BACKGROUND:The potential impact of treatment sequencing in chemoimmunotherapy combinations remains underexplored. We evaluated 2 alternative dosing schedules of chemotherapy (cisplatin and gemcitabine [GC]) and an immune checkpoint inhibitor (CPI; atezolizumab [A]) for metastatic urothelial carcinoma (mUC). METHODS:This multicenter phase II study randomized cisplatin-eligible patients with previously untreated mUC in a 1:1 ratio. The chemo-first schedule included 2 cycles of GC, followed by 4 cycles of GC + A and A maintenance. The CPI-first schedule originally included a two-cycle A lead-in, later amended to a one-cycle lead-in, followed by 6 cycles of GC + A and A maintenance. The primary endpoint was objective response rate after the protocol amendment. Secondary endpoints included progression-free survival, overall survival, and safety. RESULTS:Overall, 31 patients were randomized between 9/2017 and 2/2021 (chemo-first, n = 15; CPI-first, n = 16), with early discontinuation due to the evolving mUC management paradigm. Among the per-protocol evaluable patients (n = 19), ORR was 44% (95% CI, 14%-79%) in the chemo-first schedule and 40% (95% CI, 12%-74%) in the CPI-first amended schedule, with neither arm meeting the predefined efficacy threshold. Median follow-up was 60 months (95% CI 48-not reached [NR]). Median progression-free survival and overall survival (95% CI) were: chemo-first, 6.1 (4.4-NR) and 15 (10-NR) months; CPI-first original, 1.3 (1.1-NR) and 12 (8.4-NR) months; and CPI-first amended, 7.6 (2.0-NR) and 26 (3.6-NR) months. No new safety signals or treatment-related deaths occurred. CONCLUSIONS:This study evaluating the impact of chemotherapy and CPI dosing sequence in patients with mUC was limited by a small sample size and early discontinuation, with neither arm meeting the primary endpoint. Exploratory observations highlight CPI lead-in duration as a potential consideration for future trial design.

Nivolumab monotherapy has been approved for the adjuvant treatment of adult patients with urothelial carcinoma who are at high risk of recurrence after undergoing radical resection of urothelial carcinoma based on results of the phase 3 CheckMate 274 trial, in which adjuvant nivolumab versus placebo demonstrated improvement in the primary endpoint of disease-free survival (DFS) in high-risk muscle-invasive urothelial carcinoma (MIUC). Identification of biomarkers associated with treatment outcomes can help refine patient selection, and inform on the immunobiology of disease. To assess the relevance of key biomarkers in the adjuvant MIUC setting, extensive exploratory analyses of tumor biomarkers, including associations with DFS, were performed. Differential gene expression and gene signature analysis found that immune-related genes and pathways, in particular a high interferon-γ signature, were predictive of improved DFS in nivolumab-treated patients. Positive predictive and prognostic associations, respectively, were found for CD4 gene expression and measures of CD8 T cell infiltration. A composite predictive model suggested that high tumor cell PD-L1 expression, high CD4 gene expression, high tumor mutational burden score, receipt of neoadjuvant cisplatin and low transforming growth factor-β gene signature score made the greatest contributions to predicting improved outcomes in nivolumab-treated patients. These results reinforce studies establishing the importance of tumor biomarkers of adaptive immunity in influencing response to PD-1-PD-L1 blockade, indicating the potential predictive rather than solely prognostic nature of such findings. ClinicalTrials.gov identifier: NCT02632409 .

We previously reported results from a prospective, multicenter, phase 2 trial that demonstrated a pathologic response rate (<ypT2N0) of 63% among 57 patients with high-risk nonmetastatic upper tract urothelial carcinoma (UTUC) treated with four cycles of neoadjuvant chemotherapy (NAC) comprising gemcitabine and split-dose cisplatin. Here we report updated long-term oncologic outcomes. Outcomes included disease-free survival (DFS, non-urothelial recurrence or death from UTUC), cancer-specific survival (CSS), overall survival (OS), and bladder recurrence-free survival (B-RFS), stratified by pathologic response to NAC in the trial cohort alone (primary analysis) and in an expanded cohort including 69 additional patients (total n = 126) with high-risk nonmetastatic UTUC who received NAC followed by definitive surgery at our institution (secondary analysis). Median follow-up among surviving trial patients was 5.4 yr (interquartile range 4.6-7.5), during which 20 DFS, 11 CSS, and 18 OS events occurred. Estimated 7-yr survival rates were 60% for DFS, 77% for CSS, and 72% for OS. Responders to NAC experienced superior 7-yr DFS (78% vs 31%; log-rank p < 0.001), CSS (90% vs 56%; log-rank p = 0.002), and OS (87% vs 48%; log-rank p < 0.001). Findings were similar in the expanded cohort of 126 patients treated with NAC. B-RFS was not associated with response to NAC. These data support incorporation of NAC in the treatment paradigm for high-risk nonmetastatic UTUC.

