Citations

Abstract The B-cell maturation antigen (BCMA)–targeting bispecific T-cell engager pavurutamab (AMG 701) directs the cytotoxic T-cell response toward multiple myeloma (MM) cells. This phase 1/1b, open-label, dose-exploration and dose-expansion study evaluated the safety, tolerability, and efficacy of pavurutamab monotherapy in patients with triple-class relapsed/refractory MM (RRMM). Pavurutamab (5-18 000 μg) was administered IV weekly with step-up dosing in week 1. Overall, 172 patients received at least 1 dose of pavurutamab; 73 received the recommended phase 2 dose (RP2D; 18 000 μg), with 2 different step-up dosing regimens in phase 1b. Twelve patients had dose-limiting toxicities, which included cytokine release syndrome (CRS) and increased transaminases; none of which occurred at the RP2D. The most frequently reported treatment-emergent adverse events included CRS (74.4%), anemia (61.0%), neutropenia (47.1%), and hypophosphatemia (45.3%). Grade ≥3 infections were noted in 60 patients (34.9%). The overall response rate (ORR) was 46.5% among all patients and 65.8% (very good partial response [VGPR] or better, 60.3%) among 73 patients treated at the RP2D. At median follow-up of 17.2 months, median duration of response (DOR) was 36.6 months (95% confidence interval [CI], 22.3 to not estimable). Median progression-free survival (PFS) for all patients was 5.5 months (95% CI, 2.8-10.1) and 16.8 months (95% CI, 5.0 to not estimable) with the RP2D. Pavurutamab exposure generally increased in a dose-proportional manner, with high soluble BCMA levels correlating with lower exposure level. The acceptable safety profile, pharmacokinetics, and preliminary efficacy of pavurutamab supports anti-BCMA T-cell engager therapy in heavily pretreated patients with RRMM. This trial was registered at www.clinicaltrials.gov as NCT03287908.

ABSTRACT Intrinsic Acinetobacter -derived cephalosporinases (ADCs) in Acinetobacter baumannii are AmpC-type β-lactamases that confer resistance to β-lactam agents, typically through insertion sequence (IS) element-driven overexpression. However, the contribution of ADCs to resistance against advanced β-lactam agents has not been systematically investigated. Given the increasing clinical use of these agents, including cefiderocol, we analyzed the diversity and function of ADC variants in a global collection of carbapenem-resistant A. baumannii (CRAb) isolates. We identified 52 distinct ADC variants in a collection of 428 CRAb clinical isolates from the United States. Among these, variants carrying both a valine substitution at position 292 in the R2 loop and an alanine duplication (ADUP) in the Ω loop consistently conferred stable resistance to cefiderocol. Biochemical and crystallographic analyses demonstrated that ADC-227, which harbors a V292W substitution with an ADUP at position 218a in the Ω loop, exhibits enhanced catalytic efficiencies for ceftazidime and cefiderocol and moderately reduced inhibition by avibactam, leading to resistance not only to cefiderocol but also to ceftazidime–avibactam. Structural studies revealed conformational flexibility of the R2 loop, allowing dynamic accommodation of substrates. Collectively, the findings identify Val292, in combination with an ADUP in the Ω loop, as a mutational “hot spot” for ADCs evolution that may undermine the efficacy of newer β-lactams, including cefiderocol. These results underscore the need for ongoing molecular surveillance of A. baumannii isolates to detect and track the emergence of such variants in clinical settings. IMPORTANCE Carbapenem-resistant Acinetobacter baumannii (CRAb) has been designated as a critical priority pathogen by the World Health Organization (WHO). Cefiderocol has been introduced as a novel therapy against CRAb; however, recent clinical data highlight concerning treatment failures and excess mortality. Understanding resistance mechanisms is therefore essential to preserve the clinical utility of this agent. This study addresses a critical knowledge gap by investigating the role of intrinsic Acinetobacter -derived cephalosporinases (ADCs), which are ubiquitous in A. baumannii and diverse in sequence. By defining specific mutational patterns that endanger cefiderocol activity, this work highlights how chromosomally encoded enzymes can evolve to erode the effectiveness of newer β-lactams such as cefiderocol. These insights underscore the importance of integrating molecular surveillance into clinical practice and antimicrobial stewardship to ensure timely detection of emerging resistance in clinical A. baumannii isolates, ultimately informing treatment strategies and guiding future drug development.

