The use of poly (ADP-Ribose) polymerase (PARP) inhibitors in patients with a variety of tumor types is backed by a growing body of research. According to Maha Hussain, MD, the Genevieve Teuton Professor of Medicine and deputy director of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University in Chicago, Illinois, there is now strong justification for clinical trials of PARP inhibitors in patients with prostate cancer.

“Metastatic prostate cancer is very complex, with a marked inter- and intra-patient heterogeneity and diversity. Therapy development, from my perspective, must focus on the totality of the biology if we want better care for our patients. DNA repair deficiencies have emerged as a promising therapeutic target in metastatic castration-resistant prostate cancer [mCRPC],” Hussain said during a presentation at New York GU™: 

11th Annual Interdisciplinary Prostate Cancer Congress

She noted that there are compelling data implicating PARP-1 in the mediation of DNA repair responses to alkylating agents, cellular survival in 

deficient cells, and androgen receptor (AR)-mediated prostate cancer cellular proliferation. Further, PARP-1 interacts with the androgen signaling cascade, and castration-resistant tumor cells exhibit increased PARP-1 activity.

These data prompted a clinical trial looking at the combination of temozolomide (Temodar) and the PARP inhibitor veliparib (ABT-888) in patients with mCRPC, with the idea to replicate what was done preclinically. However, the overall results were not that promising, with a prostate-specific antigen (PSA) response rate of 8% based on 2 of 25 evaluable patients achieving a confirmed PSA decline of ≥30%. In the remaining 23 patients, 13 had stable PSA and 10 had PSA progression. None of the 16 patients with measurable disease for whom data were available achieved an objective response.

Hussain noted that the reason for this lack of significant response could be that adding PARP inhibition to castration therapy provides a better tumor effect, targeting AR-signaling and the PARP pathway simultaneously. Additionally, Hussain said, there have been no predictive biomarkers to select patients for response to this regimen, but some emerging data suggested that

 fusions could be a predictor for sensitivity to AR and PARP targeting.

In an ongoing phase II trial, investigators, led by Hussain, tested the hypotheses that targeting AR and PARP would lead to better outcomes in patients with mCRPC and that 

 fusions would serve as a predictive biomarker for the response to treatment. Every patient underwent a metastatic disease biopsy. If eligible, they were stratified either as 

 fusion positive or negative and then randomized to receive the control arm of abiraterone acetate (Zytiga) and prednisone or the experimental arm of abiraterone acetate and prednisone plus veliparib. The primary endpoint was PSA response rate.

The study was negative overall, and although there was a trend in favor of the combination treatment, this was not statistically significant. ETS fusion positivity or negativity also did not predict for a better outcome.

 However, the investigators observed that in a cohort of 80 patients with adequate tissue for tumor sequencing, 20 had DNA damage repair defects, which were either homozygous or deleterious mutations. The most frequent were 

“There was a fair amount of genomic alteration, but the 1 consistent factor was that the patients had DNA repair defects and had a response as reflected by PSA, and these responses were quite deep,” Hussain said.

PSA declines were statistically significant in patients with DNA repair defects compared with patients with wild-type disease (90% vs 56.4%, respectively; 

 = .007), and the measurable disease response rate was also higher for patients with DNA repair defects (87.5% vs 37.5%; 

“Contrary to conventional wisdom up to now, where the belief was that patients with DNA repair defects did worse, in our trial, those patients did better,” Hussain said. “This is a previously unknown observation that the patients who were on the abiraterone-only arm still did better compared with patients who had wild-type disease.”