BACKGROUND AND OBJECTIVE:Divergent differentiation and histologic subtypes are common findings in urothelial carcinoma (UC). Clinically relevant genomic alterations and oncogenic drivers of individual subtypes remain poorly defined. We characterized surgical outcomes and the genomic landscape of UC with aberrant histology (UCAH), with a focus on biomarkers and targetable alterations. METHODS:The clinical cohort comprised 3052 patients who underwent radical cystectomy (RC) with or without neoadjuvant chemotherapy. Targeted exon sequencing was performed for a genomic cohort of 1060 bladder tumors from RC or transurethral resection specimens. We characterized the frequency of oncogenic mutations and targetable alterations, and the tumor mutational burden (TMB) of each subtype. We defined the clonal relatedness of morphologically distinct regions of tumors with mixed histology. KEY FINDINGS AND LIMITATIONS:Patients with plasmacytoid, micropapillary, sarcomatoid, or mixed-histology tumors had worse cancer-specific survival than patients with pure urothelial histology. ERBB2, FGFR3, and PTEN alterations were most frequent in micropapillary, nested/squamous, and sarcomatoid UC, respectively. TMB was highest in plasmacytoid, neuroendocrine, and micropapillary tumors. Regions of mixed histology had shared clonal origins, but exceptions were observed. The retrospective design and potential for selection bias are limitations of our study. CONCLUSIONS AND CLINICAL IMPLICATIONS:UCAH tumors have distinct patterns of genomic alterations, which may be targetable via novel therapies and have implications for clinical trial inclusion. Biomarker-driven systemic therapy should be explored in patients with histologic subtypes that are associated with worse clinical outcomes.

658 Background: In the phase 3, randomized, double-blind CheckMate 274 trial, adjuvant NIVO demonstrated statistically significant and clinically meaningful disease-free survival (DFS) benefit vs PBO in pts with high-risk MIUC after radical surgery (RS) ± prior neoadjuvant cisplatin-based chemotherapy (NAC). With extended 3-y median follow-up, continued improvements in DFS were seen with NIVO vs PBO in the primary efficacy populations (intent-to-treat [ITT], tumor programmed death ligand 1 [PD-L1] expression ≥ 1%) and in pts with MIBC. Early trends in interim OS favored NIVO vs PBO in ITT and tumor PD-L1 ≥ 1% pts. Here we report additional efficacy outcomes for pts with MIBC. Methods: Pts were randomized 1:1 to NIVO 240 mg every 2 wk or PBO for ≤ 1 y of adjuvant treatment, stratified by tumor PD-L1 expression, nodal status, and prior NAC. Primary endpoints were DFS in ITT and tumor PD-L1 expression ≥ 1% pts. OS in ITT and PD-L1 ≥ 1% pts was a secondary endpoint. Analysis of MIBC pts was exploratory. MIBC OS data are from preplanned interim analyses of ITT and PD-L1 ≥ 1% pts. OS follow-up is ongoing as the prespecified statistical boundaries for significance in ITT and PD-L1 ≥ 1% pts were not crossed at the time of these analyses. Results: Of 709 randomized pts (ITT), 560 (79%) had MIBC (NIVO, n = 279; PBO, n = 281); 284 (51%) of MIBC pts had prior NAC. With median follow-up of 36.1 mo (ITT), DFS improvement with NIVO vs PBO was consistent between all pts with MIBC (hazard ratio [HR] 0.63) and those with (HR 0.58) and without prior NAC (HR 0.69; Table). For OS, HRs favored NIVO vs PBO in all pts with MIBC (HR 0.70) and the tumor PD-L1 ≥ 1% subgroup (HR 0.48), as well as in pts with MIBC with (HR 0.74) and without prior NAC (HR 0.67). Safety was consistent with previous data in ITT pts; no new safety signals were identified. Conclusions: With 3-y median follow-up, consistent benefit in DFS was observed with NIVO vs PBO in all MIBC pts and across prior NAC subgroups. The HR for OS favored NIVO in all MIBC pts, in those with PD-L1 ≥ 1%, and regardless of prior NAC status. These results continue to support adjuvant NIVO as a standard of care for high-risk MIUC and MIBC, potentially providing an opportunity for a curative outcome. Clinical trial information: NCT02632409 . NIVOn NIVOMedian(95% CI), mo PBOn PBOMedian(95% CI), mo HR (95% CI) DFS All MIBC 279 25.6 (19.2–41.8) 281 8.5 (7.3–13.7) 0.63 (0.51–0.78) With prior NAC 142 19.6 (15.6–48.2) 142 8.3 (5.6–11.2) 0.58 (0.43–0.79) No prior NAC 137 25.9 (19.2–51.5) 139 13.7 (7.8–22.1) 0.69 (0.50–0.94) OS All MIBC 279 NR (45.0–NE) 281 39.9 (29.8–52.1) 0.70 (0.55–0.90) PD-L1 ≥ 1% 113 NR (NE–NE) 117 37.6 (26.9–NE) 0.48 (0.29–0.77) With prior NAC 142 55.2 (41.8–NE) 142 40.2 (28.8–53.7) 0.74 (0.53–1.03) No prior NAC 137 NR (40.7–NE) 139 37.7 (28.7–65.2) 0.67 (0.47–0.95) NE, not estimable; NR, not reached.

