Browse Articles

ctDNA dynamics and prognostic value during first-line treatment of metastatic colorectal cancer: Analysis from the phase 3 PARADIGM study.

3573 Background: The phase 3 PARADIGM trial showed overall survival (OS) and tumor response advantages of anti-EGFR (panitumumab, PAN) over anti-VEGF (bevacizumab, BEV) therapy with FOLFOX6 in first-line metastatic colorectal cancer (mCRC) despite similar progression-free survival (PFS), highlighting limitations of imaging-based PFS as a surrogate for clinical benefit. We investigated whether ctDNA dynamics provide more refined prognostic information complementary to baseline (BL) ctDNA. Methods: Plasma samples collected from 556 patients (pts) with mCRC paired at pre-treatment (BL) and post-treatment (after treatment discontinuation) were profiled for ctDNA. Distribution of the highest variant allele fraction was modeled using a Gaussian mixture model. At pre- and post-treatment, pts were classified into 3 groups—High, Mid, and Low—according to ctDNA levels. OS, post-treatment survival (PTS), and PFS were compared across 9 ctDNA dynamic categories (eg, High→Low, High→Mid, High→High) based on changes from pre- to post-treatment. Results: Lower BL ctDNA was significantly associated with longer OS (median OS [95% CI]: Low, n = 97, 50.7 mo [44.0–65.2]; Mid, n = 159, 34.1 mo [26.9–37.1]; High, n = 300, 27.8 mo [26.2–31.3]). BL ctDNA level also correlated with tumor volume and mutation burden. Pts with lower ctDNA at treatment discontinuation had longer PTS. Incorporating ctDNA dynamics provided additional prognostic value. Regardless of BL ctDNA level, pts whose post-treatment ctDNA decreased to Low had the best survival (eg, High→Low: 50.9 mo [35.8–61.0]), while pts with persistently high ctDNA showed the poorest survival (High→High: 23.3 mo [18.2–27.8]). The prognostic value of ctDNA dynamics was consistent across treatment arms. Among pts with High BL ctDNA (PAN, n = 152; BEV, n = 148), a greater proportion achieved Low ctDNA at post-treatment with PAN vs BEV (29 [19.1%] vs 16 [10.8%], p = 0.053), whereas the proportions achieving Mid ctDNA were similar (52 [34.2%] vs 58 [39.2%], p = 0.40). In the High→Low/Mid ctDNA subsets, treatment discontinuation following curative resection was more frequent with PAN vs BEV (High→Low: 18/29 [62.1%] vs 7/16 [43.8%]; High→Mid: 11/52 [21.2%] vs 5/58 [8.6%]). OS and PTS trends were favorable with PAN vs BEV (OS; High→Low: 61.0 vs 43.1 mo, HR 0.49, 95% CI 0.23–1.04; High→Mid: 33.6 vs 26.8 mo, HR 0.74, 95% CI 0.50–1.11, PTS; High→Low: 55.1 vs 39.0 mo, HR 0.48, 95% CI 0.22–1.03; High→Mid: 20.6 vs 19.4 mo, HR 0.72, 95% CI 0.48–1.07). Conclusions: ctDNA dynamics add prognostic value beyond BL ctDNA level. In pts with high BL ctDNA, PAN yielded more conversions into low ctDNA levels and discontinuations following curative resection, with OS/PTS trends favoring PAN. These findings suggest that ctDNA dynamics may better reflect long-term clinical benefit than PFS, although standardized thresholds and prospective validation are needed. Clinical trial information: NCT02394834 ; NCT02394795 .

Machine learning approach to identify HDL as a prognostic factor for melanoma immunotherapy.

e21531 Background: Melanoma immunotherapy faces challenges due to heterogeneous patient responses. Current predictive biomarkers are not available in clinical practice. Serum lipids, crucial in tumor biology, show prognostic potential but lack consistent validation. To develop and validate a machine learning (ML) prognostic model integrating systemic lipid metabolism factors for predicting overall survival in melanoma patients receiving immunotherapy. Methods: A retrospective study of 381 melanoma patients was conducted. LASSO and Cox regression analyses identified prognostic features. Eight ML algorithms were trained and validated on a 7:3 split dataset to build the model. The best model was deployed as a publicly accessible application. We conducted SHAP analysis at 1-year, 3-year, and 5-year survival timepoints to generate variable importance rankings for each time node. To further investigate the key populations benefiting from the protective factor and explore whether this protection might be mediated through lipid regulation, we performed subgroup and interaction analyses using previously established thresholds. Results: The LASSO-Cox model demonstrated superior performance. Multivariable analysis identified mucosal subtype, advanced AJCC stage, high Lactate Dehydrogenase, and Ki67 index as risk factors, while high high-density lipoprotein cholesterol (HDL-C) was a protective factor. SHAP analysis ranked HDL-C as the most important predictive feature. Subgroup analysis revealed a more pronounced protective effect of high HDL-C in patients with hyperlipidemia. Finally, the model was deployed as a web (https://melanomaslnmodel.shinyapps.io/Shiny/) application to facilitate its potential clinical utility. Conclusions: HDL-C is a significant prognostic factor in melanoma immunotherapy. The web-based model provides an accurate risk prediction tool, highlighting the importance of monitoring lipid profiles in patient management.

Real-world use of olaparib in US veterans with metastatic castration-resistant prostate cancer: Treatment patterns and outcomes.