Table 1. PFS Response to Combination Abiraterone With Prednisone and Veliparib by Biomarker Status

Hussain et al then performed a multivariate analysis of progression-free survival (PFS) by biomarker status that incorporated clinical factors and other molecular factors. They noted that when they controlled for these factors, DNA damage repair defect was the biomarker that predicted the best outcome to PARP inhibition therapy. The median PFS for patients with DNA damage repair defects was 14.5 months compared with 8.0 months for those with wildtype disease (

Other molecular alterations also had a significant association with benefit from PARP therapy. Patients with a 

 mutation all had worse outcomes; however, DNA damage repair defects were the strongest predictor (

“When we are designing clinical trials,” Hussain said, “it is very difficult for us to understand the genomic or molecular profile of the tumor because no tumor has such a unique feature that it’s going to predict 100% response to treatment.” The main observation noted in these data was that patients with DNA damage repair defects responded to AR-targeted drugs with or without a PARP inhibitor. Another study’s findings recently demonstrated a similar observation based on germline data, affirming that these patients with mCRPC seem to respond better than expected to AR-targeted therapy.

In the single-arm phase II TOPARP-A trial, a group of heavily pretreated patients with mCRPC were given the PARP inhibitor olaparib (Lynparza) as an experimental treatment and underwent tumor sequencing.4 “Interestingly, there were 16 patients of a cohort of about 50 patients with [the] DNA repair defect, and 14 of the 16 responders were biomarker positive, and this translated into what I would consider meaningful clinical benefit in terms of delaying [progression] and in PFS,” she commented.

Table 2. Select Clinical Trials of PARP Inhibitors in Prostate Cancer

Hussain noted that the trial showed that about 90% of mCRPC tumors harbor potentially clinically actionable molecular alterations. Several of these molecular alterations appear to be novel, and there are clinical trials starting that address some of those. However, she said that an important finding of the TOPARP trial was that over 20% of patients with mCRPC harbor DNA damage repair pathway defects, specifically in

Clinically, in other cancers, these are considered the “canonical” DNA damage repair defects. In prostate cancer, it seems there are other potential 

ness alterations, but Hussain posed the question of whether patients with these mutations are responsive to PARP inhibition.

The phase II BRCAAway trial is currently recruiting patients with mCRPC and DNA repair defects (NCT03012321). Patients will be entered into the study if they either have enough tissue for a biopsy or known germline mutations in 

. They will then be randomized to abiraterone plus prednisone, olaparib alone, or the combination, with the potential to cross over after progression. Patients who have a “noncanonical” alteration will be entered into a single-arm cohort to see if there’s a signal from treatment with olaparib monotherapy.

Currently, there are 6 PARP inhibitors being evaluated in prostate cancer in clinical trials (

). Hussain notes that further study is needed to fully understand DNA repair defects and how to target them most effectively.

Hussain M, Carducci MA, Slovin S, et al. Targeting DNA repair with combination veliparib (ABT-888) and temozolomide in patients with metastatic castration-resistant prostate cancer. Invest New Drugs. 2014;32(5):904-912. doi: 10.1007/s10637-014- 0099-0. Hussain M, Daignault S, Twardowski P, et al. Abiraterone + prednisone (Abi) +/- veliparib (Vel) for patients (pts) with metastatic castration-resistant prostate cancer (CRPC): NCI 9012 updated clinical and genomics data. 

2017;35(suppl; abstr 5001). meetinglibrary.asco.org/record/144554/abstract.

Antonarakis ES, Lu C, Luber B, et al. Germline DNA-repair gene mutations and outcomes in men with metastatic castration-resistant prostate cancer receiving firstline abiraterone and enzalutamide [published online February 10, 2018]. 

Mateo J, Carreira S, Sandhu S, et al. DNA-repair defects and olaparib in metastatic prostate cancer. 

 2015;373(18):1697-708. doi: 10.1056/NEJMoa1506859.

Robinson D, Van Allen EM, Wu YM, et al. Integrative clinical genomics of advanced prostate cancer. 

 2015;161(5):1215-1228. doi: 10.1016/j.cell.2015.05.001.

Articles

The use of PARP inhibitors in patients with a variety of tumor types is backed by a growing body of research, and there is now strong justification for clinical trials of these agents in patients with prostate cancer.

