Browse Articles

A systematic review and meta-analysis evaluating role of AI-, ML-, and DL-based models for predicting recurrence risk after curative surgical resection of colorectal cancer liver metastases.

e15517 Background: Recurrence following curative-intent hepatic resection for colorectal cancer liver metastases (CRLM) remains common, affecting up to 70% of patients mostly within the first postoperative year. Conventional clinicopathologic risk stratification tools offer limited discrimination and insufficiently capture biological and spatial heterogeneity. Artificial intelligence (AI), machine learning (ML), and deep learning (DL) approaches enable integration of high dimensional imaging, molecular, immune, and clinical data, and may improve postoperative recurrence risk stratification. Methods: We conducted a systematic review and random-effects meta-analysis comparing the discriminative performance of classical logistic regression (LR) and ML/DL/AI models for predicting postresection recurrence after curative-intent resection of CRLM. PubMed, Scopus, and Web of Science were searched from inception through January 2026 for studies reporting LR- or ML/DL/AI-based prediction of recurrence or time to recurrence, quantified using the area under the receiver operating characteristic curve (AUC) or concordance index. Eligible studies enrolled adults after curative resection and incorporated clinical, pathological, radiomic, or multi-omic predictors; studies lacking discrimination metrics were excluded. To avoid duplication, the best-performing model per study was selected. Discrimination estimates were logit-transformed and pooled using restricted maximum likelihood random-effects models, generating mean AUCs with 95% confidence intervals (CIs) and 95% prediction intervals (PIs). Funnel plot asymmetry was assessed using unweighted Egger tests. Results: Seven LR model evaluations were included, yielding a pooled AUC of 0.711 (95% CI 0.667-0.750; 95% PI 0.583-0.812), consistent with moderate discrimination for postresection recurrence. Seven ML/DL/AI model evaluations demonstrated a pooled AUC of 0.720 (95% CI 0.658-0.775; 95% PI 0.566-0.835), indicating comparable overall performance with a modestly higher point estimate. Egger testing showed no significant asymmetry for LR models (t = 1.65, df = 5, p = 0.160) while ML/DL/AI models exhibited significant asymmetry (t = 2.923, df = 5, p = 0.033), raising concern for potential publication or reporting bias. Conclusions: AI-, ML-, and DL-based models provide clinically meaningful discrimination for predicting recurrence risk following curative resection of CRLM, with pooled performance exceeding conventional risk stratification. Models incorporating imaging, molecular, and clinical features, may enhance risk stratification. Prospective validation, standardized recurrence endpoints, and external calibration are essential to support clinical implementation and postoperative risk stratification.

Updated safety and efficacy of puxitatug samrotecan (Puxi-Sam, AZD8205) in patients (pts) with endometrial cancer (EC) or ovarian cancer (OC): Phase 1/2a BLUESTAR study.

5515 Background: B7-H4, a transmembrane glycoprotein that negatively regulates T cells, is highly expressed in EC and OC. Puxi-Sam (AZD8205), a B7-H4–directed topoisomerase I inhibitor antibody–drug conjugate, showed manageable toxicity and promising antitumor activity in BLUESTAR (NCT05123482) dose-escalation. Here, we report updated safety and efficacy results as EC and OC expansion cohorts are fully enrolled. Methods: Eligible pts were ≥18 years old with relapsed/metastatic B7-H4–positive (≥25% tumor cell staining by central immunohistochemistry) EC or OC and an ECOG PS ≤1. Pts had progressed on prior standard-of-care therapy including platinum-based chemotherapy. Pts with EC received Puxi-Sam at 2.0 or 2.4 mg/kg IV Q3W and pts with OC received Puxi-Sam at 1.6 or 2.4 mg/kg IV Q3W. The primary objectives were to assess safety and tolerability; secondary objectives included assessment of antitumor activity per RECIST 1.1. Results: As of October 30, 2025, 93 pts with EC received Puxi-Sam at 2.0/2.4 mg/kg and 78 with OC at 1.6/2.4 mg/kg. Pts with EC had a median age (min–max) of 63.5 (52–78)/65 (34–81) years, respectively, and median prior lines of therapy (LOT) was 1. Pts with OC had a median age of 58 (28–79)/59 (35–74) years, respectively, and median prior LOT was 2. Treatment-related adverse events (TRAE) occurred in 92.9%/88.2% of pts with EC (2.0/2.4 mg/kg); 42.9%/47.1% had Grade ≥3 TRAEs, most commonly neutropenia (23.8%/31.4%) and anemia (16.7%/27.5%). TRAEs occurred in 87.9%/97.8% of pts with OC (1.6/2.4 mg/kg); 30.3%/75.6% had Grade ≥3 TRAEs, most commonly neutropenia (24.2%/60.0%) and anemia (9.1%/37.8%). One pt (1.1%) with EC and 5 (6.4%) with OC discontinued treatment due to TRAEs. Antitumor activity of Puxi-Sam was most notable in EC at 2.4 mg/kg, with an objective response rate (ORR) of 48% and durable response of 7.1 months; at 2.0 mg/kg in EC, ORR was 34.1%. In OC, ORR was 12.1% at 1.6 mg/kg and 24.4% at 2.4 mg/kg (Table). Conclusions: Puxi-Sam showed a favorable safety profile and robust antitumor efficacy, supporting continued development, and is now being investigated in the Phase 3 BLUESTAR-Endometrial01 (NCT07044336) study. Clinical trial information: NCT05123482 . Efficacy (interim response evaluable pts). EC 2.0 mg/kgn=41 EC 2.4 mg/kgn=50 OC 1.6 mg/kgn=33 OC 2.4 mg/kgn=45 ORR, % (95% CI) 34.1 (20.1–50.6) 48.0 (33.7–62.6) 12.1 (3.4–28.2)* 24.4 (12.9–39.5) Complete response, n 1 1 0 0 Partial response, n 13 23 4 11 Stable disease, n 17 21 22 26 Progressive disease, n 10 5 5 8 Median duration of response, months (95% CI) 6.2 (5.5–NE) 7.1 (4.5–NE) 5.8 (2.8–NE) 7.0 (4.0–NE) Disease control rate at 12 weeks, % (95% CI) 70.7(54.5–83.9) 86.0(73.3–94.2) 54.5(36.4–71.9) 64.4(48.8–78.1) Median progression-free survival, months (95% CI) ‡ 7.0(4.5–9.0) § 8.1(6.8–9.2) ¶ 4.8(2.8–5.8) 5.7(4.1–9.5) *2 pts were non-evaluable. ‡ Full analysis set. § n=42. ¶ n=51. NE, not estimable.

Detection of mutational signatures in advanced cancer patients using clinical-grade specimens.