5071 Background: Olaparib, a targeted therapy for metastatic castration-resistant prostate cancer (mCRPC), has demonstrated clinical benefits in patients with homologous recombination repair (HRR) gene alterations, as shown in the PROfound trial. As the largest integrated healthcare system in the US, the Veteran’s Health Administration (VHA) offers insights into olaparib use among a diverse population. We characterized the treatment patterns and outcomes of patients with mCRPC treated with olaparib. Methods: We identified all VHA patients with mCRPC who received olaparib between May 2020 and December 2023. We then performed a retrospective chart review of data from May 2018 to June 2025 to capture pre- and post-treatment data. Demographics, baseline characteristics, biomarker testing and treatment sequencing were summarized. We analyzed time to event outcomes: time to next therapy (TTNT), and overall survival (OS) via Kaplan-Meier methods, both starting from olaparib initiation. Results: We identified 477 mCRPC patients receiving olaparib. Median age at initiation was 75, older than subjects in PROfound (median age 69). Most patients were non-Hispanic White (69%), followed by Black/African American (20%) and Hispanic/Latino (6%). Between 2020 and 2023, olaparib was most commonly initiated in ≥5th line after prostate cancer diagnosis (46%), followed by 4 th (25%), 3 rd (22%), and 2 nd line (6.5%). All patients had received an androgen receptor pathway inhibitor prior to olaparib. Median time from HRR testing to olaparib initiation was 5 months. Median TTNT was 7 months; OS was 12 months. Use of olaparib in an earlier line post first NHA was associated with numerically longer OS (17 months for 1st line vs. 8 months for 4th or later). Conclusions: Within the VHA, olaparib showed favorable outcomes despite older age and late-line use, supporting effectiveness in routine practice and in a more diverse population with substantially higher representation of Black/African American and Hispanic/Latino individuals than in clinical trials. Understanding these treatment patterns provides insight into clinical practice and helps guide towards optimal integration of olaparib into management of mCRPC. Kaplan-Meier estimates for time to event outcomes. #Events/Total Median Time (95% CI) (months) Time to Next Treatment - All Patients 449/477 7 (6-8) - Olaparib Line of Treatment Post NHA 1st line 100/111 9 (7-10) 2nd line 151/162 8 (7-10) 3rd line 92/96 6 (5-8) 4th line or later 91/92 5 (4-6) Overall Survival - All Patients 395/477 12 (11-13) - Olaparib Line of Treatment Post NHA 1st line 79/111 17 (12-22) 2nd line 133/162 15 (12-17) 3rd line 85/96 10 (8-12) 4th line or later 88/92 8 (6-9)

Cost per patient per month for a median of 3 months: Real-world value signals of KRAS ^G12C inhibitors in U.S. claims for non–small cell lung cancer.

e23078 Background: KRAS G12C inhibitors have demonstrated efficacy in clinical trials for KRAS G12C–mutated non–small cell lung cancer (NSCLC), but U.S. real-world evidence on treatment durability, safety signals, healthcare utilization, and costs remains limited. Methods: We conducted a retrospective cohort study using the Highmark insurance claims database to evaluate adults with KRAS G12C–mutated NSCLC treated with sotorasib and/or adagrasib. Outcomes included treatment duration, time to treatment discontinuation (TTD; a claims-based durability metric used as a pragmatic surrogate for progression-free survival in the absence of radiographic data), adverse-event–related claims, emergency department (ED) visits, healthcare utilization, and total and per-patient-per-month (PMPM) costs during baseline versus follow-up. Medication costs for KRAS G12C inhibitors were estimated using CMS-imputed pricing to mitigate disclosure of negotiated rates and ensure analytic stability given the small sample size. Overall survival (OS) was estimated using Kaplan–Meier methods, and Cox proportional hazards models evaluated associations between time from diagnosis to KRAS G12C inhibitor initiation and OS. Results: The cohort included 53 patients with a median age of 67 years (IQR 62–73); 64% were female. Age was independently associated with worse OS (HR 1.12 per year, 95% CI 1.04–1.20; p = 0.003). Median treatment duration was 97 days (IQR 25–300). Median total costs increased from $121,055 at baseline to $141,843 during follow-up, with PMPM costs rising from $20,176 to $21,272. Adverse-event–related claims occurred in 40% of patients. Median TTD was 97 days overall and varied by treatment strategy, with the longest durability observed among patients receiving sequential KRAS G12C inhibitors (median 210 days, IQR 165–390). Conclusions: In this U.S. claims analysis, KRAS G12C inhibitor therapy was associated with short real-world treatment durability (median TTD ~3.2 months) and substantial PMPM costs (~$21K), underscoring the economic impact of these agents in routine practice. Estimated survival probabilities were 16.7% at 1 year and 5.6% at 2 years from treatment initiation, lower than those reported in pivotal trials, suggesting a potential effectiveness–value gap in real-world care. Limitations include retrospective claims-based ascertainment, lack of radiographic progression data, small sample size, absence of a control group, and residual confounding.

Temporal trends and sociodemographic disparities in place of death among adults with pancreatic cancer in the United States (1999–2023).