Abstract Purpose: This multicenter, multi-surgeon retrospective study aimed to identify risk factors for postoperative cerebrospinal fluid (CSF) leak following endonasal resection of craniopharyngioma, while evaluating the "perception gap" through a surgeon survey. Methods: A retrospective review was conducted on 416 patients who underwent endoscopic transsphenoidal surgery (ETS) for craniopharyngioma from 20 institutions. Factors were compared between patients with and without postoperative CSF leak, and between Early (2007-2015) and Late (2016-2025) Epochs. Complementing the clinical data, a survey of 19 neurosurgeons captured expert perspectives on risk stratification and management strategies. Results: Overall postoperative CSF leak rate was 13.5% (56/416 patients). Univariate analysis identified predominantly cystic tumors (34% vs. 21%, p = 0.034)and intraoperative lumbar drain (LD) use ( p < 0.028) as associated with postoperative CSF leak. BMI ( p = 0.587), prior surgery ( p = 0.576), and tumor size ( p = 0.363) were not significant. In the multivariable analysis, LD use was associated with a higher postoperative CSF leak rate (OR 1.91, 95% CI 1.06–3.46; p = 0.030). Between Epochs, nasoseptal flap (NSF) utilization increased from 70.7% to 87.6% ( p <0.001). NSF was protective (OR 0.28, 95% CI 0.07–0.92; p = 0.037) in the Early Epoch; no factors were significant in the Late Epoch. The surgeons’ survey identified prior surgery and intraoperative high flow leaks as primary risks; however, their LD protocols diverged from clinical data. Conclusion: Despite increased use of NSF, CSF leak persists. The study highlights a significant divergence between expert perception and clinical data regarding lumbar drains.

Summary Background Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease characterized by aberrantly activated, apoptosis-resistant profibrotic lung (myo)fibroblasts. Prior research has demonstrated that lung fibroblasts from patients with IPF exhibit resistance to DNA damage, suggesting that this behavior contributes to their persistent survival and continuous proliferation. We propose that elevated levels of the DNA damage repair protein RAD51 regulate myofibroblast activation and apoptosis and provide a potential therapeutic target to impede fibrosis progression. Methods Human lung fibroblasts were transfected with siRNA against RAD51 or treated with RAD51-specific inhibitor B02 and markers of fibrosis, DNA damage, apoptosis, metabolic reprogramming, and mitochondrial dynamics were assessed. The preclinical efficacy of B02 was evaluated in human precision cut lung slices (PCLS) and in a mouse model of pulmonary fibrosis. Findings RAD51 expression was significantly upregulated in the lungs and lung fibroblasts of IPF patients. Knockdown or inhibition of RAD51 in fibroblasts reduced profibrotic marker expression, suppressed mTORC1 signaling and mitochondrial function, and increased apoptosis susceptibility. Pharmacological inhibition of RAD51 shifted the profibrotic phenotype towards a fibrosis-resolving state in human and mouse PCLS, and in a bleomycin-induced mouse model of lung fibrosis. Interpretation The inhibition of RAD51 exerts therapeutic benefits in lung fibrosis by promoting apoptosis. Our findings identify that inhibiting RAD51 with B02 in fibroblasts impairs DNA repair and induces metabolic reprogramming, making it a potential therapeutic target. Research in context Evidence before this study Pulmonary fibrosis (PF) is characterized by excessive fibroblast activation and subsequent deposition of extracellular matrix (ECM) proteins, which ultimately disrupt normal lung architecture. A significant contributing factor to the pathogenesis of pulmonary fibrosis is the presence of fibroblasts that are resistant to apoptosis, preventing normal wound healing. Recent studies highlight the DNA repair protein RAD51 as effective in protecting fibroblasts from death induced by chemotherapy and ionizing radiation. These finding suggested that RAD51 could have a role in fibroblast activation and apoptosis resistance in pulmonary fibrosis. Added value of this study We demonstrated that RAD51 is important for maintaining apoptosis-resistant fibrotic fibroblasts and their metabolic abnormalities. Our findings indicated that TGFβ-mediated upregulation of RAD51 reduces DNA damage, activates multiple pathways related to fibroblast activation and proliferation, and induces metabolic reprogramming, ultimately regulating apoptosis. Mechanistically, RAD51 inhibition enhanced p53 acetylation at lysine 120 and upregulated the expression proapoptotic proteins PUMA/BAK in mitochondria, promoting apoptosis. Pharmacological inhibition of RAD51 using the specific inhibitor B02 during the fibrotic phase of experimental lung disease effectively ameliorated pulmonary fibrosis. Implications of all the available evidence Our findings establish that RAD51 plays an important role in the survival of apoptosis-resistant fibrotic fibroblasts. We propose that reducing RAD51 expression leads to the metabolic reprogramming of activated fibroblasts, resulting in decreased mitochondrial respiration, reduced ATP levels, and diminished glycolysis or glutaminolysis. These observations suggest that targeting energy metabolism through RAD51 inhibition could be a viable strategy to enhance apoptosis, thereby creating a therapeutically targetable pathway in fibrotic cells. These findings highlight the potential of RAD51 as a therapeutic target for the treatment of IPF.

