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Fluid‐Crystallization Synergy for >26% Efficiency Fully Ambient‐Printed SAM‐Based Perovskite Photovoltaics

ABSTRACT While lab‐scale spin‐coating in inert environments has delivered record efficiencies for perovskite solar cells (PSCs) employing self‐assembled monolayers (SAMs), their fabrication via fully ambient‐air printing—a prerequisite for low‐cost industrialization—remains unreported. Here, we report the first PSCs exceeding 26% efficiency based on fully ambient‐air printed SAMs and perovskite films and elucidate the governing role of SAM physicochemical properties through fluid‐crystallization synergy. SAMs with higher surface energy ( γ ) flatten the perovskite ink meniscus, attenuating the temperature gradient and Marangoni stress along the gas‐liquid interface, thereby enabling more uniform perovskite deposition and smoother films. Simultaneously, γ systematically modulates perovskite crystallization by delaying nucleation onset and shifting the growth mode from continuous to instantaneous on higher‐ γ SAMs. The fluid–crystallization synergy yields a record power conversion efficiency (PCE) of 26.31% (certified 25.85%), a benchmark for all reported ambient‐air printed devices, including non‐SAM‐based counterparts. The approach further enables scalable fabrication, achieving a champion PCE of 22.3% in 13.04 cm 2 mini‐modules with over 90% performance retention after 1200 h operation under the ISOS‐L‐1 protocol. This work establishes a quantitative link between SAM physicochemical properties and perovskite fluid dynamics and crystallization thermodynamics in ambient‐air printing, providing guidance for perovskite photovoltaics toward scalable ambient manufacturing.

Slow PPi release enhances fidelity of the SARS-CoV-2 RNA dependent RNA polymerase

PSG copy number amplification and association with poor survival in early-stage female lung adenocarcinoma patients.

8028 Background: Pregnancy-specific glycoproteins (PSGs) are essential for maintaining maternal immune tolerance by modulating innate and adaptive responses to prevent fetal rejection. Given our prior finding that increased PSG expression is associated with worse outcomes for female lung cancer patients, we aimed to investigate whether copy number alterations (CNAs) show the same sex-dependent effect on survival in early-stage disease. Methods: We evaluated the sex-specific impact of PSG CNAs across two lung adenocarcinoma (LUAD) cohorts: The Cancer Genome Atlas (TCGA) (n = 503; 269 females, 234 males) and MSK-IMPACT (n = 3,863; 2,450 females, 1,413 males). CNAs were retrieved from cBioPortal for the TCGA cohort and determined via the FACETS algorithm on BAM files for the MSK-IMPACT cohort. Overall survival (OS) differences between patients with and without PSG copy number amplification were analyzed using Kaplan-Meier curves along with log-rank tests. Additionally, we examined the association between tumor stage and the prognostic impact of PSG copy number amplification. Results: In the TCGA cohort, female patients with PSG copy number amplification exhibited significantly worse OS compared to those without (HR = 1.96, p = 0.0039), while no significant survival difference was observed in males (HR = 1.37, p = 0.1902). This sex-specific trend was further validated in the MSK-IMPACT cohort, where the association between PSG copy number amplification and poor OS was highly significant in females (HR = 1.46, p = 7.5×10 -6 ) but relatively weaker in males (HR = 1.29, p = 0.0089). Notably, the prognostic impact of PSG copy number amplification was stage-dependent; while no significant survival differences were found for either sex in Stage 4 disease across both cohorts, the effect was highly pronounced in early-stage female patients. In the TCGA cohort, female patients with early-stage disease showed increasingly significant survival disparities between patients with and without PSG copy number amplification as stage decreased (Stage ≤ 3: HR = 1.81, p = 0.0182; Stage ≤ 2: HR = 2.03, p = 0.0129; Stage 1: HR = 2.51, p = 0.0047), whereas no such associations were found in males. Similarly, in the MSK-IMPACT cohort where tumor stage was dichotomized (Stages 1–3 vs. Stage 4), female patients with Stage ≤ 3 disease showed a strong survival difference between patients with and without PSG copy number amplification (HR = 1.86, p = 1.79×10 -5 ), which remained significantly stronger than the association observed in the male patients (HR = 1.49, p = 0.0129). Conclusions: Our findings raise the question of the potential role of PSG-mediated immune modulation in promoting tumor progression in early-stage female lung cancer patients, and suggest that there may be value in sex-stratified approaches to clinical risk assessment and in therapeutic targeting.

Factors associated with adjuvant chemotherapy initiation delays among breast cancer patients in a metropolitan healthcare system.

e12541 Background: Adjuvant chemotherapy initiation (ACI) delays in breast cancer patients are a critical concern, as they are linked to poorer survival outcomes. There are multiple factors associated with these delays, including patient-level factors (e.g., race, ethnicity, and insurance status), cancer-specific considerations (e.g., cancer stage and subtype), and system level barriers. Developing targeted interventions necessitates a greater understanding of ACI contributing factors. In this study, we examined factors associated with ACI delays among a cohort of women diagnosed with breast cancer in a metropolitan healthcare system. Methods: This study has been approved by the Social and Behavioral Research Panel of Northwestern University’s Institutional Review Board (IRB; study number STU00219464).Our cohort included people whose legal sex was female who had a first-time diagnosis of breast cancer receiving adjuvant chemotherapy at Northwestern Medicine between March 2022 and August 2025. Patient clinical and sociodemographic data were extracted from the Northwestern Medicine Electronic Data Warehouse. ACI delay was defined as a greater-than or equal-to-90-days interval between breast cancer surgery date and date of ACI. Multivariable logistic regression models were used to identify factors associated with ACI delay including race, ethnicity, insurance, area deprivation index (ADI) score, and cancer stage and subtype. Results: Of the 637 patients included in this analysis, the majority were White (80.8%), non-Hispanic (89.8%), had private insurance (57.9%), and stage I breast cancer (78.6%). The median number of days between breast cancer surgery and ACI was 47, and 10.4% (n = 66) of patients experienced ACI delay. Patients with higher odds of ACI delay identified as Hispanic ([OR],2.0;95%CI,0.26-16.2), had Medicaid ([OR],2.7;95%CI,0.33-21.7), stage III breast cancer ([OR],7.71;95%CI,0.56-105.46), or progesterone receptor negative subtype ([OR],3.82;95%CI,1.04-14.1). Patients who had lower odds of ACI delay identified as Black/African American ([OR],0.24;95%CI,0.01-4.36), other race ([OR],0.44;95%CI,0.03-6.02), or had Medicare ([OR],0.33;95%CI,0.02-6.85). ADI score was not significantly associated with ACI delay ([OR],0.98;95%CI,0.32-3.02). Conclusions: The present analysis indicated that Hispanic ethnicity, having Medicaid, stage III breast cancer, and progesterone receptor negative subtype were associated with higher odds of ACI delay when compared with their respective reference groups, while non-White race and having Medicare was associated with lower odds of ACI delay. These findings can be used to guide in the development of interventions that address barriers to timely ACI.