Background and objective:Cisplatin-based chemotherapy has been a cornerstone of therapy for advanced/metastatic urothelial cancer (mUC). However, no genomic characteristics have been validated as prognostic biomarkers for this therapy. We sought to identify prognostic biomarkers using plasma cell-free (cf)DNA collected in a phase 3 cooperative group trial. Methods:We analyzed pretreatment cfDNA from a cohort nested in CALGB 90601 (Alliance), a first-line trial of gemcitabine/cisplatin with bevacizumab or placebo in mUC. We examined associations between cfDNA features and overall survival (OS), progression-free survival (PFS), and treatment response. Key findings and limitations:Baseline cfDNA was sequenced from 201 patients with mUC. There was no statistically significant association between alterations in DNA damage response (DDR) genes and response to cisplatin-based chemotherapy (12/24; 50% response rate in DDR+ vs 60/145; 41% response rate in DDR-; p = 0.4), OS (hazard ratio [HR] 0.78, 95% confidence interval [CI] 0.50-1.22; p = 0.3) or PFS (HR 0.77, 95% CI 0.48-1.22; p = 0.3), although the DDR analysis was underpowered owing to the low frequency of DDR gene alterations. Higher variant allele frequency (VAF) in circulating tumor (ct)DNA was associated with shorter OS (HR 2.51, 95% CI 1.26-5.00; p = 0.009) and PFS (HR 2.18, 95% CI 1.02-4.67; p = 0.045). Shorter OS was associated with cfDNA alterations in TERT (HR 1.59, 95% CI 1.15-2.19; p = 0.005), PIK3CA (HR 1.91, 95% CI 1.20-3.04; p = 0.006), and ERBB2 (HR 1.64, 95% CI 1.08-2.49; p = 0.019). Conclusions and clinical implications:Among patients with mUC treated with cisplatin-based chemotherapy, high pretreatment VAF in ctDNA and alterations in the TERT promoter, PIK3CA, and ERBB2 were associated with poor prognosis. Patient summary:We looked at the link between tumor DNA present in blood and outcomes after chemotherapy for patients with advanced bladder cancer. Higher amounts of tumor DNA in blood and mutations in specific cancer genes were linked to worse survival. The results may help in the design of new studies to improve survival for patients with advanced bladder cancer.This trial is registered on ClinicalTrials.gov as NCT00942331.

Supplemental Table 4 contains SIR analysis, overall and with synchronous pairs removed, for males and females

The Supplemental Materials and Methods describes the SIR formula in detail.

Supplemental Table 1 shows scoring of tumor pairs related to hereditary cancer syndromes. Supplemental Table 2 shows pooled analysis of all tumors, and Supplemental Table 3 shows pooled analysis in those with 5+ tumors. Supplemental Table 6 shows details of genotype-phenotype associations by germline variant for all genes. Supplemental Table 7 shows LOH sensitivity analysis. Supplemental Figure 1 shows how tumor pairs are defined. Supplemental Figure 2 shows synchronous primaries.

