Caroline Seymour

Combination treatment with the IL15RaFc superagonist N-803 (Anktiva) and BCG was associated with prolonged complete responses (CRs) and disease-free survival (DFS) in patients with BCG-unresponsive non–muscle invasive bladder cancer with carcinoma in situ (CIS) and papillary histology, according to a recent study.

The findings, from the phase 2/3 QUILT-3.032 trial (NCT03022825), were presented at the 2022 AUA Annual Meeting.

At a median follow-up of 23.9 months in patients with CIS, the CR rate was 71% (95% CI, 60.1%-80.5%). The 12- and 24-month CR rates were 60% (95% CI, 45%-72%) and 52% (95% CI, 40%-65%), respectively.

At a median follow-up of 20.7 months in patients with papillary disease (n = 77), the median DFS was 23.6 months. The 12-, 18-, and 24-month DFS rates were 57% (95% CI, 44%-68%), 53%, and 48% (95% CI, 34%-60%), respectively.

“In animal models the combination of BCG plus IL15 further augments that T- and NK-cell response and results in memory T cells, and for that we designed phase 2/3 QUILT-3.032 study,” lead study author Karim Chamie, MD, MSHS, associate professor of urology at UCLA, said during the presentation.

QUILT-3.032 enrolled patients with historically confirmed BCG-unresponsive disease with persistent or recurrent CIS, with or without recurrent Ta/T1 disease, within 12 months of receiving sufficient BCG.

The population was divided into 2 cohorts: those with CIS (n = 83; cohort A) and those with papillary histology (n = 77; cohort B).

In the study, patients received 50 mg of intravesical BCG plus 400 µg of N-803 every week for 6 cycles followed by 6 cycles of maintenance therapy in patients who achieved CR for up to 2 years with the option to extend therapy. Patients who did not achieve CR but experienced response were allowed to receive another 6 cycles of re-induction with the combination.

The primary end point was CR at any time; secondary end points included duration of CR, cystectomy avoidance, and time to cystectomy. Safety end points included serious adverse effects (AEs) and immune AEs.

Regarding baseline demographics, the median age was 72.8 years in cohort A and 71.7 years in cohort B. Most patients were male and above the age of 65 years in cohorts A (87% and 84%) and B (74% and 74%), respectively. Most patients in cohorts A and B had an ECOG performance status of 0 (82% and 77%), followed by 1 (18% and 17%), and 2 (0% and 6%), respectively. The mean number of prior transurethral resections of the bladder tumor was 4 in both cohorts.

In terms of disease type, most patients in cohort A had CIS (70%), followed by CIS/Ta (19%), CIS/T1 (11%), high-grade Ta (0%), T1 (0%), and Ta/T1 (0%) disease. In cohort B, most patients had T1 (44%), followed by high-grade Ta (43%), CIS/T1 (5%), Ta/T1 (4%), and CIS/Ta (1%), and CIS (1%) disease.

The mean number of prior BCG doses was 16.6 in cohort A and 12.3 in cohort B.

Additional efficacy findings from cohort A demonstrated that the median duration of response (DOR) was 24.1 months (95% CI, 9.9–not reached). The percentage of patients whose DOR was at least 12, 18, and 24 months was 62% (95% CI, 48.0%-73.5%), 55% (95% CI, 40.1%-67.3%), and 52% (95% CI, 37.0%-64.9%), respectively.

In cohort A, the cystectomy rate was 7% in responders and 15% overall.

The 12-, 18-, and 24-month rates of bladder cancer–specific progression-free survival were 92% (95% CI, 83.4%-96.4%), 91% (95% CI, 81.2%-95.4%), and 91% (95% CI, 81.2%-95.4%, respectively. The bladder cancer–specific overall survival rate was 100%.

Regarding the efficacy in cohort B, 95% of patients (n = 73) avoided radical cystectomy, meeting the secondary end point for the cohort.