Cardiotoxicity and efficacy outcomes of SPEDOX-6 for targeted treatment of soft tissue sarcomas.

e23534 Background: Soft tissue sarcomas (STSs) are extremely aggressive & deadly rare tumors with multiple subtypes. Early diagnosis is very difficult & STSs are frequently diagnosed only at advanced stages. Doxorubicin (DOX) has remained only standard of care for past 45 years with low efficacy and high dose-dependent cardiotoxicity. Better agents are urgently needed. Methods: Our patented single protein encapsulation (SPE) platform allows encapsulation of small-molecule drugs by a single protein (albumins or globulins) to make new generation nanodrugs that have no artificial nanoparticles, no chemical bond to drugs and proteins. SPEDOX-6 was successfully prepared by encapsulated 9 DOX molecules into binding pockets of each human serum albumin (HSA) molecule, which was confirmed and characterized by UV, fluorescence, membrane dialysis, size-exclusion HPLC and dynamic light scattering techniques. SPEDOX-6 provides a novel approach for improving DOX’s efficacy and reducing its side effects by targeting cancer cells with low neonatal Fc receptor (FcRn) levels. Results: In mouse model, free DOX concentration in heart tissue of SPEDOX-6 was 4 to 8 times lower than DOX, suggesting much lower cardiotoxicity. PK profiles shown that SPEDOX-6 has shown a significant 48X increase of SPEDOX-6 total exposure upon its encapsulation. In rat model, a toxicokinetic study indicates that the total exposure for SPEDOX-6 increases17X higher, compared to DOX. Cardiotoxicity from a high dose of 50 mg/kg of SPEDOX-6 was undetectable, in contrast to observable cardiotoxicity from a single dose of 5–10 mg/kg DOX. In mouse model efficacy study on HT-1080 (STS), SPEDOX-6 remarkably suppresses HT-1080 (the lowest FcRn level) with 3 out of 10 mice attaining tumor-free status. SPEDOX-6 at 30 mg/kg is significantly better than Doxil at 4 mg/kg (MTD) and DOX at 3.5 mg/kg (MTD) in inhibiting SK-ES-1 (Ewing sarcoma, with the highest FcRn level) tumor growth, but SPEDOX-6 has less efficacy against SK-ES-1, relative to HT-1080. For MB-MDA-231 (TNBC, a medium FcRn level) model, SPEDOX-6 has shown superior anticancer efficacy in comparison to DOX. Conclusions: Combined with above 3 mouse model studies, SPEDOX-6’s antitumor efficacy displays an inverse relationship with FcRn levels, thereby providing a potential mechanism for SPEDOX-6’s targeted STS treatment. With “Orphan Drug Designation” status, SPEDOX-6’s current human phase Ib/IIa clinical trials for treating STS underway (NCT07064018) will provide more information on establishing the correlation between antitumor efficacy of SPEDOX-6 and FcRn levels of cancer tissues. SPEDOX-6 may become the first targeted cancer therapy based on the FcRn level, revolutionizing STS’s treatments.

Barriers and facilitators of advance care planning in cancer patients in southeast Alabama: An observational study.

e24039 Background: Advance Care Planning (ACP) plays a crucial role in ensuring that patients facing serious illness, such as cancer, can make decisions about their end-of-life care in line with their values and preferences. While ACP is recognized as essential for improving patient outcomes and reducing unnecessary medical interventions, many cancer patients still face challenges in initiating or completing ACP discussions and documentation. This study seeks to explore cancer patients' awareness of ACP, identify the barriers and facilitators to its implementation, and assess the perceived benefits. Methods: The study surveyed adult cancer patients from oncology clinic at Southeast Health Medical Center (n=111). Participants were selected based on their active participation in cancer treatment or being in remission, regardless of cancer type. A structured survey was administered, assessing patients’ awareness of ACP, prior discussions with healthcare providers, barriers to and facilitators of ACP, and the perceived benefits of ACP. Results: Of 200 surveys, 111 responses were received (response rate 55%), the median age was 62.9 years, with 68% participants female, 32% male. 36% of females and 42% of males were familiar with ACP. 31% of patients age 51 and older were familiar with ACP prior to cancer diagnosis. Most participants reported at least one barrier to ACP. The most frequently reported barrier was “the uncertainty of disease progression”, followed by “lack of information” and “emotional discomfort”. “Family Opposition” and “cultural or religious beliefs” were ranked low on reported barriers. 60% believed that ACP should only be discussed when all curative options are exhausted. The most frequently reported facilitators of ACP were, “understanding benefits of advanced care planning”, “clear information from healthcare providers”, “support from family and friends”, and “access to counseling or support groups” in descending order. There was no statistical significance between reported barriers and facilitators of ACP p=.997, X 2 =2.52. Conclusions: Fewer than half of surveyed patients were familiar with ACP, and most reported at least one barrier to engagement. Perceptions that ACP is only appropriate after exhausting curative options, uncertainty about disease course, emotional discomfort, and limited provider communication were common obstacles. Participants had hesitation discussing end-of-life topics, likely related to limited ACP education and variable health literacy in this population which may have attenuated response. Although no statistically significant associations between barriers and facilitators were detected, low familiarity and pervasive barriers across groups highlight need for earlier, longitudinal ACP integration, provider education, and culturally sensitive, standardized workflows in community oncology to support value-concordant care.

