 146. [Medline].
Keywords
prostate brachytherapy, radioactive seed implantation therapy, interstitial brachytherapy, prostate cancer, prostate adenocarcinoma, adenocarcinoma of the prostate, radioactive implant therapy, prostatic brachytherapy, prostate therapy, adjuvant prostate cancer therapy, seed therapy, iodine-125, palladium-103, organ-confined prostate cancer, organ confined prostate cancer, iridium-192, radiopharmaceutical for prostate cancer, radioactive isotope therapy, HDRB, high dose rate brachytherapy