3137 Background: The underlying extrinsic and/or intrinsic mutational processes underlying tumor development lead to genome-wide “passenger” alterations that can be identified as mutational signatures. Mutational signatures are known to be both prognostic and predictive in certain clinical contexts. Whole genome sequencing (WGS) based approaches are optimal for detection of mutational signatures but to date studies using formalin fixed paraffin embedded (FFPE) clinical grade specimens are limited. Methods: Archival DNA specimens from tumors of United States Veterans that underwent clinical sequencing in the VA National Precision Oncology Program were subjected to 30X WGS. Somatic alterations were identified by a tumor-only variant calling method employing filtering of variants found in the dataset at >10% frequency and putative germline variants found in multiple databases and germline WGS from the Million Veteran Program (MVP). Mutational signatures were identified using deconstructSigs. Results: WGS was performed on 134 tumor samples with matched germline WGS from MVP; variants were called using the tumor-only variant calling pipeline in addition to tumor-normal calling. Tumor-only WGS derived tumor mutational burden (TMB) was highly correlated with TMB from clinical targeted sequencing (White, R2=0.48; Black, R2=0.63; Other, R2=0.85) and with TMB from tumor-normal variant calling (White, R2=0.96; Black, R2=0.63; Other, R2=0.85). We used our tumor-only variant calling pipeline on WGS from 397 tumors. The median (+SD) number of mutations per tumor varied per tumor type, with the lowest number in head and neck squamous cell carcinomas (12445+4186 mutations) and highest in melanoma (119089+259854 mutations). Overall, 66 single base substitution (SBS) mutational signatures were identified. The SBS1 clock signature was found in 339 of 397 tumors. The SBS4 smoking mutational signature was found in 100% of small cell lung cancers (n=5), 76% of lung squamous cell cancers (n=38), 50% of lung adenocarcinomas (n=50), 36% of cancers of unknown primary (n=14), 29% of bladder cancers (n=7), and 14% of HNSC (n=36), but was not found in any other cancer type. The SBS7a UV mutational signature was found in 80% of melanomas (n=10) and 7% of cancers of unknown primary, but not in any other cancer type. Finally, the SBS6 and SBS15 mismatch repair mutational signatures were found in 10 and 12 of 16 MSI-high tumors, respectively. Conclusions: We have established a pipeline for evaluation of mutational signatures from tumor-only WGS of clinical grade FFPE tumors. Preliminary analysis shows identification of expected mutational signatures. Work is ongoing to determine whether ancestry matched panel of normals improves signature identification and to determine the prognostic and/or predictive ability of mutational signatures in a variety of clinical contexts which could greatly expand the clinical utility of WGS in advanced cancers.

Effect of treatment delay on outcomes with adjuvant chemotherapy vs chemoradiotherapy in R1-resected biliary tract cancers.

e16267 Background: R1 margins after biliary tract cancer (BTC) resection are associated with high recurrence risk. The role of adjuvant radiotherapy and the impact of delayed adjuvant therapy remain incompletely known. We compared overall survival (OS) with adjuvant chemotherapy (AC) versus adjuvant chemoradiotherapy (ACRT) and evaluated whether treatment delay modifies outcomes in R1-resected BTC. Methods: We conducted a retrospective cohort study using the National Cancer Database, including adults (≥18y) with intrahepatic cholangiocarcinoma (ICC), extrahepatic cholangiocarcinoma (ECC), or gallbladder cancer (GBC) diagnosed from 2011–2019 who underwent definitive surgery with R1 margins and received adjuvant therapy. Treatment was categorized as AC or ACRT and stratified by timing: timely ( < 60 days from surgery) versus delayed (≥60 days). Kaplan–Meier analyses compared OS across groups. The log-rank test was used to compare time-to-event outcomes between groups. Multivariable Cox regression adjusted for age, sex, race/ethnicity, facility type, Charlson–Deyo comorbidity score, and stage. Results: Among 87,340 BTC patients, 1,182 (1.4%) underwent R1 resection and received adjuvant therapy; 52.1% initiated adjuvant therapy timely, and 47.9% experienced a delay. Treatment distribution was: timely AC 29.6%, delayed AC 26.2%, timely ACRT 22.5%, delayed ACRT 21.7%. In the overall cohort, timely ACRT was associated with improved median OS compared with timely AC (25.2 vs 13.7 months; p < 0.001) and reduced mortality on multivariable analysis (HR 0.59, 95% CI 0.48–0.73; p < 0.001). In ECC, timely ACRT improved median OS compared with timely AC (28.7 vs 19.0 months; p = 0.03) and delayed AC (28.7 vs 25.1 months; p = 0.04), with reduced mortality risk (HR 0.61, 95% CI 0.42–0.88; p = 0.008). In GBC, delayed ACRT was associated with improved OS versus timely AC (22.7 vs 10.3 months; p < 0.001) and delayed AC (22.7 vs 14.7 months; p = 0.006), also demonstrating reduced mortality risk (HR 0.53, 95% CI 0.39–0.72; p < 0.001). In ICC, OS differences were not statistically significant (p = 0.46). Conclusions: In R1-resected BTC, ACRT was associated with improved OS compared with AC alone, particularly in ECC and GBC. In GBC, delayed ACRT remained associated with improved OS, suggesting radiotherapy may mitigate the adverse impact of delayed postoperative therapy in selected high-risk patients. Univariable and multivariable survival analysis of adjuvant chemoradiotherapy versus chemotherapy in R1-resected biliary tract cancers. Univariable Median OS (mo) Univariable p-value Multivariable* HR (95% CI) Overall Timely AC vs Timely ACRT 13.7 vs 25.2 <0.001 Ref vs 0.59 (0.48-0.73)<0.001 Gallbladder Adenocarcinoma Timely AC vs Delayed ACRT 10.3 vs 22.7 <0.001 Ref vs 0.53 (0.39-0.72)<0.001 Extrahepatic Cholangiocarcinoma Timely AC vs Timely ACRT 19.0 vs 28.7 0.03 Ref vs 0.61 (0.42-0.88)0.008

A phase II study to evaluate the safety and efficacy of BB-1701 in combination with sintilimab in patients with HER2 expression or mutation in locally advanced/metastatic breast cancer or NSCLC.