Patient-reported impact of a digital breast cancer survivorship community in Saudi Arabia.

e13788 Background: Breast cancer survivors in conservative societies often face cultural, social, and logistical barriers to peer support and structured survivorship care. Digital platforms may mitigate these constraints while preserving cultural sensitivity. “Najia” is a professional-patient partnership initiative with a digital-first breast cancer survivorship community established over 10 years ago that has evolved into a sustainable hybrid model integrating education, peer support, advocacy, and in-person activities. We evaluated participant-reported perceptions of Najia’s core functions. Methods: An anonymous, Arabic-language survey was distributed both on-site during a "Najia" annual summit and online via a mobile web platform. The survey included seven items assessing four predefined domains: education (knowledge acquisition), support (psychological and emotional support), belonging (peer learning and sense of community), and advocacy (recommendation to others). Responses were categorical (Yes / No / I don’t know). Descriptive analyses were performed. Results: A total of 110 responses were analyzed. Most respondents identified as Najia members (90.8%), with additional respondents expressing interest in joining. Within the education domain, 98.1% reported improved knowledge related to coping with breast cancer. In the support domain, 99.1% reported receiving psychological and emotional support through Najia. Across the belonging domain, 97.2% reported benefiting from shared peer experiences, and 97.2% reported feeling part of a supportive community. Participation in Najia-organized activities, including meetups and annual summits, was associated with improved quality of life for 86.0% of respondents. In the advocacy domain, 100% of respondents indicated willingness to recommend Najia to others. Analysis of concordance across survivorship domains is shown in Table 1. Conclusions: These findings support the role of culturally adaptable, sustainable digital survivorship communities in oncology care, particularly in settings where formal survivorship infrastructure and peer support remain limited. Moreover, the high concordance across survivorship domains suggests that Najia delivers an integrated participant experience in which education, support, belonging, and advocacy are closely aligned. Concordance of key survivorship domains within the najia community. Domain pair Respondents endorsing both domains n / N (%) Interpretation Knowledge gain × Emotional support 107 / 107 (100%) Educational benefit co-occurred with perceived emotional support Emotional support × Sense of belonging 106 / 106 (100%) Emotional support and belonging were aligned Sense of belonging × Peer learning 102 / 102 (100%) Belonging overlapped with learning from peers Sense of belonging × Recommendation 106 / 106 (100%) Belonging was accompanied by advocacy intent

Clinical outcomes of [ ¹⁷⁷ Lu]Lu-DOTA-TATE ( ¹⁷⁷ Lu-DOTATATE) vs everolimus (EVE) in managing patients (pts) with gastroenteropancreatic-neuroendocrine tumors (GEP-NETs): Real-world analysis of the PRIME initiative.

e16316 Background: GEP-NETs arise from neuroendocrine cells of the digestive tract (88%) or pancreas (12%). Therapies for progressive GEP-NETs include surgery, somatostatin analogs (SSA), chemotherapy, targeted therapy, and radioligand therapy. 177 Lu-DOTATATE is a radiolabeled SSA approved for progressive GEP-NETs based on NETTER-1 and shown to be an effective first-line therapy for Grade 2 and 3 GEP-NETs in NETTER-2. Prior to 177 Lu-DOTATATE approval, EVE, a mammalian target of rapamycin inhibitor, was the recommended therapy for progressive GEP-NETs. Here we describe pt characteristics and real-world outcomes of 177 Lu-DOTATATE vs EVE in pts with GEP-NETs. Methods: This was a retrospective, non-interventional, cohort study of pts treated with 177 Lu-DOTATATE or EVE using data from the open-source IQVIA Longitudinal Prescription and Pt Centric Medical Claims databases between Jul 1, 2017-Feb 28, 2025, representing the largest analysis of real-world GEP-NET data to date. Pt characteristics were assessed using descriptive statistics from 6 months prior to the index date (date of earliest evidence of 177 Lu-DOTATATE or EVE initiation). Following propensity-score matching of cohorts, overall survival (OS) and time to next systemic treatment (TTNT) were assessed with Kaplan-Meier and Cox models from index date to the end of follow-up. Results: The study included 5367 pts treated with 177 Lu-DOTATATE (n = 3410) or EVE (n = 1957). Prior to matching, pt characteristics were comparable between 177 Lu-DOTATATE and EVE groups, with a median (range) age of 67 (18-85) vs 65 (18-85) years. Prior exposure to systemic therapies was higher with 177 Lu-DOTATATE (68%) vs EVE (59%), with only 5% prior EVE exposure in the 177 Lu-DOTATATE group. The most common comorbidities in pts included hypertension (38% vs 37%); liver, gallbladder, and pancreatic diseases (29% vs 28%); and diabetes (24% vs 26%) for 177 Lu-DOTATATE vs EVE, respectively. Post-matching, the median (95% Cl) TTNT was not reached (NR) (70.2 months-NR) with 177 Lu-DOTATATE (n = 1559) vs 29.0 (25.2-34.6) months with EVE (n = 1559) (p < 0.0001). In pts who initiated a subsequent therapy (16% vs 38%) during the study, the median (range) TTNT was 20.5 (2.1-74.0) vs 8.0 (0.7-73.5) months with 177 Lu-DOTATATE vs EVE, respectively. Overall, 76% vs 73% of pts treated with 177 Lu-DOTATATE vs EVE were still alive at the end of follow-up. Cox proportional hazard and sensitivity analyses showed a robust, significant survival benefit for 177 Lu-DOTATATE vs EVE, with a hazard ratio (95% Cl) of 0.74 (0.59-0.92) for OS (p = 0.007). Conclusions: OS benefit and lower and less frequent treatment initiation after 177 Lu-DOTATATE vs EVE treatment, suggests a clinical benefit of 177 Lu-DOTATATE vs EVE with lower therapy burden in pts with GEP-NETs.

Sequence of similar-payload ADCs: Does it make sense in real-world HER2-low advanced breast cancer?—The Portuguese national study.