12035 Background: Location of death is a critical quality metric for pancreatic cancer due to its rapid trajectory and high symptom burden. While home-based hospice is promoted, it is unclear if shifts from hospital death have been equitable. We analyzed 25-year national trends and independent predictors of place of death. Methods: We analyzed CDC WONDER death certificate data (1999–2023) for pancreatic cancer decedents aged ≥20 years (ICD-10 C25.x). Place of death categories: Home, Hospice/Nursing Facility, Inpatient, or Outpatient/ER. We calculated annual trends and used multinomial logistic regression to estimate adjusted odds ratios (aOR) with 95% confidence intervals (CI), adjusting for age, sex, race/ethnicity, urbanization, and year. Inpatient death served as the reference category. Results: Of 899,332 deaths, acute care hospital deaths declined (34.0% to 21.0%) while home (48.6% to 56.1%) and hospice/nursing facility deaths (15.7% to 21.3%) increased. However, significant disparities persisted. Compared to Non-Hispanic Whites, Black patients were less likely to die at home (aOR 0.55; 95% CI, 0.54–0.56) or in hospice/nursing facilities (aOR 0.63; 95% CI, 0.62–0.65) and significantly more likely to die in Outpatient/ER settings (aOR 1.57; 95% CI, 1.51–1.64). Hispanics were less likely to die in hospice/nursing facilities (aOR 0.57; 95% CI, 0.55–0.58). Rural residents had lower odds of hospice/nursing facility death (aOR 0.89; 95% CI, 0.87–0.91) vs. large metro. Younger age (20–64) was associated with hospital death. Conclusions: Despite substantial shifts from hospital to home settings, Black and Hispanic patients remain significantly less likely to access hospice and more likely to die in emergency settings. These findings highlight structural inequities requiring targeted interventions to ensure high-quality end-of-life care for minority populations. Multivariable adjusted odds ratios (aOR) for place of death in pancreatic cancer. Predictor Comparison Decedent's Home (aOR) Hospice/Nursing Facility (aOR) Outpatient or ER (aOR) Black vs. White 0.55 (0.54–0.56) 0.63 (0.62–0.65) 1.57 (1.51–1.64) Asian vs. White 0.74 (0.72–0.76) 0.51 (0.49–0.53) 0.85 (0.77–0.95) Hispanic vs. Non-Hispanic 0.92 (0.90–0.94) 0.57 (0.55–0.58) 1.01 (0.94–1.08) Rural vs. Large Metro 1.08 (1.06–1.10) 0.89 (0.87–0.91) 0.92 (0.88–0.97) Male vs. Female 0.90 (0.89–0.91) 0.78 (0.77–0.79) 1.09 (1.05–1.13) Age 85+ vs. 20–64 1.79 (1.75–1.82) 3.69 (3.61–3.76) 0.66 (0.62–0.71) Age 75–84 vs. 20–64 1.39 (1.37–1.41) 1.91 (1.88–1.94) 0.81 (0.78–0.85) Age 65–74 vs. 20–64 1.18 (1.17–1.20) 1.33 (1.31–1.36) 0.89 (0.85–0.92) Abbreviations: aOR, adjusted Odds Ratio; CI, Confidence Interval; ER, Emergency Room; Ref, Reference Group.

Efficacy of Lu-PSMA–based treatment strategies in metastatic hormone-sensitive prostate cancer: A systematic review and meta-analysis.

e17114 Background: Lutetium-177-PSMA-617 (Lu-PSMA) has demonstrated significant survival benefit in metastatic castration-resistant prostate cancer; however, its role in metastatic hormone-sensitive prostate cancer (mHSPC) remains under investigation. This systematic review and meta-analysis aim to assess the efficacy of early integration of Lu-PSMA in high-volume mHSPC. Methods: Following PRISMA guidelines, a systematic search of PubMed/MEDLINE, Embase, CENTRAL, and ClinicalTrials.gov was conducted from inception through January 1, 2026, using MeSH terms and keywords related to Lu-PSMA, PSMA radioligand therapy, mHSPC, and randomized trials. Randomized phase II trials comparing Lu -PSMA-based therapy with standard treatment in high-volume mHSPC and reporting progression-free survival (PFS) were included. Hazard ratios (HR) and 95% confidence intervals (CI) were pooled using a random-effects model. Pooled estimates were derived using the Freeman–Tukey transformation with Knapp–Hartung adjustment, implemented in R (version 4.5.2). Results: Two randomized phase II trials comprising 160 patients (Lu-PSMA n = 78; control n = 82) were included. In the post-docetaxel consolidation trial, 30 patients with synchronous high-volume mHSPC and residual disease after ADT plus docetaxel were randomized. Median age was 69 vs 68 years; ECOG performance status ranged from 0–2; and all patients had completed 6 prior docetaxel cycles. Lu-PSMA consolidation resulted in higher objective response rates (53% vs 7%) and greater achievement of undetectable PSA at 6 months (60% vs 13%), with no grade ≥3 toxicity. In the upfront sequential trial, 130 patients with de novo high-volume mHSPC received Lu-PSMA followed by docetaxel or docetaxel alone with ADT. The median age was 69 years; 91% had high-volume disease by conventional imaging, and 8% had visceral metastases. Undetectable PSA at 48 weeks was more frequent with Lu-PSMA (41% vs 16%), and Lu-PSMA was associated with longer PSA progression-free survival and radiographic progression-free survival. Grade ≥3 adverse events were similar between arms (29% vs 27%) and largely attributable to docetaxel. In pooled analyses, Lu-PSMA-based strategies significantly improved PSA progression-free survival (HR 0.60; 95% CI, 0.40–0.90; I² = 0%; τ² = 0) and radiographic progression-free survival (HR 0.55; 95% CI, 0.34–0.92; I² = 0%; τ² = 0). Conclusions: Lu-PSMA-based strategies demonstrate promising clinical activity in patients with mHSPC, with consistent improvements in both biochemical and radiologic PFS across different treatment settings. These findings provide rationale for ongoing and future phase III trials of Lu-PSMA-based intensification strategies in this subset of patients.