2632 Background: BB-1701, a HER2-targeting antibody-drug conjugate (ADC) containing eribulin, has demonstrated promising antitumor activity in the clinical studies in breast cancer (BC) patients with HER2 low expression and non-small cell lung cancer (NSCLC) patients with HER2 mutation. Currently, there are no approved treatment options of ADC in combination with anti-PD-1 antibody for metastatic BC patients with HER2 low expression and NSCLC patients with HER2 mutation. We report the preliminary efficacy and safety results from the ongoing phase 2 study (including dose escalation and dose expansion) of BB-1701 in combination with Sintilimab (an anti-PD-1 antibody) in advanced or metastatic BC patients with HER2 low expression and NSCLC patients with HER2 mutation. Methods: Patients enrolled were ≥18 years of age; had confirmed locally advanced/metastatic HER2 low-expressing BC or HER2 mutated NSCLC, an ECOG PS <2 and measurable lesion(s) (per RECIST v1.1); and disease progression after ≥1 lines of prior standard therapies. HER2 expression was confirmed by IHC or NGS/PCR before patient enrollment. BB-1701 was administered at 1.2 mg/kg Q3W or 1.6 mg/kg Q3W, and sintilimab is administered at 200 mg Q3W. Results: As of 26 January 2026, a total of 12 patients with HER2 low-expressing BC or HER2 mutated NSCLC have been enrolled and treated, 6 patients at each dose level of BB-1701 during dose escalation. Median age is 63 years, 91.7%/8.3% patients were female/male, and 16.7%/83.3% patients have ECOG PS 0/1. The median number of prior systemic therapy lines was 2.0/1.0 for BC and NSCLC. All patients experienced at least one treatment-emergent adverse events (TEAEs). The most common (≥20%) reported all grade TEAEs are alanine aminotransferase increased, aspartate aminotransferase increased, γ-glutamyltransferase increased, hypercholesterolemia, peripheral neuropathy, anemia and Urinary tract infection. Three grade 3 TEAEs are γ-glutamyltransferase increased, pneumonia and open globe injury. There has been no grade 4 or grade 5 events as of data cut-off date. One treatment emergent serious adverse event is open globe injury. All patients were evaluable for efficacy. Among 5 BC patients, 4 patients achieved partial response (PR) with disease control rate (DCR) of 80.0%. Among 7 NSCLC patients, 2 patients achieved PR and 2 patients had stable disease (SD) with DCR of 57.1%. Details of data will be presented at the ASCO meeting. Conclusions: BB-1701 in combination with Sintilimab shows encouraging antitumor activity and a manageable safety profile in HER2 low-expressing BC patients and HER2 mutated NSCLC patients. The further dose expansion study is guaranteed based on the preliminary data from dose escalation study. Clinical trial information: CTR20241422.

A novel bispecific RDC+ADC theranostic approach to overcome trastuzumab deruxtecan resistance and tumor heterogeneity.

e15150 Background: Resistance to single-antigen HER2-targeted ADCs, such as trastuzumab deruxtecan and trastuzumab emtansine, poses a significant challenge in HER2-positive cancers, often due to tumor heterogeneity and antigen expression downregulation. To address this unmet medical need, we developed RB02 and B836, first-in-class bispecific radionuclide drug conjugates (RDC) and ADCs leveraging the proprietary Nanolattix Biolattix technology platform. RB02-RDC and B836-ADC are engineered to target both HER2 and Tissue Factor (TF), an attractive therapeutic target overexpressed in various tumor types. Methods: The therapeutic potential of B836 was evaluated through in vitro binding and internalization assays. In vivo efficacy was assessed in comparison to trastuzumab deruxtecan. Safety and toxicokinetic studies for B836-ADC were conducted in cynomolgus monkeys. The theranostic potential of RB02-177Lu was evaluated using SPECT/CT imaging in animal models and xenograft tumor models to monitor tumor accumulation, spatial and timing dynamic distribution, and clearance. Results: In vitro experiments demonstrated that B836 achieved significantly enhanced cancer cell binding and internalization compared to single-target ADCs. In vivo studies of B836 showed superior anti-tumor efficacy over trastuzumab deruxtecan. In safety studies, no systemic toxicity was detected for B836-ADC at doses up to 5 mg/kg in cynomolgus monkeys. SPECT/CT imaging analysis revealed the specific spatial and timing dynamic distribution of RB02-177Lu after i.v. injection. RB02-177Lu demonstrated rapid and specific tumor accumulation with retention over 7 days and non-target clearance by 4 hours post-injection. Conclusions: These collective findings support the continued clinical development of RB02-RDC + B836-ADC as a promising bispecific RDC+ADC theranostic and synergistic drug combination approach in oncology.

Survival outcomes of human epidermal growth factor receptor 2 (HER2)–amplified and HER2-mutated left-sided colorectal cancer (CRC) patients treated with anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (mAbs).

3543 Background: Current guidelines support the use of anti-EGFR mAbs in left-sided CRCs without mutations in KRAS , NRAS and BRAF . Recent reports indicated that HER2-amplified CRCs might respond worse to anti-EGFR mAbs, whereas HER2-mutated CRCs and their response to anti-EGFR mAbs remained relatively unexplored. In this study, we assembled the largest collection of HER2-altered (amplified or mutated) CRCs to date from a real-world database with the goal of describing the impact of these alterations on anti-EGFR mAb therapy. Methods: Patients profiled by Caris Life Sciences with microsatellite stable, left-sided CRC without mutations in KRAS / NRAS / BRAF who received anti-EGFR mAbs (cetuximab or panitumumab) were included in this study. Microsatellite stability, amplifications (copies ≥6), and pathogenic or likely pathogenic mutations were identified by NGS. Patient outcomes were obtained from insurance claims data. Overall survival (OS) was calculated from start of anti-EGFR mAbs to time of last clinical contact. Time on treatment (ToT) was calculated from start to end of anti-EGFR mAbs. Hazard ratios and p-values were calculated using the Cox proportional hazards model and log-rank test. Results: A total of 3217 patients were included for analysis. Patients were stratified into 3 cohorts: HER2-amplified (N=114), HER2-mutated (N=46), and HER2-normal (N=3057). The HER2-mutated group was older than the HER2-amplified and the HER2-normal groups (median: 64.5 vs 56 and 58 years, p=0.006); no other significant differences were found in patient demographics. The HER2-mutated group had worse OS and ToT than the HER2-normal group (median OS 12.4 vs 25.9 months, HR 1.57, p=0.013; median ToT 4.3 vs 6.7 months, HR 1.40, p=0.036). The HER2-amplified group showed no significant differences in OS but worse ToT compared to the HER2-normal group (median OS 26.1 vs 25.9 months, HR 0.98, p=0.856; median ToT 5.8 vs 6.7 months, HR 1.25, p=0.035). In multivariate Cox regressions accounting for age, gender, and receipt of HER2-targeted therapy, the HER2-mutated group had worse OS and ToT compared to HER2-normal group (OS HR 1.66, p=0.007; ToT HR 1.55, p=0.007), while the HER2-amplified group showed no significant differences in OS and ToT compared to HER2-normal group (OS HR 1.14, p=0.398; ToT HR 1.26, p=0.073). Conclusions: In this large, real-world cohort of KRAS / NRAS / BRAF wild-type, left-sided CRCs receiving anti-EGFR mAbs, HER2-mutated patients had worse ToT and OS than HER2-normal patients, whereas HER2-amplified patients showed no difference in OS compared to HER2-normal patients. These findings suggest that alternative treatment studies should be explored in HER2-mutated left-sided CRCs, underscoring the importance of additional biomarker-directed studies in this patient cohort.