1140 Background: New-generation Antibody-Drug Conjugates (ADC) have expanded treatment options for HER2-low advanced breast cancer (ABC), regardless of hormone receptor (HR) status. Sacituzumab govitecan (SG) and trastuzumab deruxtecan (T-DXd) are used sequentially in clinical practice, but real-world data on efficacy, sequencing and potential cross-resistance are limited. We aimed to evaluate efficacy, sequencing patterns and predictors of outcome in a national real-world cohort of HER2-low ABC. Methods: We conducted a multicenter, retrospective real-world cohort study including patients with HER2-low ABC treated sequentially with SG and T-DXd, regardless of sequence, across 14 Portuguese centers. Eligible patients initiated the first ADC between 2023 and 2025 and received ≥1 cycle of both ADCs. The primary endpoint was progression-free survival (PFS), evaluated for the first (PFS1) and second ADC (PFS2). Secondary endpoints included objective response rate (ORR), primary resistance to the second ADC (PFS2 ≤3 months) and safety. PFS was analyzed using time-to-event methods. For exploratory analyses, PFS1 and PFS2 were dichotomized at the median and associations with longer PFS were assessed using chi-square tests. Predictors of PFS2 were explored in an exploratory multivariable Cox regression model. Results: Sixty-four patients were included; 36 (56%) had HR-positive disease and 28 (44%) were HR-negative. Median age at ADC1 initiation was 51 years (27–79). T-DXd was used as the first ADC (ADC1) in 34 (53%) patients and was more frequently administered as ADC1 in HR-positive disease. A total of 22 (34%) patients received ≥1 intermediate line, mainly chemotherapy (91%). Median PFS1 was 8.9 months (95% CI 5.8–9.7) and median PFS2 was 2.7 months (95% CI 2.1–3.2). PFS2 was consistently shorter than PFS1 across subgroups, independent of treatment line, with 43 (70%) patients presenting primary resistance to the second ADC. ORR to ADC2 was 3%. No significant differences in PFS1 or PFS2 were observed by ADC sequencing. Longer PFS1 was not associated with improved PFS2 (p=0.44). In the multivariable model, none of the evaluated variables, including the use of ≥1 intermediate line between ADCs, were significantly associated with longer PFS2 (all p>0.05). No new safety signals were observed; rates of dose reductions and interruptions were consistent with known safety profiles of SG and T-DXd. Conclusions: In this national real-world cohort of HER2-low ABC, clinical benefit from a second ADC was limited, with shorter PFS and frequent early progression, irrespective of sequencing order. Importantly, no baseline clinical factors predicted PFS2. These findings may suggest clinically relevant cross-resistance between ADCs with similar payloads and highlight shared resistance mechanisms as a key challenge in optimizing ADC sequencing.

AI–assisted survival prediction in glioma: Meta-analysis of prospective and controlled studies.

e14000 Background: Accurate survival prediction in glioma is critical for individualized treatment planning, prognostic counseling, and clinical trial stratification. Artificial intelligence (AI)–based models, including machine learning and deep learning approaches, integrate radiomic, genomic, and clinical data beyond conventional prognostic tools. However, performance varies across studies, and comparative accuracy and generalizability remain uncertain. We conducted a meta-analysis of prospective and controlled studies evaluating AI-based overall survival (OS) prediction in adult glioma. Methods: PubMed, Embase, Cochrane Library, IEEE Xplore, and ClinicalTrials.gov were searched for prospective studies, controlled validation cohorts, or head-to-head comparisons published between January 2015 and December 2025. Eligible studies included adults (≥18 years) with histologically confirmed WHO grade II–IV glioma reporting OS prediction metrics (C-index, AUC, or Brier score) derived from MRI-based, radiogenomic, or multimodal AI models. Random-effects meta-analysis (DerSimonian–Laird) was performed. Heterogeneity was assessed using I², and risk of bias using PROBAST. Results: Twenty-two controlled studies including 9,314 patients met inclusion criteria. AI-based models demonstrated significantly higher OS prediction accuracy than standard prognostic tools. The pooled C-index for AI models was 0.81 (95% CI, 0.78–0.84; I² = 39%) compared with 0.69 (95% CI, 0.66–0.72) for conventional models, corresponding to a pooled mean improvement of 0.12 (p < 0.001). For 12-month OS prediction, AI models achieved a pooled AUC of 0.84 (95% CI, 0.80–0.87) versus 0.73 (95% CI, 0.70–0.76). Deep learning models showed higher accuracy (C-index 0.84) than traditional machine learning approaches (0.79). Multimodal AI models integrating imaging, genomic, and clinical data demonstrated the highest performance (C-index 0.87). External validation cohorts showed reduced accuracy (C-index 0.75), indicating limited generalizability. Acceptable calibration was reported in 64% of studies, while incomplete calibration reporting remained a major source of bias. Conclusions: AI-based survival prediction models significantly outperform conventional prognostic tools in glioma, particularly deep learning and multimodal approaches. Reduced performance in external validation highlights the need for larger, harmonized datasets and prospective trials to support clinical implementation. Pooled results of AI vs. standard prognostic models. Outcome AI Model (Pooled) Standard Model Effect Size 95% CI I² C-index (OS) 0.81 0.69 +0.12 0.09–0.15 39% AUC (12-mo OS) 0.84 0.73 +0.11 0.07–0.15 42% Deep Learning C-index 0.84 — — 0.81–0.87 33% Machine Learning C-index 0.79 — — 0.76–0.82 28% Multimodal AI C-index 0.87 — — 0.84–0.90 31% External Validation 0.75 — — 0.71–0.78 44%

Mediterranean CD19 genetic variations and potential influence on CAR T-cell therapy efficacy: Implications for population-tailored immunotherapy.

7008 Background: CAR T-cell therapy has transformed the treatment of B-cell malignancies. However, relapse due to CD19 antigen escape remain a major challenge, often driven by genetic variants affecting CD19 structure, leading to CAR-T resistance. Mediterranean populations including Arabs, remain underrepresented in genomic studies. The Arabian prevalence and functional impact of CD19 variants is unknown. Methods: We analyzed and annotated CD19 NGS data from a Mediterranean cohort comprised of 1,305 Arabian individuals. The overall allele frequencies were compared to global databases. Clinically reported resistance mutations were prioritized based on published CAR T-cell studies. Hardy-Weinberg Equilibrium (HWE) was also assessed. Results: This study characterizes functionally significant CD19 polymorphisms in a Mediterranean population, with particular focus on the clinically relevant L174V (rs2904880) variant known to associate with CAR-T therapy resistance. 174V was seen in this cohort with a Minor Allele Frequency (MAF) of 76.3%., and a variant allele homozygosity (V/V) of 65.2%. Conclusions: Our cohort displayed elevated V174 homozygosity compared to other populations, including Europeans, Americans, and South Asians, potentially predisposing to diminished CAR-T efficacy. These findings indorse population-adjusted CAR-T product development, and implementation of pre-therapy CD19 genotyping protocols to identify at-risk patients. Development of CARs targeting conserved CD19-epitopes, or combinatorial antigen approaches is warranted to mitigate resistance.