Notably, the efficacy of the combination was retained across all subgroups in both cohorts.

Regarding safety, the combination was well tolerated across both cohorts. Grade 1 and 2 treatment-related AEs (TRAEs) included dysuria (22%), pollakiuria (19%), hematuria (18%), fatigue (16%), micturition urgency (12%), chills (7%), bladder spasm (6%), pyrexia (5%), urinary tract infection (5%), noninfective cystitis (4%), nocturia (3%), diarrhea (3%), nausea (2%), positive bacterial test (2%), cystitis (2%), influenza-like illness (2%), and urinary tract pain (2%).

Grade 3 TRAEs occurring in less than 1% of patients included arthralgia, bacteremia, dysuria, encephalopathy, escherichia bacteremia, hematuria, myalgia, pain in extremity, pollakiuria, sepsis, urinary tract infection, and decreased urine flow.

The rate of serious TRAEs was 1%, there were no immune-related AEs, and only 3% of patients underwent a treatment-related discontinuation.

Notably, the activity of N-803 was localized to the bladder, and there were no systemic IL-15 levels per pharmacokinetic analysis.

Chamie K. IL-15RaFc superagonist N-803 with BCG in BCG-unresponsive non-muscle invasive bladder cancer (NMIBC) CIS and papillary cohorts. Presented at: 2022 AUA Annual Meeting; May 13-16, 2022. New Orleans, LA. PLLBA-01.

Articles

At a median follow-up of 20.7 months in patients with papillary disease (n = 77), the median DFS was 23.6 months.

N-803 plus BCG yields prolonged complete responses and DFS in NMIBC

 Interdisciplinary Prostate Cancer Congress® and Other Genitourinary Malignancies, Leonard G. Gomella, MD, explained how the ever-expanding application of genetic and genomic testing has launched the game-changing precision medicine era in prostate cancer. 

“Precision medicine is here for prostate cancer. It’s not a fantasy anymore. We’re using it every day more and more,” said Gomella.

Genomic or genetic germline testing is done to inform treatment decisions and screening in an individual and their family members for other at-risk cancers, Gomella said. Almost all the genes that are associated with inherited prostate cancer are found in the DNA damage response and repair pathway and include 

, the latter of which increases individual and familial risk for other hereditary cancers, including breast, ovarian, pancreatic, colon, gastric, and Lynch syndrome.

“The DNA damage response genes increase the risk of developing prostate cancer and, more importantly, aggressive, life-threatening, metastatic prostate cancer,” Gomella said, adding the disease is typically defined by a Gleason score of 8 or higher, positive nodes, metastases, and poor survival.

 gene mutation have a 2.6-fold increased risk of developing aggressive prostate cancer during their lifetime, and that risk is increased 8.6-fold by the age of 65 years.

“If you identify someone who has an inherited germline mutation, you really need to pay attention to that patient,” Gomella said, adding that germline mutations are found in more than 11% of prostate cancer cases and up to 25% of metastatic castration-resistant cancers.

, although uncommon, is an androgen receptor gene mutation that is the most significant inherited gene for prostate cancer and one that is almost always found in aggressive cancers in family members diagnosed before the age of 55 years.

Prostate cancer–specific genetic testing panels on the market include ProstateNext by Ambry Genetics, the Prostate Cancer Panel by GeneDx and Invitae, and the Hereditary DNA Repair Panel for Prostate Cancer by NeoGenomics. General cancer panels that also screen for relevant gene mutations include Myriad’s myRisk and Color Genomics/Genome Dx’s Hereditary Cancer Panel.

The use of such panels is first informed by a patient’s family history, said Gomella, who emphasized to urologists that asking about an individual’s history of inherited prostate cancer should be augmented by any history of breast and ovarian cancer, melanoma, and Lynch syndrome.

After such information has been gathered, a genetic counselor can be brought in to discuss testing options, result types, cancer risks, insurance complications, and reproductive implications.