Diagnostic accuracy of urine-based HPV testing for cervical neoplasia and cancer: A landmark systematic review and meta-analysis.

e17506 Background: Urine-based human papillomavirus (HPV) testing offers a non-invasive screening alternative that could improve accessibility. We quantified diagnostic accuracy of urine HPV tests for detecting cervical intraepithelial neoplasia grade 2 or worse (CIN2+), CIN3+, and cervical cancer. Methods: We searched PubMed, Embase, Scopus, and Web of Science through January 2026. Studies evaluating urine HPV testing against histologically confirmed disease were included. Bivariate random-effects meta-analyses using the Reitsma model pooled sensitivity and specificity. We analyzed different biomarker types (high-risk HPV DNA, mRNA, methylation), population and test characteristics, and examined disease threshold effects through meta-regression. Results: Fifty-five studies (72 arms, n=38,009) were included. For CIN2+, pooled sensitivity was 81.4% (95% CI: 77.5-84.7%) and specificity 59.3% (95% CI: 50.2-67.8%). hrHPV DNA tests (k=45) showed sensitivity 82.7% and specificity 58.2% (AUC 0.812). hrHPV mRNA (k=2) had lower sensitivity (45.1%, p=0.001) but higher specificity (68.4%). Methylation markers (k=2) achieved balanced performance: sensitivity 78.0%, specificity 75.2% (AUC 0.832). Performance improved with disease severity. For cancer (k=6), sensitivity was 91.8% (95% CI: 85.4-95.5%) and specificity 84.1% (95% CI: 74.2-90.6%; AUC 0.943). Meta-regression confirmed significant disease threshold differences (p<0.022). Conclusions: Urine-based HPV testing, particularly hrHPV DNA assays, demonstrates promising accuracy for CIN2+ and excellent performance for cancer detection, supporting expanded screening access. Standardization and larger studies of methylation markers are needed. Diagnostic performance of urine HPV testing by disease threshold and biomarker type. Analysis Subgroup Studies Participants Sensitivity % (95% CI) Specificity % (95% CI) Accuracy % DOR AUC Disease Threshold Cancer 6 894 91.8 (85.4-95.5) 84.1 (74.2-90.6) 86.8 59.05 0.943 CIN3+ 17 11,141 83.7 (78.0-88.1) 53.9 (36.3-70.6) 64.8 5.98 0.814 CIN2+ 49 25,974 81.4 (77.5-84.7) 59.3 (50.2-67.8) 69 6.36 0.800 Biomarker (CIN2+) hrHPV DNA 45 25,159 82.7 (79.0-85.8) 58.2 (48.3-67.4) 68.9 6.63 0.812 hrHPV mRNA 2 277 45.1 (35.6-54.9) 68.4 (54.3-79.8) 59.6 1.78 0.455 Methylation 2 538 78.0 (67.4-86.0) 75.2 (62.3-84.8) 77.1 10.79 0.832 Overall All studies 55 (72 arms) 38,009 82.8 (79.8-85.4) 60.7 (52.9-68.0) 68.2 7.42 0.819 CI, confidence interval; DOR, diagnostic odds ratio; AUC, area under curve; hrHPV, high-risk HPV; CIN, cervical intraepithelial neoplasia. All estimates from bivariate random-effects meta-analysis (Reitsma model) against histology reference standard. Meta-regression p-values: disease threshold p=0.019 (sensitivity), p=0.022 (specificity); biomarker p=0.001 (sensitivity). Heterogeneity I²: 34.7-50.8%.

Teliso-V monotherapy and EGFR-TKI combinations in c-Met–over-expressing NSCLC: A systematic review and meta-analysis.

e20714 Background: c-Met protein over-expression is frequent in non-small cell lung cancer (NSCLC) and is linked to poor prognosis. Telisotuzumab vedotin (Teliso-V) is an antibody–drug conjugate that targets c-Met overexpression to deliver a cytotoxic payload. We synthesized efficacy for Teliso-V monotherapy and combinations with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs). Methods: Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA), we searched PubMed, Embase, and major conference proceedings through January 2026 for prospective Teliso-V trials in c-Met–positive advanced NSCLC (immunohistochemistry (IHC) H-score ≥150 or ≥25% 3+ staining). Records were deduplicated, screened, and full texts were assessed, yielding 7 eligible cohorts from 5 prospective trials. Primary outcomes were objective response rate (ORR) and disease control rate (DCR), analyzed separately and stratified by regimen (monotherapy vs combination). Pooled proportions were estimated using random-effects generalized linear mixed models (GLMMs) (random-intercept logistic regression; logit scale). Between-cohort variance (tau-squared) was estimated by maximum likelihood; heterogeneity was summarized using I-squared (I²). Individual cohort confidence intervals (CIs) used Clopper–Pearson; 95% prediction intervals were computed. Results: Monotherapy (k=5 cohorts; N=224) yielded pooled ORR 24.0% (95% confidence interval 16.5–33.6; 95% prediction interval 12.4–41.2) with moderate heterogeneity (I²=52.7%), consistent with clinical and cohort-size differences. Pooled DCR was 60.3% (53.7–66.5) with no observed heterogeneity (I²=0.0%). Combination therapy (k=2 cohorts; N=74) yielded pooled ORR 40.3% (27.7–54.4; 95% prediction interval 24.7–58.3); heterogeneity estimates are imprecise and should be interpreted cautiously because only two combination cohorts were available(I²=65.0%). Pooled DCR was 81.1% (70.6–88.5; 95% prediction interval 70.5–88.5) with low heterogeneity (I²=11.8%). Conclusions: In c-Met–over-expressing advanced NSCLC, Teliso-V shows clinically meaningful activity. Pooled response rates were higher with EGFR tyrosine kinase inhibitor combinations, while disease control was consistent across settings. Findings are limited by single-arm evidence and few combination cohorts and warrant confirmation in larger, controlled studies. Pooled efficacy (percentage). Endpoint & Regimen Cohorts ( k ) Patients ( N ) Pooled Estimate % [95% CI] 95% Prediction Interval Objective Response Rate (ORR) Monotherapy 5 224 24.0 [16.5–33.6] 12.4–41.2 Combination 2 74 40.3 [27.7–54.4] 24.7–58.3 Disease Control Rate (DCR) Monotherapy 5 224 60.3 [53.7–66.5] 53.7–66.5 Combination 2 74 81.1 [70.6–88.5] 70.5–88.5

Heart failure in hospitalizations for hematologic malignancies versus solid tumors: National burden and inpatient outcomes, 2018-2022.