Artificial intelligence–enabled analysis of unstructured EHR data for identification of actionable HER2-low breast cancer phenotypes.

e13029 Background: Antibody-drug conjugates (ADCs) targeting HER2 have shown clinical effectiveness in breast cancer, even at low levels of HER2 expression, thereby widening patient eligibility. Detailed HER2 results from immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH) is often available only in unstructured clinical notes and pathology reports, leading to underestimation of HER2-low disease prevalence when relying on structured electronic health record (EHR) data alone. Artificial intelligence (AI) and machine learning methods can enable the identification of HER2-low disease by permitting the curation of data from unstructured notes. We compared HER2 status derived from 1) structured EHR fields and 2) AI-curated data from unstructured clinical documentation. Methods: ConcertAI Precision360 is a US nationwide, validated, AI-powered platform that utilizes advanced language models to deliver insights from structured and unstructured machine-curated EHR clinical data. This study focused on a subset of Precision360 breast cancer patients diagnosed on or after 1/1/2014 with HER2 results within 180 days of initial diagnosis from both 1) EHR-derived, native, structured data and 2) AI-curated data from unstructured EHR clinical notes. HER2 results as defined by the American Society of Clinical Oncology/College of American Pathologists guidelines within 180 days of initial diagnosis were included and classified as positive (IHC 3+ or IHC2+/FISH positive), low (IHC 2+/FISH negative or IHC 1+) negative, equivocal, or unknown. Results: HER2 status was available in both structured and unstructured/AI-curated data sources for 27,126 patients. HER2-low rates for structured, unstructured/AI-curated, and the combined data sources of both were 10%, 28%, and 34%, respectively. HER2-negative rates were 73%, 56%, and 52%, while HER2-positive status did not vary between the three groups (13%). Conclusions: AI-based curation of unstructured clinical notes reclassified a subset of patients, increasing the number of HER2-low patients and reducing those labeled as HER2-negative. Unstructured clinical documentation contained substantially more detailed and higher-resolution HER2 information than structured EHR fields alone. This approach can increase the identification of patients eligible for HER2-targeted therapies HER-2 status distribution from structured EHR, AI-abstracted unstructured EHR, and both sources for breast cancer patients diagnosed from 2014-2025. Structured HER(n-27,126) Unstructured/AI Curated EHR (n-27,126) Structured and unstructured EHR (n-27,126) HER2 status N % N % N % Positive 3454 12.7 3498 12.9 3575 13.2 Low 2803 10.3 7703 28.4 9328 34.4 Equivocal 583 2.1 290 1.1 121 0.4 Negative 19848 73.2 15084 55.6 13984 51.6 Unknown 438 1.6 551 2.0 118 0.4

Genomic landscape and evolutionary dynamics of <i>RAS</i> alterations in glioma: A large-scale clinicopathologic analysis.

e14077 Background: Gliomas are molecularly heterogeneous. RAS alterations ( KRAS , NRAS , HRAS ) are discussed in the 2021 WHO under a number of glioma subtypes, but their prevalence and clinical significance remains unclear. Preclinical data suggest RAS/MAPK pathway activation is a potentially actionable vulnerability. We utilized a large, clinically sequenced dataset to characterize the incidence, hotspot distribution, and longitudinal evolution of RAS -altered gliomas. Methods: We retrospectively analyzed a cohort of 1,804 patients (pts) with glioma (2,100 samples) who underwent MSK-IMPACT targeted sequencing at Memorial Sloan Kettering Cancer Center. The prevalence of KRAS/NRAS/HRAS alterations was assessed across the full cohort. Detailed genomic analysis was performed on 80 RAS -altered pts (105 samples: 99 tumors, 6 CSF), including mutations, amplifications, fusions, and co-occurring alterations at diagnosis and recurrence. Results: RAS alterations were identified in 80/1,804pts (4.4%), including KRAS (3.4%), NRAS (0.7%), and HRAS (0.3%). Histologies included glioblastoma (37.5%), oligodendroglioma (27.5%), astrocytoma (18.8%), pilocytic astrocytoma (5.0%), and other tumor types (11.2%). Among KRAS -mutant tumors, the most frequent hotspots involved codon G12 (G12D/R/A/V/C; n=20), followed by Q61H/E/L (n=7) and Q61K (n=4). Common co-alterations included TERT (54%), IDH1 (43%), CDKN2A (30%), and TP53 (8%). Longitudinal sequencing (n=19 pts) revealed KRAS alterations persistence in 32% (n=6). Notably, acquired RAS alterations at recurrence were identified in 37% (n=7/19), involving KRAS (n=3), NRAS (n=2), and multi-gene RAS alterations (n=2): KRAS/HRAS and KRAS/NRAS . Two pts with oligodendrogliomas who acquired NRAS mutations demonstrated rapid clinical progression within 12 months. Conclusions: In this large institutional cohort, RAS family alterations were observed across diverse glioma histologies. The acquired RAS mutations at recurrence may suggests these alterations can drive tumor evolution and treatment resistance. These findings underscore the importance of longitudinal genomic profiling and support the evaluation of RAS/MAPK -targeted therapies in selected glioma pts.

Longitudinal follow-up after identification of variants of uncertain significance in highly penetrant cancer predisposition genes.