Abstract Introduction: Urine cell-free DNA (cfDNA) is a promising ultra-noninvasive analyte for genitourinary cancers (GU) cancers. In this study, we investigated urine cfDNA fragmentomic features and evaluated their ability to predict the tumor tissue of origin. Methods: A total of 204 GU cancer patients and 34 healthy adults were enrolled in this prospective study. Preoperative urine was collected from 89 bladder cancer (BC) patients (64% muscle-invasive) undergoing cystectomy, 65 renal cell carcinoma (RCC) patients undergoing nephrectomy and 50 metastatic prostate cancer (mPC) patients. Urine cfDNA was isolated and sequenced at 5x genome-wide coverage on a NovaSeq S4 flow cell. To identify malignant tissue of origin, we analyzed somatic copy number alterations (CNAs), genome-wide fragment length ratios, and 4-mer end motifs. CNAs and tumor fraction (TFx) were quantified using ichorCNA in 1-Mb windows, while chromosome arm-level fragment count z-scores and fragment length ratios were calculated in 5-Mb bins across the genome. Relative frequencies of all 256 possible 4-mer end motifs were calculated for each sample. Individual logistic regression models were developed based on each fragmentomic feature using leave-one-out cross validation (LOOCV). Outputs from these models were combined into multi-feature XGBoost models. Cohort-specific end-motif enrichments were identified using Kruskal-Wallis tests with FDR correction. Motifs were then hierarchically clustered based on their cohort-wise median frequencies to define groups of motifs with shared fragmentation patterns. Results: Across urine cfDNA in the GU cohort, BC showed the highest mean TFx at 10.0%, followed by mPC at 3.6% and RCC at 2.7%. A machine learning model based on 4-mer end motifs achieved a mean ROC AUC of 0.933 with classification accuracies of 63% for healthy, 87% for BC, 72% for mPC, and 83% for RCC. This model outperformed models based on ichorCNA (AUC = 0.767), chromosome arm fragment-count z-scores (AUC = 0.827), and fragment length ratios (AUC = 0.674). Combining end motifs with other fragmentomic features did not improve prediction accuracy. Multi-feature models incorporating end motifs with ichorCNA, chromosome arm-level z-scores, or fragment-length ratios yielded mean AUCs between 0.908-0.924, lower than the end-motif only model. Kruskal-Wallis tests identified 179 of 256 end motifs (79%) as significantly different across healthy, BC, mPC, and RCC. Hierarchical clustering of cohort-level median motifs revealed distinct end motif patterns: Motifs beginning with CT were enriched in RCC; AAAA was strongly enriched in BC; and motifs beginning with CA, AC, and AG were enriched in mPC. Conclusion: Urine cfDNA 4-mer end motifs capture GU cancer-specific biological patterns that enable accurate tissue-of-origin prediction, underscoring their promise as a diagnostic tool. Citation Format: Jessica Linford, Pradeep S. Chauhan, Irfan Alahi, Yohan Kim, Arpit Panda, Nathan Colon, Ryan Mueller, Faridi Qaium, Eric H. Kim, Melissa A. Reimers, Zachary L. Smith, Woodson W. Smelser, Fabrice Lucien-Matteoni, Aadel A. Chaudhuri. Urine cfDNA 4-mer end-motif signatures outperform other fragmentomic features for tissue-of-origin classification in genitourinary cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 2590.