11074 Background: Heart failure (HF) is a common and morbid comorbidity in oncology. Whether HF burden and prognosis differ between hospitalizations for hematologic malignancies and solid tumors remains incompletely characterized at a national level. This study compared HF prevalence and HF-associated outcomes across these cancer groups. Methods: A serial cross-sectional analysis was conducted using adult hospitalizations in the 2018 to 2022 Healthcare Cost and Utilization Project National Inpatient Sample with discharge-level survey weighting. Cancer hospitalizations were classified by principal diagnosis as hematologic malignancy or solid tumor. HF was identified using ICD-10-CM I50* in any diagnosis field. Outcomes included HF prevalence, in-hospital mortality, intensive care unit utilization, shock, length of stay, and hospitalization cost. Survey-weighted multivariable regression adjusted for demographics, comorbidities, hospital characteristics, and admission factors. Models restricted to HF admissions evaluated associations between cancer type and outcomes within the HF subgroup. Results: Among an estimated 4.81 million cancer hospitalizations nationally, HF prevalence was higher in hematologic malignancies than in solid tumors (13.2% vs 8.0%, p < 0.001). After adjustment, hematologic malignancy was associated with higher odds of HF (adjusted odds ratio (aOR) 1.53, 95% CI 1.50 to 1.57). Among HF hospitalizations, hematologic malignancies had higher mortality (11.7% vs 8.0%), intensive care unit utilization (8.5% vs 7.3%), and shock (3.8% vs 3.4%) (all p < 0.001). In adjusted models restricted to HF admissions, hematologic malignancy remained associated with higher mortality (adjusted odds ratio 1.34, 95% CI 1.26 to 1.42) and intensive care unit utilization (aOR 1.15, 95% CI 1.07 to 1.23). Resource utilization was greater in hematologic malignancy HF admissions, including longer length of stay (12.1 vs 8.3 days) and higher costs ($50,518 vs $30,906; both p < 0.001). Interaction modeling showed no significant effect modification of HF-associated mortality by cancer type. Conclusions: Hospitalizations for hematologic malignancies have higher HF prevalence than solid tumor hospitalizations and demonstrate higher mortality, intensive care utilization, shock, length of stay, and costs among admissions with HF. These findings identify hematologic malignancy hospitalizations as a high-risk context for HF-associated inpatient deterioration and resource use.

Recovery with residual disparities: Real-world patterns of platinum chemotherapy use after the 2023 drug shortage.

1562 Background: The 2023 national shortages of cisplatin and carboplatin disrupted standard cancer treatment across multiple malignancies. Although the acute effects have been described, patient-level evidence of recovery in platinum chemotherapy access after supply stabilization is limited. We evaluated real-world recovery in platinum initiation across platinum-dependent cancers. Methods: We conducted a retrospective cohort study using the TriNetX U.S. Collaborative Network. Adults with platinum-sensitive malignancies, including lung, ovarian, bladder, uterine, testicular, and head and neck cancers, were identified using ICD-10-CM and ICD-O codes and assigned according to the national platinum chemotherapy shortage timeline: shortage (February 10, 2023-January 31, 2024) and post-shortage (July 1, 2024-June 30, 2025) eras. The primary endpoint was time from cancer diagnosis to first receipt of any platinum chemotherapy (cisplatin or carboplatin), analyzed using Kaplan–Meier methods and multivariable Cox proportional hazards models, adjusted for demographic characteristics, NCI Comorbidity Index, risk factors, BMI, and cancer type. Secondary analyses evaluated agent-specific initiation (cisplatin vs carboplatin) and heterogeneity of recovery across cancer sites. Prespecified subgroup analyses assessed differences in recovery by sex and race/ethnicity within matched cohorts. Results: The analysis included 33,856 patients diagnosed during the shortage and 30,256 diagnosed post-shortage. Platinum initiation improved post-shortage compared with the shortage period (adjusted hazard ratio [aHR], 1.11; 95% CI, 1.09–1.14; p<.001), with median time to initiation decreasing from 206 to 128 days. This improvement was driven primarily by increased carboplatin initiation, while cisplatin initiation continues to stall. Recovery patterns varied by cancer type, with greater improvement observed in ovarian and head/neck cancers and incomplete recovery in bladder cancer. Across eras, slower platinum initiation was observed among older patients (aHR per year increase, 0.99), male patients (aHR 0.92), and racial/ethnic minority groups, including Black (aHR 0.92) and Hispanic patients (aHR 0.90). Comorbidities associated with platinum toxicity, such as CKD (aHR, 0.79), neuropathy (aHR, 0.63), heart failure (aHR, 0.93), and liver disease (aHR, 0.84), were also associated with delayed initiation. Conclusions: After resolution of the 2023 platinum shortage, platinum chemotherapy initiation improved across multiple cancers, providing patient-level evidence of recovery in access. However, recovery was heterogeneous, driven largely by carboplatin, and modified by patient clinical and demographic factors, suggesting that restoration of drug supply does not uniformly translate into timely or equitable recovery of standard-of-care treatment.

Sleep disorder diagnosis prevalence among adult cancer patients.

e24113 Background: Sleep is commonly impacted by cancer diagnosis and treatment. Poor sleep is consistently reported to be one of the most impactful sequelae of cancer on an individual’s quality-of-life, yet the prevalence of sleep disorders among cancer patients is not well understood. As a sleep disorder diagnosis is a critical first step in the treatment or referral pathway. We sought to examine the prevalence of sleep disorder diagnoses among cancer survivors at a comprehensive cancer center. Methods: We analyzed data from all adult cancer patients who presented for an outpatient visit at our center in 2024 (N = 107,080). Medical records were queried for patient demographics (age, sex, race, ethnicity, insurance status), disease department, and sleep disorder diagnoses based on ICD-10 codes. Diagnoses were grouped into 9 standard sleep disorder categories. Descriptive statistics and logistic regressions were used to calculate sleep disorder prevalence rates and odds ratios (OR) overall, and by various characteristics. Results: At our center, 1.72% of patients had at least one sleep disorder diagnosis. The most commonly diagnosed sleep disorders were insomnia (0.76%) and sleep disordered breathing (SDB, 0.64%). All other disorders were either unspecified or diagnosed at rates < 0.1%. Most patients (94.5%) were diagnosed with a single sleep disorder. Women were more likely to be diagnosed with sleep-related movement disorders (OR: 1.60, 95% CI: 1.03, 2.47) and less likely to be diagnosed with SDB (OR: 0.34, 95% CI: 0.29, 0.40) compared to men. Those who were younger (≤39 years) were less likely to be diagnosed with SDB (OR: 0.39, 95% CI: 0.26, 0.60) compared to those ≥65 years. Middle aged adults (40-64 years) were more likely to be diagnosed with insomnia (OR: 1.33, 95% CI: 1.15, 1.54) compared to those ≥65 years. Compared to White patients, Black patients were more likely to be diagnosed with SDB (OR: 1.47, 95% CI: 1.08, 2.01). Those with Medicare were more likely to be diagnosed with SDB (OR: 1.19, 95% CI: 1.01,1.41) compared to those with private insurance. Conclusions: Over 60% of cancer patients will report sleep issues at some point during treatment, with about 20% likely to meet diagnostic criteria for insomnia alone. In the context of our findings, it is likely that sleep disorders are underdiagnosed and not consistently billed for, leading to an underestimate of the true prevalence of the problem among cancer patients in a large academic and teaching hospital. This is a missed opportunity to provide patients with clinical attention for a medical problem that poses considerable risks to physical and psychological health. It is imperative that cancer centers develop a more consistent clinical care pathway to capture sleep disorders among patients during active treatment.

Clinico-transcriptomic risk stratification to guide abiraterone treatment intensification in high-risk prostate cancer: A combined analysis of NRG/RTOG 9202, 9413, 9902, and 0521.

