Integrating PARP Inhibitors Into Advanced Prostate Cancer Therapeutics

OncologyONCOLOGY Vol 35 Issue 3
Pages: 119-125

Experts in the field review integration of approved PARP inhibitors into advanced prostate cancer clinical practice.


DNA–damage repair (DDR) pathway mutations can sensitize cancer cells to a class of cancer therapeutics known as PARP inhibitors. Given that DDR alterations can be found in up to one-third of advanced prostate cancers, PARP inhibitors have recently been established in treatment-refractory settings. We provide an updated review of the clinical data supporting the 4 PARP inhibitors that have undergone the most investigation thus far in metastatic castrate-resistant prostate cancer (mCRPC). Two of these agents are currently approved for the treatment of DDR-altered mCRPC. We end with a discussion on integration of approved PARP inhibitors into advanced prostate cancer clinical practice.

KEYWORDS: Prostate cancer, androgen inhibition, poly(ADP) ribose polymerase, PARP inhibitors, DNA damage repair, BRCA, homologous recombination

Oncology (Williston Park). 2021;35(3):119-125.
DOI: 10.46883/ONC.2021.3503.0119


Prostate cancer represents the most commonly diagnosed cancer and secondleading cause of cancer death in US men, with a projected 191,930 new cases and 33,330 deaths in 2020.1 The natural history of prostate cancer can vary; it ranges from more indolent, low-risk disease, in which patients are more likely to die from competing comorbidities, to metastatic- lethal disease or metastatic castrate-resistant prostate cancer (mCRPC), which is characterized by the eventual development of resistance to therapies against the androgen signaling axis.2

Although androgen deprivation therapy (ADT) has been a foundation of prostate cancer treatment for decades, there have been multiple recent advances in the systemic treatment of advanced prostate cancer. For example, the CHAARTED and STAMPEDE trials provided the basis for the addition of docetaxel to ADT in the first-line treatment of metastatic castration-sensitive prostate cancer (mCSPC).3,4 The addition of the novel hormonal therapy (NHT) abiraterone (Zytiga) to ADT conferred an overall survival (OS) advantage vs ADT alone in patients with untreated, locally advanced disease or mCSPC.5,6 The phase 3 ARCHES and ENZAMET trials demonstrated the superiority of the addition of enzalutamide (Xtandi) to ADT over ADT alone in mCSPC,7,8 while the phase 3 TITAN trial supported the combination of first-line apalutamide (Erleada) and ADT in mCSPC.9

Despite the advances in mCSPC that have occurred in the past 5 years, development of castrate-resistant disease often represents the final common pathway and lethal stage of advanced prostate cancer. Currently, multiple systemic agents are available in the armamentarium for mCRPC, including chemotherapy10,11; NHTs, including enzalutamide and abiraterone, both before12,13 and after chemotherapy14,15; radium-22316; and sipuleucel-T.17 However, only in the past year have targeted therapies against a specific molecular phenotype in mCRPC been established, heralding the first biomarker- driven oral therapy for prostate cancer in the era of precision medicine.

The purpose of this review is to describe the class of PARP inhibitors introduced in prostate cancer and the DNA–damage repair (DDR) pathway mutations that sensitize prostate cancer cells to these agents. We highlight pivotal clinical trials that have resulted in US FDA approvals of PARP inhibitors in mCRPC. We end with a discussion of clinical integration of PARP inhibitors for this promising class of therapeutic agents in prostate cancer.