To rechallenge or not to rechallenge? Immune-checkpoint inhibitor–associated neurotoxicity in advanced melanoma patients.

e24187 Background: Immune checkpoint inhibitors (ICIs) are a cornerstone of therapy for treatment of advanced melanoma. Neurotoxicity (N-TOX) is a known complication of ICI therapy with a frequency of 1-5%. Rechallenging with ICIs is traditionally contraindicated after occurrence of N-TOX, however this is a topic of debate, particularly in patients with progression of disease and minimal residual deficits after N-TOX. Methods: We conducted a retrospective study of 28 patients with advanced melanoma (stage 3 or 4) who developed N-TOX after ICI therapy at Moffitt Cancer Center between 2017 and 2025. Variables collected included ICI regimen, ICI duration, N-TOX syndrome, modified Rankin Scale (mRS) at nadir of N-TOX, mRS at 6-months post N-TOX, and median overall survival post N-TOX. If rechallenged with ICI later in disease course, the 6-month mRS and recurrence of N-TOX, if any, was evaluated. Results: All patients (N = 28) had advanced melanoma at onset of ICI therapy (82% stage 4, 18% stage 3). ICI regimens included PD-1 only (N = 8), PD-1/CTLA-4 (N = 16), or PD-1/LAG-3 (N = 4). The median time from start of ICI therapy to onset of N-TOX was 2.4 months (range 0.2-40.3 months). Neurotoxicity syndromes encountered in our cohort included neuropathy (N = 12), myositis (N = 9), cranial neuropathy (N = 4), myasthenia gravis (N = 3), encephalitis (N = 3), transverse myelitis (N = 1), and vasculitis (N = 1). The average N-TOX CTCAE score was 2.9 (range 2-5). Median mRS at nadir of N-TOX was 3 (range 1-6) and median 6-month mRS post N-TOX was 1 (range 0-6). 59% of patients had a 6-month mRS post N-TOX of less than or equal to 1. Median overall survival after N-TOX was 20.2 months (range 0.7-54.1 months). 48% of patients (N = 13) had progression of disease after cessation of ICI therapy. 14% of patients (N = 4, 3 with neuropathy and 1 with cranial neuropathy, mRS nadir range 2-3, all with 6-month mRS post N-TOX of 1) were later rechallenged with ICIs due to progression of disease, with no recurrence of N-TOX noted in any of these patients. Conclusions: N-TOX after ICI therapy in our cohort was usually moderately disabling at nadir, with most patients having minimal residual neurologic deficits at 6-months after N-TOX. ICIs were safely rechallenged in 4 patients in our cohort without N-TOX recurrence, suggesting that ICI rechallenge may be safe in selected patients with progression of disease and minimal residual neurologic disability after N-TOX.

Analyzing county-level factors of oncology fellowship program development from 2015-2025.

9003 Background: In the United States (US), access to oncology care varies geographically. One factor that may contribute to regional shortages is the distribution of oncology fellowship programs. We aimed to assess urban-rural trends in newly created oncology fellowship programs and to identify county-level factors associated with a higher likelihood of gaining a new oncology fellowship program. Methods: Data on all hematology/oncology and oncology fellowship positions in 2015 and 2025 were manually extracted from National Resident Matching Program (NRMP) data. A cross-sectional analysis was performed using data from 3,211 US counties to examine program development from 2015-2025. County metrics came from US Census data and physician density was calculated using the Doctors and Clinicians national downloadable file. A model was developed using Firth’s penalized logistic regression with the following predictors using 2015 data: oncologist density per 100,000 population, median household income, percentage of population with insurance, rurality (binary with rural county coded as 1), and state-level Medicaid expansion status in 2015 (binary with expansion state coded as 1). The outcome variable was counties that gained a new oncology fellowship program (n=44). Results: In 2015, there were 140 fellowship programs in the US with 1 program in a rural county (0.6%). By 2025, there were 180 fellowship programs with 3 programs in rural counties (1.7%). The total fellowship slots grew from 521 to 773 at a rate of 25.2 new fellowship slots per year. The results from the regression model are shown in Table 1. Higher household median income significantly predicted fellowship establishment (OR 1.62, 95% CI 1.25-2.06, p-value <0.001), and rurality significantly predicted no fellowship establishment (OR 0.04, 95% CI 0.01-0.14, p-value < 0.001). Conclusions: Despite robust growth in the number of oncology fellowship programs and slots, expansion into rural and underserved areas remains disproportionately small. The majority of new programs continue to cluster in urban centers, suggesting that increases in fellowship capacity have not effectively addressed geographic disparities in care. We found that new oncology fellowship programs systematically emerge in more affluent urban counties with pre-existing oncology workforces. Strategic policy interventions including location-based incentives and rural training tracks should be considered to improve the distribution of fellowship programs. Firth logistic regression model results. Variable Odds Ratio (OR) 95% Confidence Interval P-Value Intercept 0.01 0.01-0.02 <0.001 Household Median Income 1.62 1.25-2.06 <0.001 Percentage of Population with Insurance 0.74 0.51-1.15 0.17 Oncologist Density (providers per 100,000 population) 1.18 1.05-1.29 0.02 Medicaid Expansion Status 3.13 1.57-6.55 0.001 Rurality (RUCC) 0.04 0.01-0.14 <0.001

The association of baseline fatigue and severe cancer treatment toxicity by comorbid conditions: A pooled analysis.

11036 Background: Fatigue is commonly reported by patients with cancer. Patients who report fatigue are at greater risk of severe adverse events during treatment. However, it is unknown whether the relationship between baseline fatigue and toxicity risk persists after accounting for comorbid conditions. Methods: Data from 6 SWOG phase 2/3 clinical trials in advanced cancer (1999 to 2018) were pooled. Baseline fatigue (classified by 5-point Likert scale) was analyzed as any vs none. Patients were linked to Medicare claims by SSN, date of birth, and sex to identify comorbidities at study registration. Adverse events (AEs) were classified using the Common Terminology Criteria for Adverse Events. The primary outcome was severe (≥ grade 3) events. Odds ratios (ORs) were calculated using generalized estimating equations, clustered by study, and adjusted for age, sex, race, and obesity. Interaction tests between fatigue and each comorbidity were examined. Results: Among 1195 patients (median age, 73; 13.1% female; 11.8% Black; 74% prostate cancer), 629 (52.6%) had ≥1 severe AE. Among patients with ≥1 comorbid condition, those with any fatigue had a 132% (OR=2.32, 95% CI, 1.26-4.27, p=.007) increased risk of having severe AEs; among patients with no comorbidities, the association was nearly identical (OR=2.33, 95% CI, 1.51-3.60, p<.001; p-interaction=.97). Those with any fatigue had a twofold or greater risk of severe AEs across all comorbidities (Table). The association between fatigue and severe toxicity was greater for those with anemia (interaction p=.03) and those with depression (interaction p=.02). Conclusions: The association between baseline fatigue and severe treatment toxicity persisted after accounting for comorbid conditions, indicating baseline fatigue is an independent risk factor. The association was stronger among patients with anemia and those with depression, suggesting these conditions may amplify the risk of baseline fatigue. These findings support early identification of baseline fatigue and targeted supportive interventions for these high-risk populations. Association of baseline fatigue and severe toxicity by comorbid conditions. No comorbidity Comorbidity Comorbidity OR (95% CI) p-value OR (95% CI) p-value p-interaction Depression 2.24 (1.28-3.92) 0.005 4.32 (2.58-7.23) <0.0001 0.02 Anemia 2.15 (1.30-3.57) 0.003 3.05 (1.35-6.87) 0.007 0.03 Respiratory disorders (COPD, sleep apnea) 2.30 (1.35-3.94) 0.002 2.73 (0.99-7.55) 0.05 0.58 Hypothyroid 2.30 (1.34-3.95) 0.003 2.64 (1.33-5.23) 0.005 0.57 Diabetes 2.29 (1.35-3.89) 0.002 2.41 (1.24-4.71) 0.01 0.73 Hypertension 2.26 (1.36-3.78) 0.002 2.37 (1.25-4.50) 0.008 0.73 Cardiovascular disease 2.42 (1.39-4.22) 0.002 2.04 (1.15-3.63) 0.02 0.25 Autoimmune diseases 2.33 (1.34-4.04) 0.003 1.99 (1.15-3.43) 0.01 0.7 Any comorbidity (all comorbidities) 2.33 (1.51-3.60) <0.001 2.32 (1.26-4.27) 0.007 0.97