5000 Background: Outcomes for some patients with ≥high-risk localized prostate cancer (HR-PCa) who receive radiation therapy (RT) remain poor. Current guidelines recommend intensification with abiraterone/prednisone (AAP) in select patients; however, the current guideline-defined candidate population may be suboptimal. Methods: This is a secondary analysis of available biopsy samples from NRG/RTOG 9202, 9413, 9902, and 0521. The primary objective was to determine if a specific subgroup of ≥HR-PCa patients had sufficiently poor prognoses to derive a clinically meaningful benefit from AAP intensification. The prognostic impact of the Decipher 22-gene genomic classifier (GC; Veracyte, San Diego, CA) was first evaluated for metastasis-free survival (MFS, primary), overall survival (OS), and distant metastases (DM). GC scores were analyzed using both continuous (per 0.1 GC units) and pre-specified categorical cutpoints: ≤ intermediate transcriptomic risk (IR-PCa, GC≤0.6), HR-PCa (GC:0.6-0.85), and very high risk (VHR-PCa, GC > 0.85). A tree-based model was then used to combine clinical and transcriptomic risk category. Results: This study characterized outcomes of 427 patients (64% NCCN HR-PCa; 36% NCCN VHR-PCa) with a median follow-up of 10.4 years. Continuous GC score was observed to discriminate risk when adjusted for age, PSA, grade, T-stage, and treatment received for the endpoints of MFS (HR GC :1.19 [95% CI:1.10-1.29], p < 0.001), DM (HR GC :1.31 [95% CI:1.13-1.51], p < 0.001), and OS (HR GC : 1.18 [95% CI: 1.09-1.28], p < 0.001). MFS and OS were estimated using the Kaplan-Meier method by pre-specified GC subgroup within each NCCN risk group (HR-PCa, VHR-PCa). Based on outcomes by subgroup, a novel clinico-transcriptomic risk stratification system was constructed, where patients receive 1 point for NCCN/GC HR categorization and 2 points for NCCN/GC VHR categorization. The combined risk score ≥3 subgroup had a prognosis similar to the STAMPEDE M0 control arm, whereas the combined score ≤2 subgroup had a substantially better prognosis. Utilizing this system could enhance the specificity of AAP recommendations, increasing the candidate pool eligible for AAP intensification by approximately 20% and identifying approximately 25% of NCCN VHR in whom the therapeutic ratio of AAP may be less favorable. Conclusions: This study defines a novel clinico-transcriptomic risk stratification system to augment current clinical eligibility for AAP intensification. This system may increase the population who benefit from AAP by approximately 20% and simultaneously identify approximately 25% of NCCN VHR patients who may avoid AAP intensification. Acknowledgement: We would like to acknowledge Dr. Felix Feng for his contributions in his capacity as the former GU Committee Chair.

Neoadjuvant chemoimmunotherapy before chemoradiation vs chemoradiation alone for stage IIB-IIIC1 carcinoma of the cervix: A phase II open-label randomized controlled trial (NeoCHIMERA).

TPS5631 Background: Locally advanced cervical cancer (FIGO 2018 stages IIB–IIIC1) remains a major cause of cancer-related mortality in low- and middle-income countries. Concurrent chemoradiation (CCRT) with brachytherapy is the current standard of care; however, rates of persistent disease and distant failure remain substantial, particularly in patients with bulky tumors or nodal involvement. Although advances in radiotherapy have improved outcomes, survival in resource-constrained settings continues to lag behind that in high-income countries. Recent randomised trials have demonstrated improved outcomes with two distinct strategies: delivery of dose-dense induction chemotherapy followed by timely initiation of chemoradiation, and the addition of immunotherapy with pembrolizumab to concurrent chemoradiation followed by maintenance therapy for up to one year. Despite these advances, concerns about radiotherapy dose and technique in induction chemotherapy trials, and the feasibility of prolonged maintenance immunotherapy in resource-limited settings, have limited widespread adoption. The optimal dose, timing, and duration of immunotherapy in locally advanced cervical cancer remain undefined. This study was designed to evaluate whether short-course neoadjuvant chemo-immunotherapy administered prior to standard CCRT can improve early tumor response with an acceptable safety profile while preserving treatment feasibility across diverse healthcare settings. Methods: The NeoCHIMERA trial is a multicenter, open-label, randomized phase II study designed to evaluate this hypothesis. Eligible patients include those with biopsy-proven FIGO 2018 stage IIB–IIIC1 cervical carcinoma (squamous, adeno, or adenosquamous histology) who are treatment-naïve and suitable for CCRT. Participants will be randomized 1:1 to the experimental or control arm, stratified based on stage and histology. The experimental arm will receive six weeks of neoadjuvant carboplatin (AUC 2) and paclitaxel (60 mg/m²) weekly, combined with low-dose nivolumab (40 mg IV every three weeks for two cycles), followed by standard CCRT (cisplatin 40 mg/m² weekly with external beam radiation and brachytherapy). The control arm will receive CCRT alone. The primary endpoint is complete clinical response at 3 months after completion of chemoradiation. Secondary endpoints include safety, treatment completion rates, event-free survival, quality of life, and cost-effectiveness from a societal perspective. A total of 154 patients (77 per arm) will be accrued. One interim safety analysis is planned after 40 patients with predefined stopping rules for excess toxicity. Thirty-three of the planned 154 participants have been recruited. This study is registered with the Clinical Trials Registry of India (CTRI/2025/04/085540). Clinical trial information: CTRI/2025/04/085540.

Oncologic safety and patient-reported outcomes of sentinel lymph node biopsy omission in early breast cancer: A meta-analysis of randomized controlled trials.

e12618 Background: Sentinel lymph node biopsy (SLNB) has replaced axillary lymph node dissection for axillary staging in clinically node-negative early breast cancer (BC) as randomized controlled trials (RCTs) suggest that omission of SLNB may result in non-inferior oncologic outcomes in selected low-risk patients. However, the impact of SLNB omission on recurrence and patient-reported outcomes (PROs) remains incompletely defined. This meta-analysis aims to evaluate the oncologic safety of omitting SLNB and its effects on PROs in early BC. Methods: RCTs comparing surgical omission versus standard SLNB in clinically and sonographically node-negative early BC patients undergoing breast-conserving therapy (BCT) were identified through searches of PubMed, Embase, and Cochrane. Outcomes of interest included disease-free survival (DFS), distant recurrence, axillary recurrence, overall mortality, breast cancer-specific mortality, and PROs including global health status and functional domains. Random-effects models were used, reporting hazard or odds ratios with 95% confidence intervals; heterogeneity was assessed using I². When individual patient data were unavailable, quantitative data were extracted from graphical representations using PlotDigitizer. All analyses were performed using RevMan version 5.4. Results: Four RCTs met inclusion criteria, encompassing 6,329 patients randomized to SLNB omission (4,636) versus standard SLNB (1,693). Omission of SLNB resulted in non-inferior DFS (HR 0.90, 95% CI 0.73–1.11, I² = 0%), with no significant differences in distant recurrence (OR 0.97, 95% CI 0.66–1.41, I² = 0%), overall mortality (OR 0.59, 95% CI 0.15–2.30, I² = 86%) and BC-specific mortality (OR 1.55, 95% CI 0.49–4.90, I² = 0%) between groups. Notably, axillary recurrence was significantly lower in the SLNB omission group (OR 0.35, 95% CI 0.17–0.73, p = 0.005, I² = 0%). Patient-reported outcomes at 6 months revealed no significant differences in global health status (MD −0.49, 95% CI −2.08 to 1.10) or physical functioning (MD −0.22, 95% CI −2.16 to 1.73) between groups. However, role functioning at 6 months was significantly better in the SLNB omission group (MD 1.96, 95% CI 0.17 to 3.76), though this difference was not sustained at 12 months (MD −1.37, 95% CI −3.02 to 0.27). Conclusions: In patients with clinically and sonographically node-negative early BC undergoing BCT, omission of SLNB was associated with non-inferior oncologic outcomes compared with standard SLNB. SLNB omission was associated with a modest improvement in role functioning at 6 months, without differences in global health or physical functioning. These findings support axillary de-escalation in low-risk patients, although longer follow-up is needed to confirm durability and refine patient selection.