Abstract Background: Adhering to 2018 World Cancer Research Fund (WCRF)/American Institute for Cancer Research (AICR) Cancer Prevention Recommendations is reportedly associated with better survival among long-term colon cancer survivors (likely affected by immortal time bias). Thus, it is important to validate survival benefits by assessing adherence shortly after diagnosis, and further investigation is needed to examine its association with chemotherapy outcomes. Methods: Using an NCI-sponsored adjuvant chemotherapy trial conducted in patients with stage III colon cancer (CALGB/SWOG 80702; NCT01150045), we included 1,666 patients who returned valid Willett food frequency questionnaires (FFQ) at chemotherapy initiation and derived WCRF/AICR scores accordingly (higher score suggesting higher adherence). The primary outcome was disease-free survival (time from FFQ completion to recurrence or death), and secondary outcomes were reduced relative dose intensity (RDI; &lt;85% suggesting worse completion) and severe toxicities (grade ≥3 for any chemotherapy-related toxicity). To estimate the associations of WCRF/AICR scores (quartiles) with survival and chemotherapy outcomes, we conducted multivariable Cox proportional hazards regression for disease-free survival and multivariable logistic regression for reduced RDI and severe toxicities. Results: Compared to those in the lowest quartile of the WCRF/AICR score, patients in the highest quartile had significantly better disease-free survival (hazard ratio: 0.75 [0.58, 0.98], Ptrend = 0.02) and lower risk of reduced RDI (odds ratio [OR]: 0.74 [0.54, 1.00], Ptrend = 0.03), but not for severe toxicities (OR: 1.24 [0.93, 1.67], Ptrend = 0.11). Conclusions: In patients with stage III colon cancer, higher adherence to WCRF/AICR recommendations was associated with better survival and chemotherapy completion, but not for severe toxicities. Funding: https://acknowledgments.alliancefound.org Citation Format: En Cheng, Chao Ma, Qian Shi, Anthony F. Shields, Peter T. Campbell, Ardaman P. Shergill, Katherine A. Guthrie, Felix Couture, Philip Kuebler, Pankaj Kumar, Benjamin Tan, Smitha S. Krishnamurthi, Kimmie Ng, Eileen M. O'Reilly, Justin C. Brown, Philip A. Philip, Jeffrey A. Meyerhardt. Associations of WCRF/AICR recommendations with survival and chemotherapy outcomes in colon cancer: CALGB/SWOG 80702 (Alliance) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 5038.

Abstract The CoMMpass study (NCT01454297) is a prospective, longitudinal observational study involving 1,141 newly diagnosed multiple myeloma (NDMM) patients. Bone marrow aspirates from the study participants were collected for comprehensive molecular characterization of tumor (using bulk RNA sequencing and whole genome sequencing) and tumor immune microenvironment using 3’ single-cell RNA sequencing (scRNA-seq). To support exploration of this rich multi-omic dataset, we developed CoMMpass Explorer (CE), an intuitive interactive platform that enables real-time analysis of clinical and genomic data from CoMMpass. A central feature of CE is cohort building, where users can filter and stratify patients by clinical, genomic, and survival data elements to create custom cohorts for analysis. CE provides five main views: Overall Summary for clinical feature distribution, Kaplan-Meier curves, and multivariate Cox proportional hazards models; Mutational Profile for visualizing and comparing somatic mutations; Tumor Profile for bulk differential expression and gene set enrichment; Immune Microenvironment for comparing cell type abundance and cell cycle dynamics between cohorts using scRNA-seq data; and Pseudo-Bulk, which aggregates single-cell expression by cell type to enable cohort-level comparisons of transcriptional programs using DEseq2. CE reproduces prior CoMMpass studies, including WEE1 expression being associated with poorer progression-free survival (Simhal, et al.) and different mutation frequencies between African American and European American patients (Manojlovic, et al.). We further demonstrate CE’s utility by interrogating the 2025 Consensus Genomic Staging (CGS) risk classification system (Avet-Loiseau, et al). We compared CGS high-risk (HR, n=249) vs. CGS standard-risk (SR, n=573) patients. HR patients have significantly worse progression-free survival, overall survival, and time to second-line therapy compared with SR patients. Univariate models recapitulated expected differences in the clinical features that define CGS risk. Bulk tumor RNA-seq and ssGSEA