833 Background: EV has high antitumor activity and improved survival in advanced urothelial cancer both as a single agent and in combination with pembrolizumab. We hypothesized that EV primes a systemic immune response for effective T cell mediated killing. Methods: We conducted a retrospective analysis of mUC patients treated with EV at Memorial Sloan Kettering Cancer Center to evaluate its impact on peripheral blood immune cells. PBMCs were isolated from 32 patients with mUC on C1D1 and C2D1 of EV monotherapy. A 32-color spectral flow cytometry panel was used to identify T-cell subsets, and their correlation with treatment response using Wilcoxon rank sum test. Response was determined by an independent radiologist’s assessment of the first on-treatment scan according to RECIST v1.1 criteria. Results: Of 32 patients, 75% were men with median age 73. 81.3% received prior platinum-based chemotherapy and 93.8% received prior PD-1/PD-L1 immunotherapy. Partial response (PR) was observed in 16 patients, while 16 had stable disease (SD) or progressive disease (PD). At C1D1, CD8+ T cell frequencies did not correlate with response; however, a reduction in circulating CD8+ T cells at C2D1 correlated with poor response (SD + PD, p < 0.05). At baseline, high frequency of CD8+PD-1+ T cells correlated with poor response (p < 0.05). Baseline high frequencies of CD8+PD-1+LAG3+ and CD8+PD-1-LAG3+ T cells were also associated with poor response (p < 0.05). At C2D1, high frequency of CD8+TIM3+ (p < 0.05) and CD8+LAG3+ (p < 0.05) T cells correlated with non-response. Additional activation markers on CD8+ T cells at C1D1 were analyzed (Table). Within the memory CD8+ and CD4+ T cell compartments, patients with higher circulating naïve memory cells (CD45RA+CCR7+) at baseline were less likely to respond to EV (p < 0.05), while those with higher frequencies of T effector memory (CD45RA-CCR7-) and effector T cells (CD45RA+CCR7-) were more likely to respond to EV (p < 0.05). No significant correlations were found between memory T cells and response at C2D1. Conclusions: At baseline and on treatment, distinct immunophenotypes are detected in the peripheral blood of EV treated patients, potentially correlating with treatment response. Ongoing studies aim to further elucidate the influence of prior anti-PD-1/PD-L1 therapy and the combination of EV with pembrolizumab on these immunophenotypic profiles. Peripheral T cell phenotypes at C1D1 from mUC patients treated with EV. Peripheral Immune Cell at C1D1 Responders (PR, %CD45+) Non-Responders (SD + PD, %CD45+) p-value CD8+ 11.1 13.7 0.10 CD8+ Fold Change (C1D1/ C2D1) 1.07 0.74 0.04 Responders (PR, %CD8+) Non-Responders (SD + PD, %CD8+) p-value CD8+ ICOS+ 37.6 56.5 0.01 CD8+ PD1+ 40.9 64 0.04 CD8+ TIGIT+ 39.9 54.6 0.01 CD8+ LAG3+ 1.16 1.23 0.67 CD8+ TIM3+ 23.6 18.5 0.04

811 Background: We previously reported our multicenter phase II trial of neoadjuvant gemcitabine and split-dose cisplatin (GC) in 57 patients with high-grade upper tract urothelial carcinoma (HG UTUC), where 63% of patients experienced a pathological response (

Supplemental Table 5 contains the sensitivity analysis for metachronous SIR pairs using different weighted cutoffs for males and females