DNA Damage Repair Mutations and Prostate Cancer

Mechanisms of DNA damage Repair and Repair Pathways

Eukaryotic cells have evolved at least 5 major DNA repair pathways for recognizing and repairing endogenous and exogenous sources of DNA damage for the purpose of maintaining genomic integrity.18,19 For example, alkylating agents, ionizing radiation, and reactive oxygen species can cause single-strand DNA breaks (SSBs) or single-base damage that is repaired by the base excision repair (BER) pathway, while ultraviolet radiation and chemical mutagens can cause DNA crosslinks and bulky base damages that are repaired by the nucleotide excision repair (NER) pathway. Important enzymes for both BER and NER pathways include the DNA polymerases. Base mismatches formed due to replication errors during DNA replication and recombination are repaired by the mismatch repair (MMR) pathway mediated by key MMR proteins such as MLH1, MSH2, MSH6, and PMS2. Lastly, DNA double-strand breaks (DSBs) caused by ionizing radiation or collapsed replication forks, for example, are repaired by the DSB repair pathway through either homologous recombination repair (HRR) for nonhomologous end joining, the latter of which includes mediators such as Ku70, Ku80, DNA-PKcs, XRCC4, LIG4, XLF, and APLF.

DDR Alterations in Prostate Cancer

Mutations in DDR pathways have been shown to contribute to prostate cancer carcinogenesis and progression19; both somatic and germline variants, many of which are involved with the HRR pathway, have been increasingly characterized (Table 1). In the initial dataset compiled by The Cancer Genome Atlas, which includes 333 patients with localized, primary prostate cancer cases who underwent radical prostatectomies, comprehensive molecular profiling identified inactivation of multiple DNA repair genes that collectively affected 19% of patients, including BRCA2, BRCA1, CDK12, ATM, FANCD2, and RAD51C.20 In larger pooled series, the prevalence of somatic and germline DDR gene mutations ranged from 10.0% to 16.4% and 11.4% to 11.8%, respectively, in metastatic prostate cancer.21 In mCRPC, somatic mutations in BRCA1 have been shown to be more common than germline BRCA1 mutations (2.8% vs 0.8%) and somatic BRCA1 mutations in an unselected prostate cancer population (2.8% vs 1.1%), whereas somatic and germline mutations were equally common for BRCA2 (5% each) in this population. Rates of somatic mutations in mCRPC and unselected prostate cancer populations have also been similar (5.0% vs 4.9%). Germline DDR gene mutations, in general, have been shown to be more prevalent in patients with metastatic prostate cancer than those in the general prostate cancer population.21 This is also consistent with results of a multicenter study that demonstrated an incidence of germline DDR gene mutations of 11.8% among men with metastatic prostate cancer, much higher than the incidence among men with localized prostate cancer.22

TABLE 1. Commonly Altered DNA–Damage Repair Genes in Prostate Cancer

TABLE 1. Commonly Altered DNA–Damage Repair Genes in Prostate Cancer

In a cohort of 150 patients with mCRPC, whole exome and transcriptome sequencing of bone or soft tissue tumor biopsies showed higher frequencies (19.3%) of aberrations in BRCA2, BRCA1, and ATM than in primary prostate cancers.23 Notably, 12.7% of cases had loss of BRCA2 (most commonly a result of somatic point mutations and loss of heterozygosity).

PARP and Synthetic Lethality in Prostate Cancer

DNA SSBs are repaired by PARP enzymes.18 PARP inhibitors block the catalytic activity of PARP enzymes by trapping PARP on DNA at sites of SSBs, which results in the inability to repair DNA SSBs and ultimately the progression to DSBs.19,24 In cells that are deficient in HRR capacity and therefore unable to repair DSBs, the addition of PARP inhibition would become synthetically lethal ie, a phenomenon in which the combination of deficiencies results in cell death, whereas a deficiency in only 1 gene does not lead to cell death.19,24

One of the earliest prostate cancer–specific studies that demonstrated the feasibility of PARP inhibition as an anticancer therapy in mCRPC was the phase 2 TOPARP-A trial.25 In this phase 2 investigator-initiated trial, 50 patients with unselected mCRPC who had progressed after 1 or 2 lines of chemotherapy were enrolled to receive the oral PARP inhibitor olaparib at 400 mg twice daily. The primary end point was response rate, defined as a radiographic response according to RECIST, reduction in prostate-specific antigen (PSA) level 50% or greater; and/or reduction in number of circulating tumor cells from baseline. Prospectively planned whole-exome sequencing and transcriptome studies were performed on DNA from fresh-frozen tumor biopsies before treatment. The response rate was 33% of 49 evaluable patients (95% CI, 20%-48%). Sixteen patients (33%) had tumor aberrations in DDR genes, of whom 14 (88%) had response to olaparib, including 7 patients with BRCA2 and 4 with ATM aberrations (from a total of 5 patients). In these patients receiving olaparib (Lynparza), overall survival (OS) and progression-free survival (PFS) were significantly longer in those with DDR gene mutations than in those who were biomarker negative.