highlighted a more proliferative and genomically unstable transcriptional program in HR group, with upregulation of angiogenesis and cell-cycle-related pathways. In the immune microenvironment, monocytes were more abundant in the SR group. Pseudo-bulk RNA-seq of plasma cells showed overexpression of ANXA1, NSD2, IGF1R, MAF and related genes in HR. CE democratizes access to the CoMMpass multi-omic resource, allowing researchers to interrogate clinical and molecular heterogeneity. By enabling hypothesis generation and replication of published results, CE serves as a valuable tool for identifying prognostic biomarkers and meaningful patterns in gene expression, mutation profiles, and the immune microenvironment. Citation Format: Wanxing Zhang, Chaitanya R. Acharya, Steven M. Foltz, David E. Avigan, Samir Parekh, Ravi Vij, Shaji Kunnathu Kumar, Taxiarchis Kourelis, Sagar Lonial, Hearn Cho, Ioannis S. Vlachos, Sacha Gnjatic, Li Ding, Manoj Bhasin, George Mulligan. CoMMpass Explorer: An interactive platform to explore clinical and genomic data from newly diagnosed multiple myeloma patients from the landmark CoMMpass observational study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 5504.

Abstract Background: Multiple myeloma is the second most common adult blood cancer and remains incurable, despite recent advances. The IMWG/IMS recently published updated risk criteria, Consensus Genomic Staging (CGS), combining genomic events with clinical measures to identify high-risk patients (Avet-Loiseau, et al. JCO 2025). We applied CGS risk criteria to baseline samples from the Multiple Myeloma Research Foundation CoMMpass Study (NCT01454297), a prospective, longitudinal observational study that enrolled more than1100 participants between 2011-2017. Methods: We assessed patient risk following CGS criteria. Criteria 1: del(17p), with a cutoff of &gt;20% clonal fraction, and/or TP53 mutation. Criteria 2: an IgH translocation including t(4;14), t(14;16), or t(14;20) along with 1q+ and/or del(1p32). Criteria 3: monoallelic del(1p32) along with 1q+ or biallelic del(1p32). Criteria 4: beta-2 microglobulin &gt;= 5.5 mg/L with normal creatinine. Patients meeting one or more criteria were classified as High Risk. To test if risk showed association with genetic ancestry, we grouped patients into those with high African genetic ancestry and those with low African genetic ancestry. Genetic ancestry was measured using ADMIXTURE in comparison to 1000 Genomes. Results: We evaluated the CGS risk status of 877 CoMMpass patients, finding 69.2% (573/828) to be Standard Risk (SR) and 30.8% (255/828) to be High Risk (HR). HR patients showed worse progression-free survival (median PFS 26.3 months vs. 42.5 months; log rank test, p &lt; 0.0001) and overall survival (median OS 63.9 months vs. median not reached; p &lt; 0.0001). 10.6% (91/858) of patients met Criteria 1, 10.7% (93/873) met Criteria 2, 5.6% (49/877) met Criteria 3, and 8.7% (73/835) met Criteria 4. We found 14.2% (123/867) of patients to have high African-like genetic ancestry (AFR-high) and 85.8% (744/867) to have low African-like genetic ancestry (AFR-low). We observed significantly fewer HR patients within the AFR-high group (20%, 23/115) than in the AFR-low group (32.4%, 231/712) (Fisher’s exact test, p = 0.0065). The AFR-high group met HR criteria at a lower rate across all criteria, but only with Criteria 3 was the difference significant (p-value = 0.03). Higher levels of creatinine in AFR-high patients may have impacted meeting the normal creatinine requirement of Criteria 4. Conclusions: HR patients comprise 30.8% of CoMMpass subjects and show significantly worse PFS and OS than SR patients. AFR-high patients met HR criteria at a lower rate than AFR-low patients according to the CGS criteria. Clinical trials that utilize CGS criteria to determine patient eligibility may be challenged to enroll a representative patient population, including AFR-high patients. Screening and eligibility criteria should be carefully considered to mitigate potential enrollment disparities. Citation Format: Steven M. Foltz, Chaitanya R. Acharya, Alexander Gout, Yuxin Jin, David E. Avigan, Ravi Vij, Shaji Kunnathu Kumar, Sagar Lonial, Hearn Cho, Katie Wozniak, Jonathan J. Keats, Craig Cole, John D. Carpten, George J. Mulligan. Multiple myeloma risk classification of CoMMpass using Consensus Genomic Staging identifies differences between patients with high and low African genetic ancestry [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3887.