4573 Background: Enfortumab vedotin and pembrolizumab (EV/P) emerged as the new standard of care for previously untreated metastatic urothelial carcinoma (mUC), shifting the treatment paradigm. Currently, there are no guidelines for management after EV/P as the outcomes of subsequent systemic treatments, including platinum-based chemotherapy, remain unknown. Methods: Our retrospective cohort of patients with mUC treated with EV/P at Memorial Sloan Kettering Cancer Center was reviewed to identify patients receiving subsequent systemic treatments. Clinical data were collected by chart review. Response to EV/P and platinum-based chemotherapy was determined by physician assessment using RECIST v1.1. Progression free and overall survival (PFS, OS) were calculated using the Kaplan-Meier method. Results: Of 208 patients treated with EV/P between 10/2018 and 9/2024, we identified 56 patients that received any subsequent systemic treatments. In 68% of patients (n = 38), the initial post EV/P regimen administered was platinum-based chemotherapy. Other therapies included sacituzumab govitecan (n = 6), clinical trials (n = 5), trastuzumab deruxtecan (n = 4), erdafitinib (n = 2) and non-platinum chemotherapy (n = 1). In the 38 patients treated with platinum-based chemotherapy, median age was 74 years, 66% were men, 32% had upper tract primary and divergent histology/subtype component was reported in 47% of cases. One patient had prior platinum exposure (neoadjuvant treatment with rapid metastatic recurrence < 6 months). 16 patients had disease response to EV/P (observed response rate [ORR] 42%, 95% CI 27%, 59%). 36 patients (95%) received doublet therapy with gemcitabine and either cisplatin (n = 7) or carboplatin (n = 29), the two remaining patients received carboplatin/gemcitabine/paclitaxel and carboplatin/etoposide. 7 patients (18%) received maintenance avelumab following platinum. Median follow up was 5 months (IQR: 2.5-6.3). ORR was 50% (95% CI 34%, 66%), including one patient with complete response (CR; 2.9%) and 16 patients with partial response (PR; 47%). Among the patients with CR or PR, median duration of response was 3.8 months (IQR: 2.0-4.6). Median PFS was 4.4 months (95% CI 3.7, 7.8) and median OS was 12 months (95% CI 9.7, 17). Conclusions: In a real-world cohort of patients with mUC, platinum-based chemotherapy had substantial antitumor activity after EV/P, although progression-free survival and duration of response were modest. This work provides useful information to further future trial design in the post EV/P setting. Disease response with platinum-based chemotherapy after enfortumab vedotin and pembrolizumab. N=38 (%) 95% CI Observed response rate 17 (50%) 34%, 66% Complete response 1 (2.9%) 0.15%, 17% Partial response 16 (47%) 30%, 65% Stable disease 6 (18%) 7.4%, 35% Progressive disease 11 (32%) 18%, 15% Unknown 4

4574 Background: Enfortumab vedotin and pembrolizumab (EV/P) recently became the standard of care frontline treatment for patients with locally advanced or metastatic urothelial carcinoma (la/mUC). In patients treated with EV monotherapy, previous studies reported a potential association between cutaneous toxicities and improved clinical outcomes. While cutaneous toxicities are common with EV/P, the correlation with response has not been described. Methods: This is a retrospective cohort of patients treated with first line EV/P for la/mUC at Memorial Sloan Kettering Cancer Center. Clinical data were collected by chart review. Response to EV/P was defined by investigator assessment adhering to RECIST 1.1. Cutaneous toxicity events were recorded and classified as mild (managed with topical agents and/or oral antihistamines) or moderate/severe (requiring further pharmacological interventions and/or dose modifications). Association between clinical characteristics and response were analyzed using univariable and multivariable logistic regression models. Results: 186 patients who started EV/P between October 2018 and September 2024 were identified, 166 with distant metastases (89%) and 20 (11%) with locally advanced disease. Median age was 72 years, 68% were male, 31% had upper tract primary, and 44% had subtype/divergent histology component. Rates of bone, lung, and liver metastases were 29%, 24%, and 19%, respectively, and 27% had lymph node only disease. Observed response rate was 64% (119/186; 95% CI 57%, 71%), including a complete response rate of 18% (33/186; 95% CI 13%, 24%). Cutaneous toxicities occurred in 106 patients (57%), predominantly within the first 12 weeks (94/106), 70% of events were classified as mild and 30% as moderate/severe. On univariable analysis, cutaneous toxicity at any time, and before 12 weeks were significantly associated with response to EV/P, with odds ratio (OR) 2.6 (95% CI 1.44 - 4.94, p = 0.002) and 1.91 (95% CI 1.04 - 3.53, p = 0.037). Greater effect was seen based on severity: OR 2.24 (95% CI 1.17 - 4.42, p = 0.017) for mild events and OR 4.12 (95% CI 1.62 - 12.0, p = 0.005) for moderate/severe events compared to patients without cutaneous toxicity. Response to EV/P was less likely with distant metastatic disease (vs. locally advanced; OR 0.28, p = 0.05), and with bone metastases (OR 0.44, p = 0.015), and more likely with lymph node only disease (OR 2.89, p = 0.007). When adjusted for treatment setting (metastatic vs locally advanced) and time on treatment in multivariable analysis, the effect of cutaneous toxicity ≤12 weeks on response was no longer significant (OR 1.7, 95% CI 0.9 - 3.25, p = 0.11). Conclusions: In our large, real-world cohort there was a non-significant trend for response to EV/P in patients with cutaneous toxicities. Further studies are needed to define the potential correlation.