The promising results of TOPARP-A led to the initiation of the open-label, randomized phase 2 trial (TOPARP-B). Included patients have mCRPC that has been previously treated with 1 to 2 taxane regimens; they were selected for tumor DDR mutations by next-generation sequencing (NGS) and were randomized to receive olaparib 300 mg or 400 mg twice daily.26 Of 592 patients with evaluable tumor samples, 161 (27%) had DDR gene aberrations, with BRCA2 (7%), ATM (7%), and CDK12 (6%) being the most common. As in TOPARP-A, a confirmed composite response end point was used as the primary end point, and the majority of patients had received either abiraterone or enzalutamide or both in addition to prior chemotherapy. Of 92 evaluable patients (46 in each olaparib-dosing cohort), response was seen in 25 patients (54.3%; 95% CI, 39.0%-69.1%) in the 400-mg cohort and 18 patients (39.1%; 95% CI, 25.1%-54.6%) in the 300-mg cohort (P = .14). The BRCA1/2 subgroup had the highest number of composite responses and the longest median radiographic PFS of all DDR gene aberration subgroups. The 400-mg twice daily dose was associated with greater toxicity; in this cohort, 37% of patients had to reduce their dose to 300 mg twice daily, most commonly due to anemia.

PARP inhibitors have now seen advancement from early-phase studies to phase 3 registrational trials in prostate cancer, resulting in their FDA approval and the establishment of this class of agents in the treatment paradigm for mCRPC. The clinical development of PARP inhibitors in prostate cancer has been extensively reviewed elsewhere.24,27 We will focus on an overview of the 4 PARP inhibitors that have undergone the most investigation thus far in mCRPC, with a discussion on integration of approved PARP inhibitors into clinical practice (Table 2).

TABLE 2. Pivotal Clinic Trials of PARP Inhibitors in mCRPC

TABLE 2. Pivotal Clinic Trials of PARP Inhibitors in mCRPC

Pivotal Clinical Trials of PARP Inhibitors in mCRPC


Olaparib became FDA approved on May 19, 2020, for the treatment of mCRPC following progression on enzalutamide or abiraterone, based on the results of the prospective, open-label, randomized, phase 3 PROFOUND trial.28 At 206 sites in 20 countries, 4425 patients were screened for alterations in 15 prespecified genes, and 778 of 2792 (28%) had qualifying DDR mutations based on NGS from primary or metastatic tumor tissues. Patients with 1 or more alterations in BRCA1, BRCA2, or ATM were assigned to cohort A while those with alterations in the other 12 genes were assigned to cohort B. Patients were randomized 2:1 to receive standard-dose olaparib (300 mg twice daily) or the prespecified physician’s choice of enzalutamide (160 mg once daily) or abiraterone (1000 mg once daily and prednisone at a dose of 5 mg twice daily). The primary end point was PFS, with secondary end points of overall response rate (ORR) and OS. A total of 162 and 83 patients were randomized to receive olaparib and control treatment, respectively, in cohort A, while 94 and 48 patients received olaparib and control treatment, respectively, in cohort B.