DNA Repair Defects Are Strong Targets for Therapeutic Development in Prostate Cancer

Radium-223 (Xofigo) has efficacy in treating patients with prostate cancer and bone metastases, but is usually introduced into the patient's traetment plan after they have symptomatic disease. These symptoms are often painful, and the metastases can be difficult to treat at this stage. Moving radium-223 up in the treatment paradigm for these patients could provide better outcomes and longer survival, according to Richard G. Stock, MD, professor and director of genitourinary oncology at the Icahn School of Medicine at Mount Sinai in New York.

“Clearly, what we know is, when bone metastases are present, patients have a decrease in overall survival. This is a problem that needs to be addressed, and skeletal tumor burden is an independent predictor of death in patients with advanced prostate cancer,” Stock said during a presentation at New York GU™: 

Bone metastases are quite common in prostate cancer, Stock said. About 14% of the patients who undergo surgical or chemical castration will develop castration-resistant prostate cancer (CRPC), and about 90% of those patients will develop metastases in the bone. The 5-year survival rate for patients with bone metastases is about 30%.

Typically, prostate cancer progresses from nonmetastatic local disease (M0), with a possible rise in prostate-specific antigen levels and biochemical relapse, to CRPC when patients fail androgen-deprivation therapy. Patients with newly diagnosed metastatic CRPC (M1) are often chemotherapy naïve, and 4% of patients with prostate cancer present initially with M1, hormone-sensitive disease.

The treatment challenge is that prostate tumor cells may colonize the bone during this disease progression. In vitro data show that the colonization of bone tissue may be driven by chemoattraction and preferential attachment.

Prostate cancer metastases are also associated with osteoblastic activity, so the balance shifts from bone destruction to bone deposition, where the osteoblasts secrete more proteins to form excess bone beyond the body’s bone resorption capabilities. This leads to osteoblastic lesions in the mineralized bone tissue where tumor cells have gathered, and it correlates with higher levels of alkaline phosphatase and osteocalcin, which would signify liver or gallbladder toxicity.

When bone metastases are present, overall survival (OS) is lower. Results from a population-based cohort study of patients with prostate cancer showed that fewer patients with bone metastases were alive at 5 years (3%; 95% CI, 2.2%-3.4%) than patients with no bone metastases (56%; 95% CI, 54.9%-56.7%). In the study, 23,087 patients had an initial diagnosis of prostate cancer; 22,404 of those patients had no bone metastases, and 569 presented with bone metastases at diagnosis.

Investigators in the field of prostate cancer therapeutics have seen different isotopes being used to treat bone metastases in patients with prostate cancer, but most have fallen by the wayside due to bone marrow toxicities. Radium-223 has remained a standard radiotherapy since its approval by the FDA in 2013, due in part to its more favorable toxicity profile and its mechanism of action.

Radium-223 is an alpha-pharmaceutical that targets bone metastases by mimicking calcium, forming complexes with the bone mineral hydroxyapatite at areas of increased bone turnover, such as bone metastases. The short range of the alpha particles emitted (<10 cell diameters) limits damage to the surrounding normal tissue, leading to less bone marrow toxicity. The alpha particles predominantly cause double-strand DNA breaks in adjacent cells, resulting in the antitumor effect on bone metastases.

Because radium-223 is absorbed primarily by the bone marrow, there is a small risk for bone marrow—related toxicities, such as myelosuppression. However, radium-223 can also lead to adverse events (AEs) outside of the bone. The agent can be absorbed by other organs, including the gastrointestinal system, leading to AEs that can include nausea, diarrhea, and vomiting.

Stock recommended watching out for these and other AEs. “For those of us who do this in a clinical practice, we check the blood count, and it is very rare that patients have to discontinue treatment due to myelosuppression,” he said. It is important, he continued, to monitor patients with evidence of compromised bone marrow reserve closely and provide supportive care measures when clinically indicated. Radium-223 should be discontinued in patients who experience life-threatening complications despite supportive care for bone marrow failure.