Lung cancer screening for early detection of suspicious lung nodules in Latin America (LUCAS-LATAM).

TPS10631 Background: Lung cancer (LC) remains the leading cause of cancer-related death in the Latin American (LATAM) region, accounting for 1 in 10 cancer deaths, attributable to late stage diagnosis in above 85%. Clinical utility of low-dose CT (LDCT) in early detection of LC has been established. However, these trials primarily focus on smokers, excluding non-smokers, who account for over one-third of LC globally. Recent studies document a need to expand screening criteria. Prevalence of light smokers and non-smokers among LC patients in LATAM is high (35% of patients being non-smokers). Geographic and socio-economic barriers hinder early detection of LC. Despite effectiveness, access to LDCT is limited in LATAM. Artificial intelligence (AI) based algorithms have demonstrated improved accuracy in predicting the risk of LC among patients with an incidental pulmonary nodule (IPN) detected on chest radiographs. Qure.ai has developed a model (qXR) that generates a lung nodule malignancy score (LNMS) based on the nodule's characteristics in a chest X-ray (CXR): low risk or high risk. Methods: Prospective study to assess LC screening with LDCT in LATAM and prospectively evaluate qXR in CXR at the initial visit correlating with the finding of the initial LDCT in patients with other high risk criteria to develop LC. 2000 patients will be recruited in 4 LATAM countries (Mexico 700 pts, Costa Rica 300 pts, Colombia 500 pts, Argentina 500 pts) Inclusion criteria include patients ≥50 years of age with one of the following: a. exposure to wood smoke (at least 100 hours/year), b. family history of LC in a first degree relative, c. COPD and/or emphysema, d. smokers with tobacco index of 10 y or more. Exclusion criteria: a. LC diagnosis or other type of cancer 5 years prior to screening, b. loss of 10% of baseline weight 6 months before, c. ineligible for LDCT, d. life expectancy ≤5 years, and e. previous history of pulmonary nodules. The primary objective of the study is the utility of LDCT-based LC screening in identifying suspicious lung nodules in smokers and non-smokers across LATAM, with secondary objectives including: 1- Utility of qXR-LNMS of CXR for LC risk assessment to exclude low risk patients from LDCT screening, 2- Utility of LDCT-based LC screening in subjects with various risk profiles in LATAM, 3- Prevalence of lung nodules in the study population, 4-Mortality rate in the subjects diagnosed with an anomaly in the LDCT (with or without LC diagnosis). Study design: Visit 1: CXR by qXR and LDCT1 Visit 2: LDCT2 : (12/24 months as applicable ± 2 weeks)(interval of LDCT2 is determined by the findings of the Visit 1) Low risk by qXR and Lung RADS 1 or 2: repeat in 24 months Low risk by qXR and Lung RADS 3, high risk by qXR and Lung RADS 1, 2, 3: repeat in 12 months Telephonic follow-up visits (at 6 month interval post LDCT2 for 2 years) Any Lung RADS 0, 4A, 4B, 4X or S will be assed in a thoracic oncology multidisciplinary team.

Clinical outcomes of patients with RTK-RAS pathway alterations by treatment type: The MD Anderson Cancer Center IMPACT 2 study.

3151 Background: The receptor tyrosine kinase (RTK)-RAS signaling axis comprises distinct membrane receptors and downstream effectors that regulate cell proliferation and survival. Alterations in this pathway drive carcinogenesis and are associated with poor prognosis. We analyzed the outcomes of patients with RTK-RAS pathway alterations enrolled in the IMPACT 2 study (2014-2023; NCT02152254). Methods: Patients with advanced cancer underwent tumor biopsy and molecular profiling (CLIA-certified lab). Pathway analysis was conducted using the maftools R package. RTK-RAS pathway alterations were defined as those involving EGFR, ERBB2, ALK, MET, KRAS, NRAS, BRAF , and MAP2K1/2 genes. Cases were discussed at Molecular Tumor Board meetings. Patients were treated in clinical trials with investigational agents, including matched targeted therapies (MTTs) when available. We analyzed the following outcomes by treatment type (MTT vs. non-matched targeted therapy [NTT] and immunotherapy [IO] vs. non-IO): objective response rate (ORR; complete response + partial response), clinical benefit rate (CBR; ORR + stable disease≥4 months), progression-free survival (PFS), and overall survival (OS). Results: Of 491 treated patients with targetable alterations, 216 (44%) had RTK-RAS pathway alterations (median age, 62.3 years [range, 21-80]; female, 54.1%; ECOG performance status 1, 90.3%; median number of prior therapies, 3 [range, 0-10]; liver metastases, 46.3%; > 2 metastatic sites, 34.7%; high LDH, 37.0%; low albumin level, 11.1%). The most common cancers were gastrointestinal (40.3%), head/neck (10.2%), and lung (10.2%). Other tumor characteristics included PD-L1≥1%, 43.6% (58/133); MSI-H, 1.3% (2/153); and TMB-H, 10.7% (16/150). Concomitant pathway alterations were TP53 (62.5%), PI3K (26.9%), and cell cycle (34.3%) pathways. MTT targeted EGFR, n = 8; FGFR, n = 10; HER2, n = 6; BRAF+MEK, n = 3; ALK, n = 1; and MEK, n = 4 among others (n = 24). Clinical outcomes are shown in the Table. Conclusions: The ORR was 14.6% in IO-treated patients vs. 5% in the non-IO-treated group (p = 0.049), although the difference was not significant. No differences in PFS or OS were observed by therapy type in patients with RTK-RAS pathway alterations. Novel MTTs (i.e., KRAS inhibitors) that were unavailable during the study period may improve the outcomes of these patients. Identification of molecular subsets benefiting from MTT is needed. Clinical trial information: NCT02152254 . All patients MTT NTT P value IO Non-IO P value N=216 N=56 N=160 N=57 N=159 ORR (%) 14/189 (7.4) 5/50 (10) 9/139 (6.5) 0.53 7/48 (14.6) 7/141 (5) 0.049 CBR (%) 110/189 (58.2) 31/50 (62) 79/139 (56.8) 0.62 27/48 (56.3) 83/141 (58.9) 0.87 Median PFS, months(95% CI) 2.96(2.3, 3.81) 3.09(2.66, 8.02) 2.89(1.97, 4.08) 0.5 2.3(1.61, 5.42) 3.19(2.66, 4.08) 0.72 Median OS, months(95% CI) 7.36 (5.69, 9.21) 5.88(4.7, 18.28) 7.79(5.69, 9.44) 0.10 6.61(4.6, 12.76) 7.46(5.69, 9.21) 0.85