Abstract Background: Personalizing chemoradiotherapy (chemoRT) for locally advanced non-small cell lung cancer (LA-NSCLC) is limited by the lack of early biomarkers that inform response during treatment. Current circulating tumor DNA (ctDNA) molecular residual disease assays predict post-treatment outcomes but lack mid-treatment utility. ctDNA burden estimation has traditionally relied on variant-centric metrics such as maximum variant allele fraction (Max VAF), which rely on mutation-specific signals and may be confounded by histology-dependent shedding variability, allelic imbalance, and clonal hematopoiesis. Here we present circulating tumor fraction estimate (ctFE), a machine-learning composite score that integrates VAF distributions, copy-number alterations, and germline B-allele frequency deviations to approximate global tumor burden using a widely available, tumor-naïve clinical platform. Methods: A burden-based ctFE threshold was derived using pre-treatment plasma from a prospective phase II clinical trial of MR-guided hypofractionated chemoRT (LA-WU, n=26), locked, and applied unchanged to early mid-treatment samples (day 10-14). To test scalability and generalizability, its prognostic performance was validated in two real-world cohorts: 94 LA-NSCLC patients receiving definitive chemoRT (LA-RW) and 309 oligometastatic NSCLC patients receiving consolidative RT (OM-RW). ctFE and Max VAF were compared as continuous predictors across cohorts. Results: ctFE consistently outperformed Max VAF. In LA-WU, pre-treatment ctFE was associated with overall survival (OS HR=1.15, p=0.04) and progression-free survival (PFS HR=1.84, p=0.009), whereas Max VAF was not. Mid-treatment ctFE remained prognostic for PFS (HR=1.14, p=0.026). Early ctFE dynamics defined three molecular response groups with marked OS separation: consistently low, responder, and nonresponder groups (median OS 60.8 vs 13.0 vs 2.9 months, respectively; p&lt;0.001). In multivariable models including both biomarkers, higher ctFE remained independently associated with worse survival in LA-RW (OS HR=1.88, p=0.010) and OM-RW (OS HR=1.37, p=0.040; PFS HR=1.45, p=0.008), whereas Max VAF did not. The locked ctFE threshold stratified OS across all cohorts (LA-WU HR=5.93; LA-RW HR=9.08; OM-RW HR=2.26; all p&lt;0.001). Conclusion: ctFE provides clinically meaningful pre- and mid-treatment risk stratification and consistently outperforms Max VAF across locally advanced and oligometastatic NSCLC cohorts. We show that ctFE is a biologically informative, clinically generalizable and scalable ctDNA burden metric measurable using a tumor-naïve, off-the-shelf assay, supporting its practical utility in biomarker-adapted radiotherapy strategies. Citation Format: Ayesha Hashmi, Jessica Linford, Pradeep S. Chauhan, Kaushal Parikh, Rotem Ben-Shachar, John Guittar, Malvika Pillai, Jyoti Patel, Matteo Bergsagel, Nicholas P. Semenkovich, Kenneth R. Olivier, Sean S. Park, Dawn Owen, David M. Routman, Katie N. Lee, Alex D. Sherry, Aaron S. Mansfield, Daniel Morgensztern, Ramaswamy Govindan, Clifford G. Robinson, Carmen Bergom, Saiama N. Waqar, Bruna Pellini Ferreira, Gregory R. Vlacich, Aadel A. Chaudhuri. Early ctDNA quantification by ctFE outperforms Max VAF for survival stratification across locally advanced and oligometastatic NSCLC treated with radiotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 1183.