Current guidelines recommend genetic testing/counseling in the event of:

At least 2 cases of prostate cancer in close relatives 55 years of age or younger regardless of risk category

At least 3 first-degree relatives with prostate cancer regardless of risk

Aggressive prostate cancer with a Gleason score above 7

At least 2 cases of breast, ovarian, and/or pancreatic cancer in a close relative

Metastatic prostate cancer or metastatic castration-resistant prostate cancer (mCRPC)

Somatic tumor sequencing with mutations in hereditary cancer genes

Family history of cancer at an early age of diagnosis

“Looking for genetic risk has become baked into our management of prostate cancer today,” Gomella said. “Germline and somatic testing are complementary. One does not replace the other. They should both be considered in the management of many patients with prostate cancer.”

When it comes to determining whether to biopsy patients for prostate cancer, several things can be used, including prostate-specific antigen (PSA) kinetics, the Prostate Health Index score, OPKO 4K, Prostarix, Select MDx, ExoDx, MyProstate Score, PCA3, as well as MRI and ultrasound, the Prompt Prostate Genetic Score, germline testing, and online calculators.

In terms of whether to perform a repeat biopsy, Gomella cited the ConfirmMDx, Prostate Score Mitomic Test, MyProstate Score, OPKO 4K, and PCA3 as helpful options.

“Whatever test you’re comfortable with is the most important,” Gomella said. “[At Jefferson Health,] we rotate different tests to give our residents exposure to the different potential assays that are available.”

Following biopsy, several tissue tests can be used to determine disease aggressiveness, including ConfirmMDx, Decipher, Prolaris, and the Oncotype DX genomic prostate score test.

“[These tests] are used after the biopsy. This is taking the biopsy of someone with known prostate cancer and deciding whether this a cancer, based on the characteristics beyond Gleason score, PSA, and digital rectal exam, that can be watched or [one] that requires further testing,” Gomella said.

Turning to treatment implications, Gomella explained that in the setting of heavily pretreated metastatic castration-resistant prostate cancer, in the presence of a germline or somatic 

mutation or homologous recombination repair gene mutation, patients may be eligible to receive rucaparib (Rubraca) or olaparib (Lynparza),

 respectively, and in the presence of high microsatellite instability/mismatch repair deficiency or tumor mutational burden greater than 10 mut/Mb, pembrolizumab (Keytruda).

“Many of the new treatments under study today are associated with precision medicine with the identification of a precise marker that can be used to guide treatment,” Gomella concluded.

Gomella L. The evolution of biomarkers and genetics in the management of prostate cancer. Presented at: New York GU 

 Interdisciplinary Prostate Cancer Congress® and Other Genitourinary Malignancies; March 11-12, 2022; virtual. Accessed March 12, 2022.

Rubraca highlights of prescribing information. FDA. Updated December 2016. Accessed March 15, 2022. https://bit.ly/3Ibfx9b

Lynparza highlights of prescribing information. FDA. Updated May 2020. Accessed March 15, 2022. https://bit.ly/2WLJt7u

Keytruda highlights of prescribing information. FDA. Updated March 2021. Accessed March 15, 2022. https://bit.ly/37zl8tu

The applications for germline and somatic genetic testing in prostate cancer have skyrocketed, carving out an important role in screening, diagnosis, and treatment.

Dr. Gomella explains the evolving precision medicine paradigm in prostate cancer

Results from the phase 2 ARIES trial shared during the 2022 ASCO Genitourinary Cancers Symposium showed that frontline avelumab (Bavencio) did not improve overall survival (OS) at 1 year in patients with cisplatin-ineligible, PD-L1–positive advanced urothelial cancer; however, the immunotherapy did induce a notable objective response rate (ORR) and disease control rate (DCR) with a favorable safety profile.1

At a median follow-up of 9 months, the median OS was 10 months (95% CI, 5.7-14.3). The estimated 1-year OS rate was 44.9%, and the 1-year OS rate was 40.8%.