10607 Background: ASCO and the NCCN recommend that patients with variants of uncertain significance (VUS) in hereditary cancer predisposition genes undergo periodic variant reassessment, since reclassification of VUS as pathogenic or likely pathogenic (P/LP) may alter clinical management. However, the extent to which such longitudinal follow-up occurs in practice has not been studied. Methods: Data were retrospectively reviewed from patients who underwent germline genetic testing for cancer-related indications from 2015-2025 at an adult genetics clinic in an academic-affiliated, safety-net healthcare system. Analyses were restricted to patients found to have VUS (without P/LP variants) in any of 23 highly-penetrant cancer predisposition (HPCP) genes based on the NCCN guidelines for genetic/familial high-risk assessment: APC , ATM , BMPR1A , BRCA1 , BRCA2 , BRIP1 , CDH1 , CDKN2A , CHEK2 , EPCAM , HOXB13 , MLH1 , MSH2 , MSH6 , MUTYH (biallelic), PALB2 , PMS2 , PTEN , RAD51C , RAD51D , SMAD4 , STK11 , and TP53 . The primary outcome of interest was the percent of patients who adhered to clinician recommendations for follow-up after VUS disclosure, excluding those for whom insufficient time had elapsed to assess follow-up status. Chi-square tests were used to assess if follow-up rates differed among patients with VUS that were considered “clinically concordant” (personal history of a tumor consistent with the gene’s neoplastic spectrum), “possibly concordant” (history of a relevant neoplasm in a 1st/2nd degree relative but not the patient), or “likely incidental” (no relevant personal or family cancer history). Results: Of 2028 tested patients, 25% (n = 501) were found to have one or more cancer-related VUS (without P/LP variants), including 308 with VUS in HPCP genes. At the time of initial result disclosure, 11% of these patients were discharged from further follow-up, while the remaining 89% were advised to return for variant reassessment, typically within 2 years. Adherence to these recommendations was low overall, with only 38% returning for any post-disclosure follow-up. Rates of follow-up were similar among patients with VUS classified as clinically concordant (40%), possibly concordant (34%), or likely incidental (45%); p = 0.47. Conclusions: Despite clear clinician guidance to return for variant reassessment, most patients with VUS in highly-penetrant genes did not engage in recommended follow-up, even in the presence of a clinically compatible personal and/or family cancer history. Alternative approaches to longitudinal VUS management - such as automated recontact and/or direct-to-patient notification of variant reclassifications - should be explored to mitigate the risk of loss to follow-up in this population.

Capivasertib plus fulvestrant in Chinese patients with HR+/HER2− advanced breast cancer: Interim analysis of CAPItrue.

1088 Background: After disease progression on cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) plus endocrine therapy (ET), patients (pts) with HR+/HER2- advanced breast cancer (ABC) face limited treatment options and poor prognosis, particularly those with PI3K/AKT pathway tumor alterations, which are major drivers of disease progression and treatment resistance mediated centrally by AKT. Targeting the PI3K/AKT pathway represents a mechanism-driven precision strategy to overcome CDK4/6i/ET resistance, with potential to maximize ET benefit and delay subsequent chemotherapy. In the phase III CAPItello-291 trial, capivasertib (CAPI) plus fulvestrant (FUL) improved progression free survival (7.3 vs 3.1 months, HR 0.50) versus placebo plus FUL in pts with PIK3CA/AKT1/PTEN -altered tumors. CAPItrue (NCT06635447) is an ongoing phase IIIb study of CAPI plus FUL in Chinese pts with HR+/HER2- ABC progressing on ET, with a focus on PIK3CA/AKT1/PTEN-altered disease, aiming to inform precision 2 nd line treatment following CDK4/6i progression. Methods: CAPItrue enrolled Chinese pts with HR+/HER2- ABC progressing on ET±CDK4/6i. All pts received oral CAPI (400 mg BID, 4 days on, 3 days off) and intramuscular FUL. This pre-specified interim analysis was performed in the cohort (C1) without prior FUL (conducted after the last C1 pt received ≥1 dose of study treatment). Baseline characteristics, biomarker profiles, preliminary efficacy (interim objective response rate [ORR] was evaluated in pts with ≥4 months of follow-up) and safety were summarized. Results: By Aug 20, 2025, 195 pts were enrolled in C1 and received study treatment. PIK3CA/AKT1/PTEN alterations were detected in 115 (59.0%) pts (altered group). The median age was 55.0 yrs; 64.1% were post-menopausal. Prior therapy for ABC included: 75.4%/8.7% 1/2 prior lines of ET; 65.1% CDK4/6i, 17.9% chemotherapy. The altered group showed similar characteristics. In patients with ≥4 months of follow-up, ORR was 35.6% overall (37/104, 1 complete and 36 partial responses [PR]) and 43.1% in the altered group (25/58, 25 PR). Overall, at a median follow-up of 4.1 months,92.8% had ≥1 adverse event (AE); 88.7% had AEs possibly related to CAPI; and 34.9%/11.8% had grade ≥3/serious AEs (SAE). A similar safety profile was seen in the altered group (any AE: 92.2%, grade ≥3 AE: 30.4%, SAE: 11.3%). No new safety signal was observed. Conclusions: In Chinese pts with PIK3CA/AKT1/PTEN -altered HR+/HER2- ABC previously treated with ET±CDK4/6i, CAPI plus FUL showed encouraging preliminary efficacy and safety. Follow-up is ongoing. Clinical trial information: NCT06635447 .

Incidence and predictors of delayed hematologic engraftment after autologous stem cell transplantation and early post-transplant complications: A retrospective study.