Insurance, hospital, and racial disparities in surgical treatment and mortality among patients with neuroendocrine tumors: A national analysis.

4184 Background: Neuroendocrine tumors (NETs) are the second most common gastrointestinal malignancy with increasing incidence. Surgical resection remains curative, yet population-level disparities data are lacking. We examined insurance, hospital, and racial disparities in NET surgical treatment and outcomes. Methods: Using the National Inpatient Sample (2019-2022), we identified NET hospitalizations (ICD-10: C7A, C7B, C25.4, C4A). Outcomes were surgical resection and in-hospital mortality. Multivariable logistic regression estimated adjusted odds ratios (aOR) by insurance, hospital type, and race, controlling for demographics, tumor site, and metastatic status. Results: Among 198,955 NET hospitalizations (mean age 64.9 years; 52.7% metastatic), surgical resection was 35.3% and mortality 5.2%. Medicaid (aOR 0.58, 0.56-0.60) and Medicare (aOR 0.64, 0.63-0.66) patients had significantly lower surgery odds versus private insurance (p<0.001). In localized disease, surgery rates were 58.9% (Private) vs 36.9% (Medicare). Rural patients had 50% lower surgery odds (aOR 0.50, 0.48-0.53) and 47% higher mortality (aOR 1.47, 1.34-1.61) versus urban teaching hospitals. Black patients had 19% lower surgery odds (aOR 0.81, 0.78-0.83) and 18% higher mortality (aOR 1.18, 1.11-1.25) versus White patients. Conclusions: This largest national NET analysis reveals profound multilevel disparities: Medicaid/Medicare patients are 36-42% less likely to receive surgery, rural patients face 50% lower surgical access with 47% higher mortality, and Black patients experience significant treatment and survival inequities. Findings support targeted interventions including insurance coverage expansion, rural referral networks, and equity-focused initiatives. Multilevel disparities in surgical resection and mortality among patients with neuroendocrine tumors. Disparity Type Comparison N Surgery Rate Mortality aOR (Surgery) aOR (Mortality) 95% CI P-value Key Finding Overall Cohort — 198,955 35.3% 5.2% — — — — Mean age 64.9y; 52.7% metastatic INSURANCE DISPARITIES Insurance Medicare vs Private — 29.9% vs 45.3% — 0.64 0.90 0.63-0.66 / 0.84-0.95 <0.001 36% lower surgery odds Insurance Medicaid vs Private — — — 0.58 1.26 0.56-0.60 / 1.16-1.37 <0.001 42% lower surgery; 26% higher mortality HOSPITAL DISPARITIES Hospital Rural vs Urban Teaching — — 7.0% vs 4.9% 0.50 1.47 0.48-0.53 / 1.34-1.61 <0.001 50% lower surgery; 47% higher mortality RACIAL DISPARITIES Race Black vs White — — — 0.81 1.18 0.78-0.83 / 1.11-1.25 <0.001 19% lower surgery; 18% higher mortality Localized NETs Private vs Medicare 87,100 58.9% vs 36.9% 1.7% vs 3.6% — — — — 22-point surgery gap

Use of optical genome mapping (OGM) to identify atypical or cryptic <i>KMT2A</i> (11q23) rearrangements and genomic structural mechanisms in acute myeloid leukemia.

e18537 Background: KMT2A translocation and rearrangements are recurring chromosome abnormalities in acute leukemia and define a clinically important subset of acute myeloid leukemia (AML) with implications for diagnosis, prognosis, and therapeutic planning. KMT2A fusions frequently arise through various chromosome translocations, but may result from complex, multi-break structural variants (SVs) alterations, which can be cryptic by conventional chromosome analysis and FISH testing. Optical genome mapping (OGM) enables genome-wide SV and copy number alterations (CNAs) detection and may clarify genomic mechanisms of the fusions not apparent by karyotype and FISH testing. Methods: We applied OGM to clinical cases with suspected cryptic/complex KMT2A rearrangements, and compared with karyotyping, FISH, and targeted RNA sequencing (Archer FusionPlex). OGM results were reviewed to define SV structures, genomic mechanisms, and involved genomic junction and segments. Results: Three AML cases with cryptic KMT2A fusion cases were collected and analyzed. Two cases with KMT2A :: MLLT10 fusion showed no numerical or structural abnormalities involving both chromosomes 10 and 11 by karyotyping analysis and a normal KMT2A break-apart FISH pattern. OGM revealed an insertion mechanism in both, consistent with a 3’ MLLT10 portion inserted into the KMT2A locus. In one case, an ~900 kb inserted segment included 3′ MLLT10 and downstream genes; in the other, an ~150 kb 3′ MLLT10 segment was inserted, and OGM additionally detected a duplication involving MLLT10 with an adjacent gene. One case with KMT2A::MLLT3 fusion was cryptic by karyotype; OGM resolved the mechanism as insertion of an ~600 kb segment including 5′ KMT2A into the MLLT3 locus. Notably, this case also demonstrated copy-neutral loss of heterozygosity of the short arm of the derivative chromosome 9 spanning the insertion, suggesting potential allelic enrichment of the abnormal segment. A larger cohort analysis is ongoing. Conclusions: OGM complements routine cytogenetics by detecting and clarifying atypical, cryptic and novel gene fusions, including insertion-based mechanisms that may not be detected by karyotype or FISH testing. Our experience in these three AML cases with KMT2A fusions support OGM as a complementary approach in AML and other leukemia workup, especially in settings where RNA-based fusion testing is not routinely performed. Ongoing study on additional cases will expand the cohort and explore associations between SV mechanism, clinical outcomes, and response to Menin inhibitor therapy.