“The ARIES trial confirmed the favorable safety profile of avelumab in advanced urothelial cancer. Although avelumab was unable to improve the 1-year OS rate as expected, patients able to receive at least 1 month of therapy had longer OS,” lead study author Roberto Iacovelli, MD, PhD, a medical oncologist at the Fondazione Policlinico Gemelli IRCCS in Rome, Italy, said in a presentation of the data.

Cisplatin-based chemotherapy is the standard frontline treatment in advanced urothelial cancer. However, approximately half of patients are cisplatin ineligible, and some are entirely platinum ineligible, leading to poor prognosis.

Avelumab is a PD-L1 antibody that has shown improved progression-free survival (PFS) and OS as maintenance therapy in patients with advanced urothelial cancer with responsive or stable disease after frontline platinum-based therapy.

In the ARIES trial (NCT03891238), the efficacy and safety of avelumab was evaluated in patients with cisplatin-ineligible, PD-L1–positive advanced urothelial cancer.

To be eligible for enrollment, patients must have had a histologic diagnosis of advanced urothelial cancer; an ECOG performance status between 0 and 2, and cisplatin-ineligible disease due to at least one of the following: an ECOG performance status of 2; eGFR below 60 mL/min; grade 2 or worse peripheral neuropathy or hearing loss; prior cisplatin for neoadjuvant or adjuvant chemotherapy with disease progression within 6 months.

A total of 198 patients underwent central assessment for PD-L1 expression of at least 5%, and 71 eligible patients received 10 mg/kg of avelumab every 2 weeks.

The primary end point was 1-year OS; secondary end points were median OS, median PFS, ORR, safety, quality of life, and outcome based on PD-L1 expression.

The study was designed such that 67 patients were required to show an improvement in the 1-year OS rate from 40% to 57% with 80% power and a 2-sided type I error equal to .05.

Regarding baseline characteristics, most patients were at least 65 years of age (93%; n = 55), male (77.5%; n = 55), had an ECOG performance status of 1 (47.9%; n = 34), and had a primary tumor location of the bladder (70.4%; n = 50).

A total of 11 patients (15.5%) had hemoglobin less than 10 mg/dL.

The primary location of metastasis was the lymph nodes (66.2%; n = 47), followed by the lung (43.7%; n = 31), liver (25.3%; n = 18), bone (18.3%; n = 13), and lymph nodes only (15.5%; n = 11).

Reasons for cisplatin ineligibility were a result of patients having a creatinine clearance of less than 60 ml/min (70.4%; n = 50), an ECOG performance status of 2 (31%; n = 22), grade 2 or worse peripheral neuropathy or hearing loss (5.8%; n = 4), and prior treatment with cisplatin for adjuvant intent in 6 months (12.7%; n = 9).

Additional results showed that 56 patients had a PD-L1 combined positive score (CPS) of at least 10%, 11 had a CPS below 10%, and 4 were not evaluable.

Notably, the median OS was 13 months (95% CI, 2.4-23.6) in patients with a CPS of at least 10% vs 7 months (95% CI, 2.8-11.2) in patients with a CPS below 10%, showing a numerical but not statistically significant improvement (

 = .09). The 1- and 2-year OS rates were 50.4% and 39% in the CPS of at least 10% group vs 27.3% and 13.6% in the CPS below 10% group, respectively.

The median PFS in the overall population was 2 months (95% CI, 1.4-2.6). When broken down by CPS, the median PFS was no different at 2 months (95% CI, 1.2-2.8) in patients with a CPS of at least 10% vs 2 months (95% CI, 1.1-2.9) in patients with a CPS below 10% (

The confirmed ORR, which was evaluated locally per RECIST version 1.1 criteria, was 22.5% (n = 16), consisting of 1 complete response (1.4%) and 15 partial responses (21.1%). A total of 15 patients (21.1%) had stable disease, reflecting a DCR of 43.6%.