Race-associated clinicogenomic predictors in non-small cell lung cancer treated with immune checkpoint inhibitors.

8557 Background: PD-L1 low and STK11 mutation associate with immune checkpoint inhibitor (ICI) resistance in non-small cell lung cancer (NSCLC), but appear differentially expressed among racial ethnic groups. This has not been validated in large, diverse studies. Methods: We retrospectively studied NSCLC patients 18 or older, without targetable EGFR or ALK alterations, treated with frontline ICI between January 2014 and February 2020 at MD Anderson Cancer Center and University of Illinois Chicago. We analyzed clinicogenomic and survival characteristics by race/ethnicity. Differences in clinicogenomic predictors were assessed through log-rank and chi-squared comparison of proportions tests. Survival differences were estimated via Kaplan-Meier method. Results: 1694 patients met inclusion criteria, 383 (22.6%) were minorities. Poor performance status (PS 2-3) was most frequent in African American (AA) (32.5%) and Native Alaskan/Hawaiian or American Indian (NAHAI) (27.3%) patients (p=0.005) (Table). Heavy smoking was more frequent in White (50.3%) patients. PD-L1 <1% was most prevalent among Asian (31.3%) and least prevalent among Hispanic/Latino (HL) (15.8%) patients (p=0.001). STK11 mutation rate was most prevalent in AA (14.7%) and least prevalent in HL (6.9%) and Asian (2.5%) patients (p=0.056). Median overall survival (OS) was lower (21.3, 23.5, and 24.3 months) for HL, NAHAI, and AA patients, and higher (25.4 and 30.6 months) for White and Asian patients, respectively (p<0.01). Conclusions: Our dual center study with 22% minority patient representation shows self-reported race can result in biological differences, because of ancestry and/or environmental differences. AA, HL, and NAHAI patients had lower rates of heavy smoking and different clinicogenomic patterns than White patients. AA tended towards higher prevalence of STK11 mutation—while not statistically significant, it was overall not highly represented in the sample. In line with these poor prognostic factors, AA had statistically significant lower median overall survival (OS) than their White and Asian counterparts. Asians had the lowest rates of heavy smoking and STK11 mutation, highest rates of PD-L1<1%, and highest median OS. HL had the lowest OS, with low prevalence of PD-L1<1% and STK11 mutation – future studies should evaluate other clinicogenomic factors to determine potential culprits. White Black or African American (AA) Hispanic or Latino (HL) Asian Native Alaskan/Hawaiian or American Indian (NAHAI) p-value Total cohort n=1694, No. (%) 1311 (77.4) 191 (11.3) 101 (6.1) 80 (4.7) 11 (0.5) ECOG PS 2-3 at ICI start 267 (20.4) 62 (32.5) 23 (22.8) 20 (25.0) 3 (27.3) 0.005 20+ Pack Years Smoking 659 (50.3) 77 (40.3) 26 (25.7) 19 (23.8) 5 (45.5) 4.9 ×10 -9 PD-L1 <1% 317 (24.2) 47 (24.6) 16 (15.8) 25 (31.3) 1 (9.1) 0.001 STK11 mut 129 (9.8) 22 (14.7) 7 (6.9) 2 (2.5) 1 (9.1) 0.056 Median OS (mo) 25.4 24.3 21.3 30.6 23.5 < 0.01

From diagnosis to survivorship: Mapping the lived experience of patients with cancer in the Philippines.

e13619 Background: Cancer is now the Philippines’ second leading cause of death, yet the day-to-day realities of care remain poorly documented. Mapping the patients' cancer journey is a valuable tool in cancer care, providing a deep understanding of the patient's perspective and using that knowledge to drive improvements across the healthcare system. Despite the legislation and continuing implementation of the National Integrated Cancer Control Act (NICCA), a landmark policy designed to enhance access, equity, and quality of cancer care in the Philippines, there is a gap between the law's intended impact and the actual experiences of Filipino cancer patients. Methods: We conducted a multicenter qualitative study that combined focus-group discussions with real-time patient-journey mapping among 24 adults with diverse cancers from five Philippine regions. We independently applied inductive coding and developed an initial codebook that the entire team reviewed by consensus. Codes were aggregated into higher-order themes within and across regions, and matrix tables were created showing barriers and facilitators to care according to cancer phase and care setting. The team then generated a composite patient-journey map that visually represented these themes. Results: Twenty-four adults (15 females and 9 males), with a mean age of 52.5 years, participated in five regional journey-mapping sessions. Most patients had breast, lung, or rectal cancers. Eight patients (32%) had metastatic disease, while the rest had early or locally advanced cancers. Eight participants (32%) received treatment in private hospitals, 7 (28%) received concurrent mixed private-public hospital care, 5 (20%) received treatment in government hospitals only, and 4 participants (16%) switched from private to public hospitals. Thirteen (13) participants were able to receive treatment in a CSPMAP (Cancer and Supportive-Palliative Medicines Access Program)-enabled government facility. Four care trajectories surfaced: exclusive private care, public-to-private switching, concurrent mixed-sector use, and exclusive public care. Regardless of the care trajectory, five themes shaped experience: the navigational power of family, faith, and social capital; financial and geographic hurdles that magnify distress; the decisive impact of empathic clinicians; life-course disruption and anxiety during survivorship; and persistent recourse to alternative therapies. These insights pinpoint several touch-points that could be mitigated by strengthening the implementation of the NICCA: the need for early diagnostic access, more streamlined subsidy processes, and the impact of compassionate communication. Conclusions: Patient-journey mapping thus offers a practical lens for designing Filipino-centered cancer services in a resource-limited setting.

Analysis of recurrence and risk factors in resectable early-stage adenocarcinoma with uncommon <i>EGFR</i> mutations: A comprehensive cohort study in South Korea.