On the borderline: GEJ coding as a driver for stage migration and survival difference—A SEER analysis.

e16151 Background: The classification of gastro-esophageal junction (GEJ) tumors as esophageal (ICD-O-3 C15.5, C15.2) versus gastric cardia (C16.0) differs by institutional practice. We postulated that this coding heterogeneity leads to stage migration, which could impact trial eligibility and survival comparisons by assigning different stages to physiologically comparable tumors. Methods: Using SEER Research Data (17 Registries, 2000-2022), we identified 23,892 patients individuals with adenocarcinoma at the GEJ border (C15.2/C15.5 "esophagus-coded" vs. C16.0 "stomach-coded").Overall survival (OS) and stage distribution differences (chi-square test) were the main results. Overall and stratified by AJCC 7th edition stage, we conducted Kaplan-Meier and Cox regression analyses. Log-rank tests were used to evaluate within-stage survival differences in order to identify stage migration effects. Results: Esophagus-coded tumors (n = 10,705) versus stomach-coded tumors (n = 13,187) showed significantly different stage distributions (p = 2.1×10⁻³⁷). Stomach-coded tumors had higher stage IV prevalence (43.0% vs 37.0%) and lower stage III (22.1% vs 26.5%). Advanced-stage disease (III-IV) was more common in stomach-coded tumors (65.1% vs 63.5%, p = 0.01). Overall median survival was similar (13 vs 12 months, log-rank p = 0.62), but within-stage survival differed significantly in stages II, III, and IV (p = 0.0003, p = 0.01, p = 0.004, respectively), with no difference in stage I (p = 0.11). In stage II, esophagus-coded tumors showed worse survival despite earlier nominal stage. Results persisted in sensitivity analyses restricted to specified anatomic sites excluding NOS codes (n = 19,030). Conclusions: GEJ adenocarcinomas that are otherwise the same but coded as esophageal in some settings and gastric in others show consistent stage migration and survival differences even within the same stage, indicating that coding conventions can bias stage-based comparisons. This directly affects how we design clinical trials, write treatment guidelines, and interpret comparative effectiveness studies. To make results comparable across datasets and institutions, we need either standardized GEJ classification rules or a GEJ-specific staging framework.

Efficacy and safety of CD3×CD20 bispecific antibodies in Richter transformation: A systematic review of prospective trials and comparative analysis.

e19095 Background: Richter transformation (RT), the progression of chronic lymphocytic leukemia to aggressive diffuse large B-cell lymphoma, carries poor outcomes. Chemoimmunotherapy (CIT), including R-CHOP, remains commonly used in the frontline setting, while CD19-directed CAR T-cell therapy is used mainly in relapsed/refractory (R/R) disease but is limited by toxicity and access. CD3×CD20-targeting bispecific antibodies (BsAbs) are off-the-shelf immunotherapies with emerging prospective data in RT. We systematically evaluated the efficacy and safety of BsAbs across treatment lines. Methods: We did a systematic search on PubMed, Google Scholar, and ClinicalTrials.gov. Updated studies of four trials met the inclusion criteria. Outcomes were stratified by line of therapy (first-line [1L] vs relapsed/refractory [R/R]) and regimen (monotherapy vs combination). Primary endpoints were overall response rate (ORR) and complete response (CR) per Lugano 2014 criteria. Cytokine release syndrome (CRS) was graded per ASTCT criteria. Results: A total of 138 patients were evaluated (97 monotherapy, 41 combination). In the 1L setting (n=21), epcoritamab monotherapy achieved an ORR of 57% and CR rate of 52%, with an mOS of 27.5 months, more than doubling historical CIT (R-CHOP) survival (&lt;12 months). In R/R RT, mosunetuzumab (n=20) and glofitamab (n=11) demonstrated ORRs of 40% and 63.6% with CR rates of 20% and 45.5%, respectively. The BLINART study with Blinatumomab (n=25) reported an ORR of 46% and CR of 20%. Combination regimens (n=41) showed favorable responses similar to those reported with CD19-directed CAR T-cell therapy in multicenter registries, though cross-trial comparisons are limited: epcoritamab plus lenalidomide achieved a CR rate of 73%, and epcoritamab plus R-CHOP achieved a CR of 60%. Grade ≥3 CRS occurred in &lt;9% of patients, lower than rates reported with CAR T-cell therapy (16%). Neutropenia was the most common grade ≥3 adverse event. Conclusions: CD3×CD20 bispecific antibodies demonstrate meaningful clinical activity in RT, with signals of improved frontline survival versus historical CIT and favorable efficacy and safety across R/R settings. More data from clinical trials is needed to establish clear superiority. Prospective CD3×CD20 BsAb trials in RT and comparison with R-CHOP and CAR T cell therapy. Trial / Regimen Population N ORR (%) CR (%) mOS Gr ≥3 CRS Epcoritamab + Lena R/R 11 82.0% 73.0% NR 9.0% Epcoritamab + R-CHOP R/R 30 73.0% 60.0% 16.4 mo 3.0% Epcoritamab Mono 1L 21 57.1% 52.0% 27.5 mo 7.0% Glofitamab Mono R/R 11 63.6% 45.5% NR 0.0% Mosunetuzumab Mono R/R 20 38.1% 29.0% 9.8 mo 7.0% Epcoritamab Mono R/R 20 40.0% 20.0% 11.4 mo 5.0% Blinatumomab (Seq) R/R 25 36.0% 20.0% NR 8.0% CIBMTR (CAR-T Ref) R/R 140 — — 46.6% (2-yr OS) — Kittai et al. (CAR-T Ref) 1L 69 63.0% 46.0% 8.5 mo 16.0% R-CHOP (CIT Ref) 1L — 40–60% 20.0% 6–12 mo 0.0%