A total of 28 patients (39.4%) had progressive disease and 12 (16.9%) were not evaluable.

A post-hoc analysis was also conducted in patients who received at least 1 month of therapy or 3 treatment infusions. Among 56 evaluable patients, the median OS was 16 months (95% CI, 7.5-24.5), and the estimated 1-year OS rate was 53.9%.

In the overall population, 13 patients (19.4%) remained on treatment at data cutoff.

Regarding safety, any-grade adverse effects (AEs) occurred in 67 patients (94.4%), and grade 3-5 AEs occurred in 30 patients (42.3%).

Fatal AEs were reported in 2 patients (2.8%) and were attributed to sepsis and an unknown cause.

All-grade AEs included fever (29.6%; n = 21), fatigue (28.2%; n = 20), constipation (22.5%; n = 16), anemia (21.1%; n = 15), diarrhea (19.7%; n = 14), back pain (16.9%; n = 12), pruritus (14.1%; n = 10), rash (14.1%; n = 10), hypothyroidism (12.7%; n = 9), edema of the limbs (11.3%; n = 8), abdominal pain (9.9%; n = 7), infusion reactions (9.9%; n = 7), anorexia (8.5%; n = 6), bone pain (8.5%; n = 6), hematuria (8.5%; n = 6), cough (7%; n = 5), dyspnea (7%; n = 5), vomiting (7%; n = 5), nausea (5.6%; n = 4), and sepsis ((5.6%; n = 4).

Grade 3-5 included fever (1.4%; n = 1), fatigue (1.4%; n = 1), anemia (5.6%; n = 4), abdominal pain (1.4%; n = 1), infusion reaction (4.2%; n = 3), anorexia (1.4%; n = 1), bone pain (1.4%; n = 1), dyspnea (1.4%; n = 1), and sepsis (5.6%; n = 4).

“Patients with advanced urothelial cancer who are unfit for cisplatin have a dismal prognosis. Clinical selection is critical to maximize the efficacy of available therapeutic options, including immunotherapy,” Iacovelli concluded.

1. Iacovelli R, Ciccarese C, Brunelli M, et al. First line avelumab in PD-L1+ve metastatic or locally advanced urothelial cancer (aUC) patients unfit for cisplatin (cis): 

. 2022;40(suppl 6):439. doi:10.1200/JCO.2022.40.6_suppl.439

Despite missing the primary end point, avelumab did demonstrate notable clinical activity and a favorable safety profile in the phase 2 ARIES trial.

No OS benefit at 1-year mark with upfront avelumab in cisplatin-ineligible urothelial cancer

Findings from the phase 3 MAGNITUDE trial showed that adding the PARP inhibitor niraparib (Zejula) to the antiandrogen agent abiraterone acetate (Zytiga) significantly extended radiographic progression-free survival (rPFS) in patients with metastatic castration-resistant prostate cancer (mCRPC) and homologous recombination repair (HRR) gene alterations.

Data presented during the 2022 Genitourinary Cancers Symposium showed that compared with placebo plus abiraterone, niraparib plus abiraterone led to a 47% reduction in the risk of progression or death in patients with 

 mutations and a 27% reduction in the risk of progression or death in all patients with HRR gene alterations. The median follow-up time was 18.6 months.

 population, the median rPFS was 16.6 months with niraparib plus abiraterone vs 10.9 months with placebo plus abiraterone (HR, 0.53; 95% CI, 0.36-0.79; 

 = .0014). The investigator-assessed rPFS was 19.3 months with niraparib/abiraterone and 12.4 months with placebo/abiraterone (HR, 0.50; 95% CI, 0.33-0.75; 

Among all patients with HRR gene alterations, the median rPFS was 16.5 months vs 13.7 months, respectively (HR, 0.73; 95% CI, 0.56-0.96; 