Stock also said that a key reason why radium-223 is an effective drug for patients with prostate cancer is how it’s eliminated. After an intravenous injection, less than 1% of radium-223 dichloride remains in the blood after 24 hours. Fecal excretion, the major route of elimination, removes 63% of the agent within 1 week; less than 5% is excreted through the urine.

Table. Ongoing Clinical Trials of Radium-223 in Combination With Other Agents for Patients With CRPC and Bone Metastases

In the phase III ALSYMPCA study of radium-223 in patients with symptomatic CRPC with skeletal metastases (NCT00699751), results showed that radium-223 significantly improved OS versus a placebo (median OS, 14.9 vs 11.3 months; HR, 0.70; 95% CI, 0.55-0.88; 

 <.001). In a subgroup analysis of the study, radium-223 provided benefit to patients in all subgroups.8

In a phase II prospective study of radium-223 in patients with CRPC with bone metastases (NCT01516762), results showed that the agent was well tolerated with no new safety concerns observed. The study found that patients with more advanced disease were less likely to benefit from radium-223, and investigators recommended that clinicians consider baseline characteristics and therapy sequence for greatest clinical value.

The phase II prospective study was part of an expanded access program that was approved in 2012, with the goal to monitor acute and long-term safety of radium-223 in patients with CRPC and symptomatic bone metastases. The drug was made available at qualified clinical sites to patients who could not participate in a controlled clinical trial.

Ultimately, Stock said, radium-223 is generally used early in the management of castration-resistant disease if the patient exhibits symptomatic bone metastases with or without small-volume pelvic or retroperitoneal lymph node metastases, with no evidence of visceral metastases, and with good hematologic function.

Looking to the future, there are other clinical trials testing the efficacy and safety of radium-223 in patients with prostate cancer with bone metastases combined with other therapies (

). However, Stock cautioned that in a phase III trial (NCT02043678), radium-223 was combined with abiraterone (Zytiga), which led to greater risk of fractures.

 “We now know not to use that combination treatment, although we don’t really know why it leads to the increased risk of fracture,” he said.

Cancer stat facts: prostate cancer. Surveillance, Epidemiology, and End Results Program. National Cancer Institute website. seer.cancer.gov/statfacts/html/prost. html. Accessed May 3, 2018.

Tsingotjidou AS, Zotalis G, Jackson KR, et al. Development of an animal model for prostate cancer cell metastasis to adult human bone. 

Taichman RS, Cooper C, Keller ET, Pienta KJ, Taichman NS, McCauley LK. Use of the stromal cell-derived factor-1/CXCR4 pathway in prostate cancer metastasis to bone. 

Jung K, Lein M, Stephan C, et al. Comparison of 10 serum bone turnover markers in prostate carcinoma patients with bone metastatic spread: diagnostic and prognostic implications.

2004;111(5):783-791. doi: 10.1002/ijc.20314.

Yang J, Fizazi K, Peleg S, et al. Prostate cancer cells induce osteoblast differentiation through a Cbfa1-dependent pathway. 

Nørgaard M, Jensen AØ, Jacobsen JB, Cetin K, Fryzek JP, Sørensen HT. Skeletal related events, bone metastasis and survival of prostate cancer: a population based cohort study in Denmark (1999 to 2007).

. 2010;184(1):162-167. doi: 10.1016/j.juro.2010.03.034.

Xofigo [prescribing information]. Wayne, NJ: Bayer HealthCare Pharmaceuticals Inc; 2013. accessdata.fda.gov/drugsatfda_docs/label/2013/203971lbl.pdf. Accessed May 3, 2018.

Parker C, Nilsson S, Heinrich D, et al; ALSYMPCA Investigators. Alpha emitter radium- 223 and survival in metastatic prostate cancer. 

. 2013;369(3):213- 223. doi: 10.1056/NEJMoa1213755.

Sartor O, Vogelzang NJ, Sweeney C, et al; U.S. Expanded Access Program Investigators. Radium-223 safety, efficacy, and concurrent use with abiraterone or enzalutamide: first U.S. experience from an expanded access program. 