8038 Background: This study aimed to identify clinicopathologic factors associated with recurrence in patients with surgically resected lung adenocarcinoma harboring uncommon EGFR mutations. Methods: We conducted a multicenter retrospective cohort study. The study included patients with stage I–III lung adenocarcinoma harboring uncommon EGFR mutations (G719X, S768I, or L861Q) who underwent curative-intent resection between 2010 and 2017 in South Korea. Recurrence-free survival (RFS) and overall survival (OS) were analyzed using Cox proportional hazards models. Results: A total of 48 patients were analyzed (stage I: n=33, stage II: n=6, stage III: n=9). The median age was 65 years; 56.3% were female and 66.7% were never-smokers. Mutation distribution was G719X (72.9%), S768I (16.7%), and L861Q (10.4%). Visceral pleural invasion (VPI) and lymphovascular invasion (LVI) were present in 37.5% and 16.7% of cases, respectively. During follow-up, 26 patients (54.2%) experienced recurrence and 21 (43.8%) died. Multivariable analysis identified ECOG performance status ≥1 (HR 4.55, 95% CI 1.226–16.899; P=0.024), stage III vs. I (HR 5.07, 1.181–21.771; P=0.029), and VPI (HR 3.67, 1.030–13.058; P=0.045) as independent predictors of recurrence. EGFR subtype (non-G719X vs. G719X) was not significantly associated with recurrence (P=0.428). Conclusions: Patients with surgically resected lung adenocarcinoma harboring uncommon EGFR mutations face a substantial risk of postoperative recurrence. Conventional clinicopathologic factors—particularly ECOG status, advanced stage, and VPI—outperform EGFR subtype as prognostic indicators. These findings support the need for risk-adapted surveillance and prospective evaluation of adjuvant strategies in these high-risk subsets. Univariate and multivariate Cox regression analysis for the risk factors associated with recurrence. Variables Recurrence rate* Univariate analysis,HR (95% CI) P -value Multivariate analysis,HR (95% CI) P -value ECOG 0 50.0 (19/38) - - 1≤ 70.0 (7/10) 1.64 (0.678-3.955) 0.273 4.55 (1.226-16.899) 0.024 EGFR mutation G719X 54.3 (19/35) - - Non-G719X 53.8 (7/13) 0.91 (0.377–2.210) 0.840 0.58 (0.155–2.207) 0.428 Tumor size † &lt; 2.0 cm 38.5 (5/13) - - ≥ 2.0 cm 60.0 (21/35) 1.59 (0.599–4.214) 0.353 1.75 (0.434–7.068) 0.431 Clinical stage I 48.5 (16/33) - - II 66.7 (4/6) 1.65 (0.549–4.950) 0.373 1.33 (0.368–4.801) 0.663 III 66.7 (6/9) 2.11 (0.820-5.436) 0.121 5.07 (1.181-21.771) 0.029 Lymphovascular invasion Absent 52.5(21/40) - - Present 62.5(5/8) 1.11 (0.420–2.958) 0.827 0.03 (0.001–0.841) 0.040 Visceral pleural invasion Absent 46.7 (14/30) - - Present 66.7 (12/18) 1.97 (0.893–4.334) 0.093 3.67 (1.030–13.058) 0.045 *Presented as number of recurrences / number of patients (%). † ROC curve and Youden’s index analyses were used to determine the cut-off value of primary tumor size.

Annealing-induced modifications in Al doped ZnO thin films: Correlating temperature with structural and photoelectrical properties

Clinical outcomes and treatment sequencing effects in well-differentiated grade 3 gastroenteropancreatic neuroendocrine tumors.

e16311 Background: Following the 2017 WHO reclassification, well-differentiated grade 3 neuroendocrine tumors (WDG3 NETs) were recognized as distinct from neuroendocrine carcinomas due to their unique biology. Given this recent change, outcomes data for WDG3 NETs remain limited. This study analyzes clinical outcomes and impact of treatment sequencing in WDG3 NETs. Methods: We included WDG3 gastroenteropancreatic (GEP) NET patients treated at our multidisciplinary NET clinic from 2014–2025. Median progression-free survival (mPFS) and overall survival (OS; from date of biopsy) were estimated using Kaplan–Meier methods with p-values derived from Cox regression analysis. Objective response rate (ORR) was assessed using RECIST v1.1. Subgroup analyses evaluated patients receiving multiple systemic therapy lines. Lines of treatment were categorized as first-line (1L) or second line and beyond (2L). All patients were initially treated with somatostatin analogue therapy (SSA) thus lines of treatment were counted following progression on initial SSA. Results: We analyzed 35 WDG3 GEP NET patients (primary sites: pancreas n = 27; small bowel n = 4; rectum n = 2; gastric n = 2). Median PFS by treatment was Peptide Receptor Radionuclide Therapy (PRRT) (n = 14, 11.53 months [m]), Capecitabine/Temozolomide (CAPTEM) (n = 20, 8.72 m), surgical debulking of liver metastases (surgery) (n = 11, 6.30 m), and non-CAPTEM chemotherapy (n = 10, 7.10 m). ORR was 12.5% for PRRT, 16.7% for CAPTEM, and 10% for non-CAPTEM chemotherapy. First-line PRRT (1L = 16.97 m vs 2L = 3.73 m, p = 0.04) and CAPTEM (1L = 16.27 m vs 2L = 7.20 m, p = 0.01) had significantly longer mPFS compared to later-line use. Timing of surgery did not impact mPFS (before systemic therapy = 6.30 m vs after = 6.10 m, p = 0.57). OS was not significant across treatment groups. Compared to first line non-CAPTEM chemotherapy, first line CAPTEM had longer mPFS (CAPTEM = 9.32 m vs non-CAPTEM = 5.36 m, p = 0.03), with a trend toward longer OS (CAPTEM = 31.70 m vs non-CAPTEM = 18.47 m, p = 0.09). Conclusions: In patients diagnosed with WDG3 GEP NETS receiving multiple lines of systemic therapy, treatment sequencing may be important with those receiving first-line CAPTEM or PRRT prior to other systemic therapies experiencing a longer progression free survival. mPFS (months) OS (months) ORR PRRT (n = 14) 11.53 (3.73-17.96) 35.45 (28.96-NA) 12.5% (1/8) CAPTEM (n = 20) 8.72 (4.63-16.64) 29.80 (23.83-53.67) 16.7% (3/18) Surgery (n = 11) 6.30 (5.17-NA) 45.30 (15.40-NA) - Non-CAPTEM chemotherapy (n = 10) 7.10 (5.67-NA) 27.77 (18.46-NA) 10% (1/10) 1L (n = 3) vs 2L (n = 9) PRRT 16.97 vs 3.73 p = 0.04 53.66 vs 38.86 p = 0.12 - 1L (n = 8) vs 2L (n = 8) CAPTEM 16.27 vs 7.20 p = 0.01 36.45 vs 27.30 p = 0.23 - Surgery before systemic therapy (n = 3) vs after systemic therapy (n = 5) 6.30 vs 6.10 p = 0.57 28.96 vs 45.30 p = 0.62 - CAPTEM (n = 16) vs non-CAPTEM chemotherapy (n = 7) 9.32 vs 5.36 p = 0.03 31.70 vs 18.47 p = 0.09 -