 = .0217). Here, the investigator-assessed rPFS was 19.0 months and 13,9 months, respectively (HR, 0.64; 95% CI, 0.49-0.86; nominal 

“The MAGNITUDE study results support niraparib plus abiraterone as a new first-line treatment option for patients with mCRPC and alterations in genes associated with HRR,” lead study author Kim N. Chi, MD, senior research scientist, Vancouver Prostate Centre, chief medical officer and vice president, BC Cancer, medical oncologist, BC Cancer–Vancouver, and professor, Department of Medicine, The University of British Columbia in Vancouver, BC, Canada, said in a presentation of the data.

As many as 30% of patients with mCRPC will harbor alterations in genes associated with HRR. Although these alterations reflect poor prognosis, they have also shown increased sensitivity to PARP inhibitors such as niraparib, Chi explained. Notably, the addition of an antiandrogen agent like abiraterone has been theorized to augment responses in all-comers, serving as the rationale for the randomized, double-blind MAGNITUDE trial, which evaluated the value of adding niraparib to abiraterone in patients with mCRPC with and without HRR gene alterations.

The study enrolled patients with mCRPC who had received no more than 4 months of prior abiraterone and prednisone for mCRPC; had an ECOG performance status of 0 or 1; and had a Brief Pain Inventory-Short Form worst pain score of 3 or less. Eligible patients were screened for HRR alterations in 

Based on prescreening results, patients were allocated into the biomarker-positive cohort or the biomarker-negative cohort, which had a planned enrollment of 400 and 600 patients, respectively.

Patients were randomized 1:1 to receive 200 mg of niraparib once daily plus abiraterone or placebo plus abiraterone in each of the cohorts.

The primary end point was rPFS assessed by blinded independent central review in the 

 population followed by all other biomarker populations. Secondary end points were the time to initiation of cytotoxic chemotherapy, time to symptomatic progression, and overall survival (OS). Other end points included time to prostate-specific antigen (PSA) progression, objective response rate (ORR), time to second disease progression (PFS2), time to pain progression, and patient-reported outcomes.

Patients were stratified by whether they had received prior taxane-based chemotherapy for metastatic castration-sensitive disease; prior androgen receptor inhibition for nonmetastatic castration-resistant disease or metastatic castration-sensitive disease; prior abiraterone plus prednisone for frontline mCRPC treatment; and 

The statistical analysis included a prespecified futility analysis in the biomarker-negative population after approximately 200 patients were enrolled and approximately 125 compositive events of either radiographic or PSA progression or death had occurred.

Findings from the preplanned futility analysis in 233 biomarker-negative patients failed to show the benefit of adding niraparib to abiraterone in the prespecified composite end point of radiographic or PSA progression (HR, 1.09; 95% CI, 0.75-1.59). With added grade 3/4 toxicity in the niraparib arm, the Independent Data Monitoring Committee recommended halting enrollment to this cohort.

As such, only a total of 423 patients with HRR gene alterations were subsequently randomized to niraparib plus abiraterone (n = 212) or placebo plus abiraterone (n = 211).

Regarding baseline characteristics, the median age was 69 years (range, 43-100). In the niraparib and placebo arms, respectively, 23.6% (n = 50) and 22.7% (n = 48) of patients had prior abiraterone/prednisone, 24.1% (n = 51) and 18.5% (n = 39) had visceral metastases, and 46.3% (n = 98) and 43.6% (n = 92) had 

Additional findings showed that rPFS favored niraparib across all prespecified biomarker positive subgroups.