. 2018;23(2):193-202. doi: 10.1634/theoncologist.2017-0413.

Bayer initiated expanded access program for investigational compound radium-223 chloride [press release]. Wayne, NJ: PRNewswire; February 2, 2012. prnewswire. com/news-releases/bayer-initiates-expanded-access-program-for-investigationalcompound- radium-223-chloride-138559894.html. Accessed June 6, 2018.

Important drug warning. Xofigo (radium Ra 223 dichloride): important safety information update regarding increased incidence of deaths and fractures in an investigational phase III clinical trial with Xofigo used in combination with abiraterone acetate and prednisolone/prednisone. Bayer HealthCare Pharmaceuticals Inc. hcp.xofigo-us.com/downloads/pdf/PP-600-US-3282%20Xofigo%20November%20 2017%20DHCP%20Letter%20-%20Digital%20Version.pdf. Published November 30, 2017. Accessed May 3, 2018.

Moving radium-223 (Xofigo) up in the treatment paradigm for patients with prostate cancer could provide better outcomes and longer survival, according to Richard G. Stock, MD. 

Moving Radium-223 Forward in the Treatment Timeline for Prostate Cancer With Bone Metastases

When I graduated from medical school in the 1980s and decided to pursue a career in urologic surgery, most of the residency programs in the United States took 6 years— 2 years of general surgery followed by 4 years of urology. Part of those 4 years of urologic training included, for the most part, a year spent in the research lab. There were 5-year residency programs available, but the majority at the time were built around the 2/4 construct.

I had the good fortune to be accepted into the urology program at Vanderbilt University Medical Center, and my time in the lab coincided with my first year of urology training, 3 years after medical school. This offered me a welcome respite after 2 long years of being on call every other night in general surgery, as it did for friends in other disciplines who were undergoing the same regimen.

Fortunately for me, my residency chairman at the time was committed to basic science research, particularly renal physiology and electrolyte imbalance. I was very interested in how the diversion technique of continent urinary reservoirs and orthotopic bladder reconstruction—new at the time&mdash;could result in a better quality of life without a stoma bag once a cystectomy had been performed. Consequently, I initiated 2 projects during that period. First, using a rat model and inducing unilateral obstruction of varied times, I tried to isolate the humoral factor that resulted in renal compensatory hypertrophy of the kidney. Second, in a canine model, I configured tubularized and detubularized segments of intestine, then measured and characterized peristaltic activity in these types of reconstruction.

What started as a period I initially viewed as a time away from the clinic, less stress, and not being on call became one of my most valuable experiences, because it shaped much of my clinical thinking and approach to science. (The downside was that it subjected my immune system to a daily barrage of rat and canine dander, rendering me deathly allergic.) The academic rigor necessary to approach the hypothesis and devise the study also was invaluable early in my career. Additionally, during this experience I had the good fortune to be befriended by 2 people—with strikingly diverse backgrounds&mdash;whom I would never have met otherwise.

James Phillips was a gentleman and high school graduate who essentially took care of most of the animals in the lab and assisted with anesthesia, intravenous procedures, etc, especially with the larger species. As a young teenager in Nashville, Tennessee, before World War II, he had the opportunity to work with Vivien Thomas, who would leave the Vanderbilt University labs and join Alfred Blalock, MD, at Johns Hopkins Hospital in Baltimore, Maryland, to pioneer pediatric heart surgery and correction of tetralogy of Fallot. The stories of those early days in the lab were mesmerizing.

The second was a pipe-smoking scholar whose lab was on the way to our favorite watering hole. Although I stopped by on many occasions and asked him to join us for lunch, which was always politely declined, he would often take the time to try to understand what the surgeons were doing in the lab. This was the great Stanley Cohen, PhD, who earlier, in 1986, shared the Nobel Prize in Physiology or Medicine for his discovery of the epidermal growth factor family and its receptors. My intermittent discussions in his lab would change the way I viewed cancer biology.