e19103 Background: Delayed hematologic engraftment after autologous stem cell transplantation (ASCT) may prolong cytopenias and increase susceptibility to post-transplant complications. We evaluated the incidence and predictors of delayed engraftment and summarized infectious and non-infectious complications following ASCT. Methods: In this retrospective cohort analysis, we analyzed 306 patients undergoing ASCT for hematologic and other malignancies. Engraftment was categorized as early or delayed using cutoffs of 14 days for absolute neutrophil count (ANC) recovery and 21 days for platelet recovery. Outcomes included fever and infections, antibiotic escalation intensity, and post-transplant complications. Multivariable logistic regression was used to identify predictors of delayed platelet engraftment and delayed ANC engraftment. Results: Median age was 43 years (IQR 27), and 54.6% were male. Plasma cell neoplasms (45.1%) and Hodgkin lymphoma (40.2%) accounted for most transplants. Delayed platelet engraftment occurred in 25.2%, and delayed ANC engraftment in 32.4%; 44.4% experienced delayed engraftment of ANC and/or platelets, and 13.1% had a delay in both. Infectious complications were frequent, including permanent catheter infection in 16.3% and infected admission swabs in 15.9%. Fever occurred in 92.8% (median duration 5 days) and neutropenic fever in 90.2%; post-conditioning infection occurred in 51.6%. Tier 2 (broad empiric, non-carbapenem) antibiotics were most common (60.1%), with 13.1% requiring tier 3 and 13.1% tier 4 escalation. Non-infectious complications included acute kidney injury (16.3%), septic shock (10.5%), ICU admission (4.6%), and all-cause mortality (8.0%). In multivariable models evaluating baseline clinical factors as predictors, pre-existing respiratory disease at baseline was associated with higher odds of delayed platelet engraftment (OR 2.56), whereas baseline hepatitis B status was associated with lower odds of delayed platelet engraftment (OR 0.40). Delayed ANC engraftment was independently associated with lower baseline platelet count (OR 0.994), baseline heart disease (OR 2.94), and pre-conditioning infection (OR 2.76). Conclusions: In this ASCT cohort, delayed engraftment was common, alongside a high early infectious burden and clinically meaningful complications. Baseline respiratory disease and lower baseline platelet count identified patients at higher risk for delayed platelet and ANC recovery, respectively, while baseline heart disease and pre-conditioning infection were also independently associated with delayed ANC engraftment.

Exploratory study of <i>TP53</i> mutations in circulating tumor DNA as prognostic and longitudinal monitoring biomarkers for relapsed ovarian carcinoma patients.

e17568 Background: This study aims to investigate the prognostic and recurrence monitoring applications of TP53 mutated circulating tumor DNA in platinum-resistant ovarian cancer (PROC) with pegylated liposomal doxorubicin (PLD) therapy. Methods: This is a prospective observational study (NCT05976932), and twenty-seven PROC patients with TP53 mutations were recruited with PLD treatment. CA125 levels were measured prior to each cycle of chemotherapy. While TP53 mutations in circulating tumor DNA were detected in the first three cycles of chemotherapy, and subsequent each two cycles together with radiological assessments. Three TP53 algorithms were established for prognostic evaluation and recurrence monitoring: [1] Algorithm 1, TP53 mutation burden algorithm ( TP53 mutation be detected after clearance or TP53 MAC ≥ 1000); [2] Algorithm 2, dynamic TP53MAC change algorithm ( TP53 mutation be detected after clearance or TP53MAC reach twofold of the nadir); and [3] Algorithm 3, combined algorithm (positive if either Algorithm 1 or Algorithm 2 is met). Results: The median PFS of the enrolled cohort was 114 days (95% CI: 66.51-161.50 days), and the median baseline TP53 MAC value was 72.43 (range from 0.00 to 6583.60). Results meeting the aforementioned criteria were assigned to the ‘TP53+’ group, while the others were assigned to the 'TP53-' group. Prognostic evaluation based on the first three cycles exhibit significant differences between the TP53+ and TP53- groups across all three TP53 algorithms (log-rank p =0.00327, 0.00017 and 0.00001, respectively). Algorithm 3 shows the best performance while the TP53+ group had a median progression-free survival (PFS) of 79 days (95% CI: 50.14-107.86 days), versus 159 days (95% CI: 78.21-239.79 days) in the TP53- group. Conversely, CA125 levels showed no prognostic significance ( p =0.87010). What’s more, monitoring TP53MAC during longitudinal follow-up of PROC patients may indicate the risk of recurrence earlier than radiological evidence. Specifically, Algorithm 3 achieved a sensitivity of 74.07% (95% CI: 53.72%-88.89%) and median lead time of 26 days ( one treatment cycle in advance), much better than CA125, whose sensitivity was 48.15% (95% CI: 28.67%-68.05%). Conclusions: Multiple TP53 mutation algorithms were developed in this study based on the sensitive, rapid and cost-effective digital PCR platform, demonstrating the potential of TP53 in prognostic evaluation and recurrence monitoring for PROC patients. Clinical trial information: NCT05976932 .

Bridging the access gap: First-line blinatumumab for KMT2A-rearranged infant acute lymphoblastic leukemia (ALL) in a public health system.

e23441 Background: Infant acute lymphoblastic leukemia (ALL) accounts for approximately 4% of pediatric ALL and remains associated with poor outcomes, particularly in cases with KMT2A rearrangements. While event-free survival (EFS) in older children reaches 80–85%, infants continue to experience inferior survival and substantial treatment-related toxicity. Incorporation of blinatumomab in first-line therapy has emerged as a strategy to deepen remission, achieve minimal residual disease (MRD) negativity, reduce chemotherapy exposure, and optimize conditions for hematopoietic stem cell transplantation (HSCT) in first complete remission (CR1). However, access to this therapy is limited in many low- and middle-income countries (LMICs), where cost remains a major barrier. Methods: We describe three infants with pro-B ALL harboring KMT2A::AFF1 rearrangements who received blinatumomab during CR1 within the Brazilian public health system (SUS), enabled through support from a nonprofit organization. Between November 2022 and June 2024, all patients received four cycles of blinatumomab. Ages at diagnosis were 5, 6, and 23 months, with initial white blood cell counts of 46,850/mm³, 1,073,000/mm³, and 635,000/mm³, respectively. All patients were CNS-1 and achieved CR1 prior to blinatumomab. Treatment backbones included AIEOP-BFM 2017 and Interfant-06 protocols. Results: All patients achieved and sustained MRD negativity at days 15 and 29 of blinatumomab. Treatment was well tolerated, with no adverse events above grade 1. Two patients proceeded to HSCT in CR1, while one remained in continuous remission without transplantation. All patients are alive and disease-free, with EFS ranging from 14 to 37 months. Conclusions: First-line blinatumomab was safe and effective in infants with KMT2A -rearranged ALL, enabling deep molecular responses with minimal toxicity and reduced reliance on intensive chemotherapy. This experience demonstrates that strategic partnerships with civil society organizations can overcome access barriers in public health systems, potentially lowering toxicity-related morbidity and downstream costs while delivering state-of-the-art care to highly vulnerable patients in LMICs.