Notably, the addition of niraparib to abiraterone prolonged time to initiation of cytotoxic chemotherapy (HR, 0.59; 95% CI, 0.39-0.89; 

 = .0108), time to symptomatic progression (HR, 0.69; 95% CI, 0.47-0.99; 

 = .0444), and time to PSA progression (HR, 0.57; 95% CI, 0.43-0.76; 

 = .0001) in all patients with HRR gene alterations. Moreover, the ORR was improved with niraparib vs placebo, at 60% (n = 55/92) vs 28% (n = 23/82; relative risk, 2.13; 

Similarly, niraparib delayed the time to initiation of cytotoxic chemotherapy (HR, 0.58; 95% CI, 0.33-1.01; 

 = .0495), time to symptomatic progression (HR, 0.68; 95% CI, 0.42-1.11; 

 = .1224), and time to PSA progression (HR, 0.46; 95% CI, 0.30-0.69; 

 mutations. Additionally, the ORR was improved with niraparib vs placebo, at 52% (n = 29/56) vs 31% (n = 15/48; relative risk, 1.66; 

Although data from the first interim analysis of OS were immature (HR, 0.94; 95% CI, 0.65-1.36;

 = .733), a multivariate analysis accounting for baseline characteristics showed favorable outcomes with niraparib (HR, 0.767; 95% CI, 0.525-1.119;

In terms of safety, no new signals were seen. All-grade treatment-emergent adverse effects (AEs) occurred in 99.1% (n = 210) of patients in the niraparib arm vs 94.3% (n = 199) of patients in the placebo arm. The most common all-grade AEs in the niraparib arm were anemia (46.2%; n = 98), hypertension (31.6%; n = 67), and constipation (30.7%; n = 65). The most common AEs in the placebo arm were hypertension (22.3%; n = 47), anemia (20.4%; n = 43), and fatigue (16.6%; n = 35).

Sixty-seven percent (n = 142) of patients in the niraparib arm experienced grade 3/4 AEs vs 46.4% (n = 98) of patients in the placebo arm. The most common grade 3/4 AEs in the niraparib arm were anemia (29.7%; n = 63), hypertension (15.6%; n = 33), and thrombocytopenia and neutropenia (each, 6.6%; n = 14) vs hypertension (14.2%; n = 30), anemia (7.6%; n = 16), and hepatotoxicity (4.7%; n = 10) in the placebo arm.

Dose reductions occurred in 19.8% (n = 42) of patients on niraparib with a median relative dose intensity of 99%. The most common AEs leading to dose reduction in the niraparib arm were anemia (13.2%) and thrombocytopenia (2.8%).

Additionally, 10.8% (n = 23) and 4.7% (n = 10) of patients discontinued treatment in the niraparib and placebo arms due to AEs, respectively. Deaths due to an AE occurred in 11 (5.2%) of patients on niraparib vs 7 (3.3%) of those on placebo.

Notably, no clinically significant differences in overall quality of life were seen between the study arms, according to results from The Functional Assessment of Cancer Therapy-Prostate questionnaire.

“MAGNITUDE highlights the importance of testing for HRR gene alterations in patients with mCRPC, to identify who will optimally benefit from the combination of niraparib plus abiraterone,” concluded Chi.

1. Chi KN, Rathkopf DE, Smith MR, et al. Phase 3 MAGNITUDE study: first results of niraparib (NIRA) with abiraterone acetate and prednisone (AAP) as first-line therapy in patients (pts) with metastatic castration-resistant prostate cancer (mCRPC) with and without homologous recombination repair (HRR) gene alterations. 

. 2022;40(suppl 6):12. doi:10.1200/JCO.2022.40.6_suppl.012

Findings from the phase 3 MAGNITUDE trial showed that adding niraparib to abiraterone acetate significantly extended radiographic progression-free survival in patients with metastatic castration-resistant prostate cancer and homologous recombination repair gene alterations.

Caroline Seymour

Articles

N-803 plus BCG yields prolonged complete responses and DFS in NMIBC

Dr. Gomella explains the evolving precision medicine paradigm in prostate cancer

No OS benefit at 1-year mark with upfront avelumab in cisplatin-ineligible urothelial cancer

Niraparib and abiraterone combo significantly delays mCRPC progression