For cohort A, the median PFS was significantly longer in the olaparib group (7.4 months) than in the control group (3.6 months; HR, 0.34; 95% CI, 0.25-0.47; P <.001). Among evaluable patients, the ORR was 33% (28 of 84 patients) in the olaparib group and 2% (1 of 43 patients) in the control group (odds ratio, 20.86; 95% CI, 4.18-379.18; P <.001). For the overall population (cohort A and B), olaparib resulted in longer median PFS than control treatment did (5.8 months vs 3.5 months; HR, 0.49; 95% CI, 0.38-0.63; P <.001). In the final OS analysis (secondary end point) of PROFOUND,29 median OS was 19.1 months with olaparib and 14.7 months with control therapy (HR, 0.69; 95% CI, 0.50-0.97; P = .02) in cohort A. In cohort B, median OS was 14.1 months with olaparib and 11.5 months with control therapy (HR, 0.96; 95% CI, 0.63-1.49).


The oral agent rucaparib (Rubraca), a PARP1/2/3 inhibitor, was FDA approved (accelerated approval) based on the TRITON2 study on May 15, 2020, for patients with BRCA-mutated mCRPC who have been previously treated with androgen receptor (AR)–directed therapy and a taxane-based chemotherapy.30,31 TRITON2 is an ongoing, international, open-label, single-arm, phase 2 study in which patients with pretreated mCRPC were screened by plasma or tumor NGS for a panel of 15 deleterious somatic or germline DDR alterations (Table 2). Patients who had progressed on 1 or 2 prior lines of NHT (ie, abiraterone or enzalutamide) and 1 prior line of taxane-based chemotherapy received rucaparib at 600 mg twice daily. In the BRCA-mutated cohort (n = 115), confirmed ORR was 43.5% with a PSA response rate of 54.8%, while OS has not yet matured; the 12-month OS rate was 73.0%. The median radiographic PFS was 9.0 months (95% CI, 8.3-13.5 months). Notably, response rates were similar for those with germline or somatic BRCA mutations and for BRCA1 or BRCA2 alterations.30 In the non–BRCA-mutated cohort (n = 78), rucaparib had limited activity in those with ATM, CDK12, or CHEK2 mutations, with no radiographic or PSA responses in 11 patients with confirmed biallelic ATM loss or in 11 patients with germline ATM mutations.31

A multicenter, randomized, open-label, phase 3 study (TRITON3) is ongoing and randomizing patients with mCRPC who have BRCA1/2 or ATM gene mutations and have progressed on 1 prior NHT for mCRPC to rucaparib monotherapy or investigator’s choice of abiraterone, enzalutamide, or docetaxel (NCT02975934). The primary end point will be radiographic PFS.


Talazoparib (Talzenna) is a potent PARP1/2 inhibitor that was investigated in mCRPC in the open-label, single-arm, phase 2 TALAPRO-1 study.32 Eligible patients included those with mCRPC refractory to 1 or more lines of taxane-based chemotherapy and 1 or more lines of NHT (ie, enzalutamide or abiraterone) with known/likely pathogenic variants or homozygous deletions in DDR mutations based on tumor-derived NGS. Interim results show an ORR of 28.0% in 75 patients with DDR mutations treated with oral talazoparib 1 mg daily (primary end point). The most common treatment-related adverse events (AEs) were anemia (42.5%) and nausea (32.7%). A phase 3, randomized, double-blind, placebo-controlled study (TALAPRO-2) is currently randomizing patients with mCRPC who have not received prior taxanes or NHT in the mCRPC setting to talazoparib and enzalutamide vs placebo and enzalutamide, with radiographic PFS as a primary end point in unselected patients and in those with DDR deficiencies (NCT03395197).


Niraparib (Zejula) is another oral PARP1/2 inhibitor that has seen active investigation in mCRPC. The phase 2, open-label, single-arm GALAHAD study enrolled patients who had mCRPC refractory to taxane and to AR-targeted therapy as well as biallelic alterations in select DDR genes, as ascertained by plasma or tissue-based profiling; they received niraparib 300 mg daily.33 The most common grade 3/4 treatment-emergent AEs were mainly hematologic: anemia (29%), thrombocytopenia (15%), and neutropenia (7%). The ORR was 41% in those with BRCA mutations; the median radiographic PFS and OS were 8.2 and 12.6 months, respectively. The ORR in the non–BRCA-mutated cohort was 9%; response was observed in only 2 patients, both with FANCA mutations. The phase 3, randomized, placebo-controlled, double-blind MAGNITUDE study is currently randomizing mCRPC patients who have not received systemic therapy in the mCRPC setting (except for <4 months of abiraterone prior to randomization) to niraparib and abiraterone vs placebo and abiraterone (NCT03748641). Patients will be stratified into DDR gene–mutated and non– DDR gene–mutated cohorts, and the primary end point will be radiographic PFS.