Enhanced targeted delivery of cisplatin via folate and boron-modified magnetic nanoparticles: A promising approach for cervical cancer treatment

Neoadjuvant chemotherapy and individualized de-escalation surgery for fertility preservation in stage IB1-IIA2 cervical cancer: A multicenter prospective study (FIND study).

5533 Background: Radical trachelectomy (RT) has long been the standard fertility-sparing surgery (FSS) for early-stage cervical cancer (most validated for tumor&lt;2cm), produced satisfied oncologic outcomes but adverse pregnancy outcomes. Neoadjuvant chemotherapy (NACT) offers a potential pathway for tumor downstaging, which may further expand the population eligible for FSS. Based on this, this study aimed to evaluate the oncologic and reproductive outcomes of an individualized, NACT-based fertility-preserving strategy in patients with early-stage cervical cancer (FIGO 2018 IB1–IIA2) (CSEM009, NCT02624531). Methods: This prospective, non-randomized clinical study enrolled patients aged 18–40 years with pathologically confirmed stage IB1–IIA2 squamous, adenocarcinoma, or adenosquamous carcinoma and a strong desire for fertility preservation. All patients underwent pretreatment pelvic MRI. Patients with a baseline tumor diameter &lt;1 cm proceeded directly to simple trachelectomy (ST). Those with tumors ≥1 cm received 2–3 cycles of platinum-based NACT. Individualized surgery was performed based on Post-NACT MRI: cervical conization (CON) for complete response, ST for residual disease ≤2 cm, and RT for residual disease 2–4 cm. Lymph node assessment involved sentinel lymph node biopsy (SLNB) or systematic lymphadenectomy. Primary endpoints were 5-year overall survival (OS), 5-year progression free survival (PFS), and reproductive outcomes. Results: From June 2015 to June 2023, 99 eligible patients were enrolled. Among them, 84 received NACT, and 80 ultimately underwent FSS. Median follow-up duration was 67 months (range: 7–122). For the entire cohort of 99 patients, 5-year PFS and OS were 88.9% and 93.9%, respectively. In the FSS group (n=80), 5-year PFS and OS were 91.3% and 96.3%. In FSS patients, univariate analysis identified lymphovascular space invasion (LVSI) as significantly associated with recurrence and mortality (p&lt;0.05). Patients with initial tumors ≤2 cm (n=42), 2–4 cm (n=29), and ≥4 cm (n=9) had 5-year PFS rates of 95.2%, 86.2%, and 88.9%, and 5-year OS rates of 97.6%, 93.1%, and 100%, respectively. Nineteen patients failed to undergo FSS with 5-year PFS 78.9% and 5-year OS 84.2%. Of 40 FSS patients attempting pregnancy, 19 (47.5%) achieved at least one pregnancy, resulting in 17 cumulative deliveries: 3 after conization and 14 after ST. No successful pregnancies occurred after RT. Conclusions: This prospective study demonstrates that fertility-sparing strategy involving NACT and individual less radical FSS provides favorable long-term oncologic safety and meaningful reproductive potential in patients with FIGO 2018 IB1-IIA2 cervical cancer. Clinical trial information: NCT02624531 .

Nanochemo-immunotherapy of ER-positive metastatic breast cancer (MBC) with PEG-liposomal doxorubicin (PLD) and pembrolizumab (PEM).

1060 Background: PLD is a nanomedicine containing doxorubicin, a potent immunogenic cell death inducer. Based on the pharmacological profile of PLD, we hypothesized that PLD-based chemotherapy should allow for improved immune recognition of tumor cells and activation of T cells by PD1 blockade. We report here the results of a phase 1B study with a combination of PLD and PEM in ER+/Her2 negative MBC. Methods: Patients with MBC, whose disease progressed on hormonal, CDK 4/6 inhibitors and up to 3 lines of chemotherapy, were eligible for enrollment. Primary objectives were evaluation of safety and tumor response, and secondary objectives were overall survival and pharmacokinetic analysis of PLD and PEM. In a first cohort of 15 patients, PLD 30 mg/m 2 was infused along with PEM 200 mg on day 1 every 3 weeks. In a second cohort of 20 patients, PLD 40 mg/m 2 was infused on day 1 every 4 weeks without change of PEM dose-schedule. Responding and stable patients continued treatment until disease progression or treatment intolerance. All patients were followed up on for survival. Results: 35 patients were enrolled. A total of 201 PLD and 257 PEM treatments were administered until data lock. Treatment was well tolerated with no grade 3-4 neutropenia, no cardiac events, and no grade 2 hair loss. In one patient, a severe infusion reaction to PLD was observed forcing discontinuation of PLD in the 2 nd cycle. There were 2 cases of grade 4 hepatitis, 1 case of grade 4 hemolytic anemia, and 5 cases of grades 1-2 hypothyroidism, possibly or probably related to PEM. PLD-related skin toxicity (palmar-plantar erythema, grades 1-2) was observed after 3 or more cycles, forcing treatment delays. Among evaluable patients receiving ≥3 cycles of PEM (n=30), we observed 8 partial and 2 complete responses with a long median duration of response (11 mo) and survival (28 mo). In 5 patients, near complete responses of large liver metastases were observed. Median survival was 25 mo for all patients and 26 mo for evaluable patients. Eight patients, including 1 patient still under treatment, remain alive at data lock with survival in the range of 10+ to 51+ mo. The plasma clearance of PLD was mono-exponential with high Cmax, long T½ (~3 days), slow clearance, and small Vcc. There was a significant increase of ~20% in the average AUC of PLD between the 1 st and 3 rd cycle indicating delayed clearance upon PLD retreatment. Analysis of PEM plasma levels revealed a mean T½ of ~11 days with high trough concentration by end of the cycle implying saturation of all accessible PD1 receptors. Conclusions: The combination of both dose levels of PLD with PEM is well tolerated, active, and feasible for extended treatment with durable responses. The favorable response and survival data in this heavily pretreated patient group suggest that PEM has significant contribution to the anti-tumor effect. A randomized study in ER+ MBC patients based on this regimen is warranted. Clinical trial information: NCT03591276 .