Many do not realize that residents do not get such opportunities today. Save for a few, most programs have gone back to a 5-year training, the required minimum to achieve board certification in urology; the research year is not funded by Medicare, so hospitals do not receive direct graduate medical education funds from the government. Thus, an institution that still provides basic science research time has to support that resident with internal sources or grants. The focus of research for the residents today is less about science or drug development and more about health economics outcome research and realworld practice patterns with attempts to optimize care, which are all very much needed in today’s medical environment.

However, there is still a role for urologists, even those currently in practice, to be active participants in research and become clinical scientists. Many successful groups across the United States have launched clinical research divisions within the practice that have played an important role in the development and ultimate approval of many of the new therapies for advanced prostate cancer that we prescribe, as well as some of the biomolecular markers being used for diagnosis and management. I see this trend continuing into the future. Newer technologies and treatment paradigms are constantly being introduced into the marketplace and require validation and randomized trials. There is no reason we as specialists should not be involved in these trials, as rapid accrual is essential.

We talk about creating centers of excellence and physician champions to advance care. I truly believe that by doing the research, one gets a deeper and better understanding of the disease state, which will ultimately improve care and outcomes. We should all strive to support these collaborative efforts.

Raoul S. Concepcion, MD, FACS, discusses the importance of research opportunities for residents.

A Call for Clinical Research

Greater Boston Urology (GBU), the largest physician-owned urology practice in Massachusetts, strives to offer comprehensive urologic care that includes up-and-coming diagnostics and treatments, such as the Prostate Health Index (PHI) blood test and high intensity—focused ultrasound (HIFU).

The practice also strives to improve outcomes from traditional medicine. It recognizes the necessity of prostate- specific antigen (PSA) testing to find out which patients are at risk of developing prostate cancer, but also that PSA testing is not fully reliable and may lead to unnecessary surgery and adverse events. GBU will not put a patient through a prostate biopsy or a diagnostic workup based on a single lab test because there other tests are now available to supplement the PSA and determine who is at risk. GBU utilizes the PHI test as a safer and more effective way to stratify prostate cancer risk than PSA alone.

According to Michael J. Curran, MD, practice chief executive officer, although results of national studies show prostate cancer is detected in 30% to 35% of biopsies, at GBU the use of supplemental tests has enabled physicians to achieve a positive biopsy rate of about 65%. The practice has halved the number of biopsies done on patients who may not have prostate cancer.

“There’s a tremendous benefit not only for those individual patients, but for the community, because that overall care process is going to lower the cost of delivery or urological care,” Curran said. “Because we mitigate problems with the most expensive part of the process, which is the biopsy, by reserving it for a more select group who are more likely to have prostate cancer, we can lower costs.” GBU also uses genomic testing as part of the decision- making process to decide what treatment plan would be best for patients with prostate cancer. “We can identify the patient through genomic testing who may be at much lower risk for having cancer-causing morbidity or mortality in the future, and some patients with prostate cancer can go on to a surveillance program instead of active intervention,” Curran said.

The practice strives for minimally invasive outcomes for other genitourinary cancers. Most partial or radical nephrectomies are done laparoscopically or robotically. At all GBU locations, advanced therapeutics for superficial bladder cancer treatment are offered in-office. For treatment of testicular cancer, patients are referred outside the practice for chemotherapy and radiation, although GBU coordinates with those cancer centers to manage care effectively and has in-house labs for diagnostic tests.

“There’s not much need for our patients to go outside our practice when they have complex oncology needs or if they have relatively common cancers, such as bladder and prostate,” Curran said. “We are comfortable managing those patients, and we try to cater to them; it’s very easy to get the patient to a doctor who’s going to be best for their needs. This way, the patients not only have a good outcome for their disease, but they also have a good experience.”