Incorporating PARP Inhibitors Into Clinical

Practice for mCRPC PARP inhibitors have already been approved for multiple malignancies, including ovarian cancer, breast cancer, and pancreatic cancer.34,35 The recent approvals of olaparib and rucaparib offer promising efficacy in patients with treatment-refractory mCRPC, in whom therapeutic options have been limited. As this class of agents continues to undergo rapid clinical development and clinical implementation, several factors must be considered when incorporating PARP inhibitors into routine prostate cancer management.

Choosing the Right Patient

Aside from microsatellite instability, which is found in less than 3% of all prostate tumors, DDR mutations represent a predictive biomarker that can currently guide targeted therapies in patients with advanced prostate cancer.36 In the phase 3 PROFOUND trial, DDR alterations from a predefined 15-gene panel were found in 778 of 2792 (28%) patients.28 However, as exploratory analyses of PROFOUND and TRITON2 have shown, not all DDR mutations are equal in eliciting response to PARP inhibitors in mCRPC. Exploratory gene-level analyses in PROFOUND showed that in the intention-to-treat population, HRs for death for the comparison of olaparib versus the control were 0.42 and 0.59 for patients who had alterations only in BRCA1 and BRCA2, respectively, while the HR for those with non-BRCA genes was 0.95 (95% CI, 0.68- 1.34).29 There was an improved median OS of 17.4 months with olaparib vs 12.6 months with control (HR, 0.64; 95% CI, 0.39-1.08) after prior taxane therapy in patients with only BRCA1 or BRCA2 alterations. A more pronounced effect of previous taxane use was seen in those with only ATM mutations, however; for them, median OS was improved with olaparib (17.6 months) compared with control (12.4 months; HR, 0.45; 95% CI, 0.22-0.95). It should be noted that these subgroup analyses were not powered to detect a treatment effect across these subgroups, so these results should be interpreted with caution.

A similar theme was observed in the TRITON2 study, as no radiographic or PSA responses were seen in 11 patients with confirmed biallelic ATM loss or 11 patients with ATM germline mutations.31 Instead, the bulk of responses to rucaparib was observed in patients with BRCA1 or BRCA2 mutations, while in patients with mCRPC having non-BRCA DDR mutations, responses were seen only in those with PALB2, FANCA, BRIP1, and RAD51B mutations.30,31 Higher PSA responses have also been seen in those with BRCA2 vs BRCA1 mutations and biallelic vs monoallelic loss, but the number of patients with BRCA1 mutations and monoallelic loss was small.30 One can argue, based on the constellation of these findings, that the approved indications for olaparib and rucaparib should be limited to those with mCRPC harboring BRCA1 or BRCA2 mutations, with perhaps the potential to benefit those with select non-ATM DDR gene mutations. Of note, the rucaparib label is restricted to those with deleterious BRCA mutations only (germline and/or somatic) while the olaparib label applies to the DDR genes prespecified in PROFOUND (Table 2).37,38 In both PROFOUND and TRITON2, deleterious DDR alterations were identified with tumor-based NGS of archival or recent biopsy tissues (Foundation Medicine) from primary or metastatic disease, while TRITON2 permitted plasma-based NGS as well.28,30 The FDA also approved the FoundationOne CDx (Foundation Medicine, Inc) assay for selection of patients with mCRPC carrying DDR gene alterations and the BRACAnalysis CDx test (Myriad Genetic Laboratories, Inc) for BRCA1/2 alterations as companion diagnostics for olaparib treatment.