Abstract Background: Bacillus Calmette-Guérin (BCG) remains the most efficacious and widely studied intravesical therapy for NMIBC, but less than 50% of BCG-exposed patients will respond to a second course of BCG. One mechanism of resistance to BCG is an immunosuppressive tumor microenvironment with myeloid-derived suppressor cells (MDSCs), tumor associated macrophages (TAMs), and Tregs that abrogate the anti-tumor immune response. IL-6 is associated with MDSCs and BCG resistance. Gemcitabine (Gem), however, has been shown to selectively inhibit MDSCs, TAMs, and Tregs. This observation served as the biologic rationale for our recently completed Phase I trial of combination chemoimmunotherapy with intravesical Gem and BCG for BCG-exposed high-grade (HG) NMIBC (NCT04179162) that demonstrated excellent tolerability and preliminary efficacy (96% complete response at 6-month follow-up). We sought to evaluate immune modulation with the addition of Gem to BCG as determined by changes in urinary cytokine/chemokine levels. Methods: Patients with BCG-exposed papillary HG NMIBC (Ta/T1) +/- carcinoma in situ recurring within 24 months of BCG therapy were treated with intravesical Gem twice weekly (weeks 1,4,7,10; 8 total doses) and intravesical TICE BCG weekly (weeks 2,3,5,6,8,9; 6 total doses) followed by SWOG maintenance BCG for responders. Urine specimens were collected prior to treatment and on weeks 4, 8, 12, 24, and 52 weeks after on-trial treatment initiation. Urinary cytokines present in the supernatant were evaluated using a 96-plex immuno-oncology proximity extension assay (Olink®). Cytokines with < 75% of values below the lower limit of detection of the assay were not evaluated. We performed an exploratory analysis of select pre-specified cytokines using a linear mixed model. Mean changes and 95% confidence intervals (CI) are presented with global p-values testing for a change in cytokine levels at any timepoint. Results: Urine samples were available for all 25 patients in the Phase I study. A total of 25 proteins on the panel were excluded due to low detection. Chemokines associated with T-cell trafficking (CXCL9, CXCL10, CXCL11) increased during induction treatment through 3 months of follow up and then returned to baseline after the completion of treatment (p<0.001 for each cytokine). IL-6 decreased after initiation of treatment and remained low through 12 months of follow up (-2.7, 95% CI -3.8, -1.7; p<0.001). Notably, the one patient who had a recurrence also had a rise in IL-6 after an initial decline while on treatment. Conclusion: We found evidence that the addition of intravesical gemcitabine to BCG favorably augments the tumor microenvironment based on changes in urinary cytokine/chemokine profiles. Additional tumor and urinary correlatives are ongoing. Based on the the robust preliminary efficacy demonstrated in the ongoing phase I/II trial (NCT04179162), a prospective randomized controlled trial comparing GemBCG to BCG alone for BCG-exposed NMIBC is planned through the National Clinical Trial Network (Alliance A032303). Citation Format: Christopher D. Gaffney, Syed M. Alam, Jessica A. Lavery, Merve Basar, Neeta D'Souza, Christian Hernandez, Melissa McCarter, Patricia Moran, Kristen Stasi, Kara Worth, Daniel Sjoberg, Guido Dalbagni, Timothy Donahue, Sherri Donat, Dean Bajorin, Bernard H. Bochner, Alvin Goh, Judy Sarungbam, Hikmat Al-Ahmadie, Eugene J. Pietzak. Urinary cytokine profiles reflect rationale for treatment with gemcitabine and Bacillus Calmette-Guérin (BCG) in BCG-exposed high-risk non-muscle invasive bladder cancer (NMIBC) [abstract]. In: Proceedings of the AACR Special Conference on Bladder Cancer: Transforming the Field; 2024 May 17-20; Charlotte, NC. Philadelphia (PA): AACR; Clin Cancer Res 2024;30(10_Suppl):Abstract nr B007.