GBU formed in 2011 as a merger of independent urology practices primarily in southern Massachusetts and has since grown to a team of 14 urologists, 1 urologic gynecologist, 1 pathologist, 4 physician assistants, and 79 other employees. They have 8 office locations in southeastern Massachusetts: Dedham, Falmouth, Framingham, Milton, North Easton/Brockton, Norwood, Plymouth, and Sandwich. The practice covers about 15% to 20% of total urology services in the state. All of the urologists practice general urology, with some concentrating on robotic surgery, advanced diagnostic techniques (primarily for prostate cancer), advanced therapeutics, or urologic gynecology.

The team can handle all aspects of urologic malignancies, managing patients with all stages of prostate cancer, and is currently the only group in New England offering HIFU for patients with prostate cancer.1 According to Curran, GBU was one of the first practices in the region to offer 3D MRI fusion biopsy of the prostate and is the only independent urology practice in New England where a patient can get the PHI blood test.

In addition to physicians, GBU has administrators and other background support to share the responsibility for successful management. This includes a chief operations officer, a vice president of operations, a legal firm and a political lobbyist on retainer, and a certified coder and medical billing expert in GBU’s centralized billing office.

GBU maintains its commitment to staying abreast of new technologies and techniques by keeping its physicians in control of the business. The practice reasons that the people who provide healthcare should be the same people who make the decisions about what technology or techniques to employ to deliver the best care.

At larger practices that are owned by hospitals or other entities that are not physician controlled, bureaucratic roadblocks may arise when physicians want to adopt new technology. The physicians first have to appeal to the institution or a board of directors to get the approval and funding, with the risk that their request could be turned down. GBU does not have this problem. “[Our independence] allows us a lot of freedom in adopting and incorporating new technology,” Curran said.”

The practice’s philosophy is that physicians should also control how income is allocated. “The physician is the person who’s been put there to understand the medical needs of the patient and where their cash should be applied,” Curran said. Therefore, the physicians at GBU decided to maintain their control to provide the best care possible to their patients, as well as run the business as well as possible.

Although many practices are merging or partnering with larger nonurological entities, Curran believes that this trend does not necessarily equate with providing good healthcare. “Rather than turning to hospital networks, insurance networks, or venture capital, [practices] should be turning to their colleagues in the specialties or complementary specialties they’re in to align with people who have the same goals as they do,” he said.

When a new technique or technology is developed, the physicians who own GBU meet and discuss whether it is justified from a medical perspective to add it to their practice. When they agree to adopt it, they bring their case to the chief operations officer, who decides whether making the addition makes sense financially or it would be better to partner with a facility that has the technique or technology already. For example, they have relationships with all of the major radiation centers in the area and are able to provide external beam radiotherapy for their patients with prostate cancer.

According to Curran, technology adoption can be done in a matter of hours or days instead of the weeks or months it would take for larger organizations, allowing GBU to consistently offer the latest and best care possible. This makes the practice stand out in the Boston metropolitan area, which has some of the largest and most distinguished medical centers in the country.

Another reason for offering the latest treatments is that patients tend to be well informed about them, mostly due to having the ability to research their disease online. They even ask for these treatments when they come into the office. “We view that as a really good thing. The more knowledge a patient has, the better that patient is going to be for themselves,” Curran said.

Treatment sites. Commercial treatments and clinical trials. Focused Ultrasound Foundation website. fusfoundation.org/the-technology/treatment-sites/treatmentsites/ list. Accessed May 11, 2018.

Greater Boston Urology strives to offer comprehensive urologic care that includes up-and-coming diagnostics and treatments, such as the Prostate Health Index blood test and high intensity–focused ultrasound. 

June 2018 | Oncology Live Urologists in Cancer Care®

DNA Repair Defects Are Strong Targets for Therapeutic Development in Prostate Cancer

Moving Radium-223 Forward in the Treatment Timeline for Prostate Cancer With Bone Metastases

A Call for Clinical Research

Urology Practice Keeps Up With Technology Through Physician-Owned Business Model