Choosing the Right PARP Inhibitor

Unlike olaparib and rucaparib, talazoparib and niraparib, although under active investigation, have not been FDA approved for mCRPC. Of the 2 PARP inhibitors approved for mCRPC harboring select DDR mutations, olaparib is approved for those with mCRPC who have progressed on the NHTs enzalutamide or abiraterone,28 while rucaparib is approved in patients with mCRPC who have been treated with an NHT and a taxane-based chemotherapy.30 Therefore, olaparib offers earlier access to a PARP inhibitor along the mCRPC treatment continuum (ie, if taxanes have not been used), but it has still shown benefit, on subgroup analysis, in those previously treated with taxanes—45% of patients treated with olaparib in PROFOUND had received prior docetaxel.28 In TRITON2, 36.5% of patients treated with rucaparib had previously received ≥2 AR-directed therapies; 93.9% had received prior docetaxel in the castrate-resistant setting; 10.4% had received sipuleucel-T; and 12.2% had received radium-223, therefore showing efficacy in a heavily pretreated population.30

Ultimately, olaparib was granted regular FDA approval, based on its higher level of evidence (phase 3 PROFOUND trial), while rucaparib was granted accelerated FDA approval—meaning that clinical trial data (TRITON2) strongly suggest benefit, but level of proof is not yet available. One could also argue that rucaparib is approved in mCRPC patients with BRCA mutations only, while olaparib is approved for a more expanded DDR gene panel beyond BRCA mutations; as discussed earlier, however, the majority of responses to PARP inhibitors in this setting have been observed in those with BRCA1/2 only.37,38 When separating these groups, only 12% of mCRPC cases have defects in BRCA1 or BRCA2 and only 8% to 18% have defects in non-BRCA DDR genes.25,28,30 A head-to-head comparison of the efficacy of PARP inhibitors in prostate cancer does not exist. The choice of PARP inhibitor in routine clinical practice therefore depends on not only the DDR alterations detected but also the treatment setting of the patient with mCRPC; the receipt of specific prior lines of systemic therapy as per FDA labeled indications must be taken into account. With the development of other PARP inhibitors in this arena, debate will continue regarding the ideal agent to use in prostate cancer. Such decisions would need to incorporate level of evidence, safety and tolerability, quality-of-life metrics, cost effectiveness, and discussions of provider and patient preferences that should underlie the physician-patient relationship.


In the updated survival analysis of the phase 3 PROFOUND trial, the median duration of olaparib therapy was 7.6 months vs 3.9 months with control.29 Of 256 patients randomized to the olaparib group, 46% of patients had interruptions of olaparib due to AEs (vs 19% in control), 23% required dose reductions due to AEs (vs 5% in control), and 20% discontinued treatment due to AEs (vs 8% in control). Grade ≥3 AEs were seen in 52% of patients, with anemia (23%) and fatigue (3%) the most common. Median duration of rucaparib therapy was 6.5 months in TRITON2, with treatment interruptions due to AEs occurring in 56.5% (most commonly due to anemia, thrombocytopenia, or fatigue), dose reductions occurring in 40.9%, and treatment discontinuations occurring in 7.8%.30 Grade ≥3 AEs due to rucaparib occurred in 60.9% of patients, with the most common being anemia (25.2%), thrombocytopenia (9.6%), and fatigue (8.7%). Although no new cancers, pneumonitis, myelodysplastic syndrome, or acute myeloid leukemia were observed in the 30-day safety follow-up with olaparib in PROFOUND, 1 case of fatal acute myeloid leukemia occurred in a patient with mCRPC who had germline BRCA2 deficiency diagnosed 54 days after the discontinuation of olaparib (15.7 months duration of olaparib exposure).29

In short, anemia and fatigue are the most common and significant AEs, or class effect, of PARP inhibitors in patients with mCRPC. Toxicity profiles appear to be similar between the 2 FDA-approved PARP inhibitors, with nearly half of men treated with these drugs requiring either treatment interruptions or dose reductions. Of note in PROFOUND, men without surgical castration were required to continue luteinizing hormone–releasing hormone analogue therapy with olaparib; while in TRITON2, men were required to receive a concomitant gonadotropin-releasing hormone analogue, or to have had prior bilateral orchiectomy facilitated by rucaparib. Therefore, PARP inhibitor therapy should not be considered a way to spare patients from undergoing hormonal therapy.29,30


PARP inhibitors have demonstrated promising efficacy and manageable toxicities in pretreated patients with mCRPC: a high-risk group in desperate need of additional treatment options. With continued development of this class of agents in advanced prostate cancer, more work should be focused on the subgroup of patients with non–BRCA DDR mutations who could bene t from PARP inhibition. Also, ongoing trials seek to establish PARP inhibitors in earlier treatment settings (eg, rst-line metastatic prostate cancer and nonmetastatic prostate cancer). Lastly, with greater clinical implementation of and familiarity with PARP inhibitors in prostate cancer, development of rational combination strategies with this drug class would be warranted to further exploit its anticancer potential.

ACKNOWLEDGMENT: This work was supported by grants from the Department of Defense (W81XWH-19-1-0388 to NAB and W81XWH-19-1-0406 to JG), the National Cancer Institute (CA233452 to NAB), and US Department of Veterans Affairs (BX001040 to NAB).

FINANCIAL DISCLOSURE: JG—consultant to Amgen, Astellas, Elsevier, Exelixis, QED Therapeutics. EP—consultant to Bayer, Genentech/Roche, research funding Pfi zer. TD—consultant to Janssen, contracted research Merck. HS—stock and other ownership interests Radiogel, consultant to Janssen, other relationship to Caribou Publishing. MK—consultant to Augmenix, Varian Medical Systems. ZZ— contracted research Janssen. SJF—consultant to Janssen, Sanofi , Pfi zer, Astellas, Bayer, Dendreon, Merk, AstraZeneca. RF—consultant to Accelera, Bristol Myers Squibb, CBT Pharmaceuticals, Johnson & Johnson, Precision Health Economics. NB, HK, AG—nothing to disclose.

Gong is a is a medical oncologist of the Gastrointestinal Disease Research Group, Pancreatic Cancer Research Group, and Urologic Oncology Program in the Samuel Oschin Comprehensive Cancer Institute at Cedars-Sinai.

Posadas is director of the Translational Oncology Program and the medical director of the Urologic Oncology Program at the Samuel Oschin Comprehensive Cancer Institute at Cedars-Sinai Medical Center.

Bhowmick is director of the Cancer Biology Program and a professor biomedical sciences and medicine at the Samuel Oschin Comprehensive Cancer Instituteat Cedars-Sinai Medical Center.

Kim is director of the Cedars-Sinai Academic Urology Program and associate director of Surgical Research in the Samuel Oschin Comprehensive Cancer Center.

Daskivich is a urologic oncologist in the Cedars-Sinai Urology Academic Program and the director of Health Services Research for the Cedars-Sinai Department of Surgery.

Guptais an expert in robotic surgery and urologic oncology and is the chairman of the Robotic Surgery Steering Committee at Cedars-Sinai.

Sandler is a radiation oncologist at the Samuel Oschin Comprehensive Cancer Instituteat Cedars-Sinai Medical Center.

Kamrava is an associate professor of radiation oncology and director of Brachytherapy Services at the Samuel Oschin Comprehensive Cancer Institute at Cedars-Sinai Medical Center.

Zumsteg is an assistant professor in the Department of Radiation Oncology at Cedars-Sinai Samuel Oschin Comprehensive Cancer Institute.

Freedland is director of the Center for Integrated Research in Cancer and Lifestyle, co-director of the Cancer Genetics and Prevention Program, and associate director for Faculty Development at the Samuel Oschin Comprehensive Cancer Institute.

Figlin is the associate director of the Academic Development Program and director of the Division of Hematology/ Oncology at Cedars-Sinai Oschin Comprehensive Cancer Institute.


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