Golcadomide (GOLCA), a potential, first-in-class, oral CELMoD, plus rituximab (R) versus investigator’s choice (IC) in patients (pts) with relapsed/refractory follicular lymphoma (R/R FL) who have received ≥ 1 line of systemic therapy: GOLSEEK-4, a phase (Ph) 3, randomized study.

TPS7102 Background: Follicular lymphoma (FL) is the most common indolent non-Hodgkin lymphoma (NHL), typically presenting as advanced-stage at diagnosis. With current SOC (chemoimmunotherapy [CIT] and maintenance), many pts can achieve remission; however, FL remains incurable, with shorter remissions and overall survival (OS) following relapses. Treatments for R/R FL, including CIT or R-lenalidomide (R 2 ), offer limited long-term benefit. T-cell-redirecting therapies in ≥ 3L provide better efficacy but are limited by tolerability and logistical challenges. An unmet need persists for effective, well-tolerated, convenient options for R/R FL pts after ≥1L of systemic therapy. GOLCA is a potential, first-in-class, oral CELMoD designed for the treatment of lymphoma, with preferential distribution to lymphoid organs and enhanced activity in lymphoma cell lines. GOLCA induces rapid and deep degradation of Ikaros and Aiolos, leading to direct cell killing and immunomodulatory activity. GOLCA 0.4 mg + R was studied in heavily pre-treated R/R FL pts (including those given lenalidomide [LEN] and T-cell redirecting therapies) in the Ph 1/2 CC-99282-NHL-001 study, resulting in objective response rate 97%, complete response rate 78% and tolerable safety, suggesting benefit vs SOC (Chavez et al., ASH 2025, #1006). As a result, the Ph 3 study, GOLSEEK-4 (NCT06911502) was initiated. Methods: GOLSEEK-4 is a global, randomized, Ph 3 study evaluating fixed-duration, chemo-free GOLCA + R vs IC (R 2 or R-chemo) in R/R FL after ≥1 prior lines of therapy. Included: adults (≥18 yr) with grade 1-3A R/R FL or cFL, PET-positive disease with measurable lesions (Lugano criteria), ECOG 0–2 (or 3 if due to lymphoma), require treatment based on modified GELF, and ≥1 prior regimen, including anti-CD20 + alkylating agent. Prior T-cell-redirecting therapy allowed. Excluded: composite DLBCL/FL, transformed NHL, CNS involvement, those who are R/R or intolerant to all options in IC arm. Approximately 400 pts will be randomized 1:1 to GOLCA (0.4 mg QD, Days 1–14 per 28-day cycle) + R for 5 cycles, then GOLCA monotherapy for 7 cycles (12 cycles total) or IC (R 2 for 5 cycles then LEN monotherapy for 7 cycles, or R-CHOP or R-Bendamustine for 6 cycles). Randomization will be stratified by disease progression within 24 months (mo) vs &gt;24 mo from initial CIT, prior lines (2L vs 3L+), and IC regimen. Pts will be followed for at least 5 yrs. Recruitment began July 2025. Primary endpoint: progression-free survival (IRAC). Secondary endpoints: overall response rate (IRAC), OS, complete metabolic response, minimal residual disease, time to next therapy, duration of response. Safety is exploratory. Acknowledgement: BMS ChatGPT4 used to revise existing text with human author input (Jan 26). Clinical trial information: NCT06911502 .

A phase 1, first-in-human study of DS9051, a novel targeted protein degradation molecule, in patients with advanced/metastatic adrenocortical carcinoma (ACC) or metastatic castration-resistant prostate cancer (mCRPC).

TPS3179 Background: ACC and mCRPC are difficult-to-treat malignancies. mCRPC typically progresses despite androgen deprivation and androgen receptor pathway inhibitor (ARPI) therapy, with or without taxanes. Similarly, treatment options for ACC are limited and prognosis is generally unfavorable. DS9051 is a targeted protein degradation molecule that has been designed to selectively degrade a key protein involved in the development and progression of both ACC and mCRPC via a novel mechanism. It leverages the ubiquitin-proteasome system, where DS9051 acts as a bridge to link the target protein and E3 ligase, initiating ubiquitination and degradation of the target protein. Methods: DS9051-079 (NCT07189403) is a Phase 1, first-in-human, open-label, multicenter study of DS9051 (N≈40). Patients must be adults with histologically confirmed advanced or metastatic ACC (Stage III–IV) or mCRPC and an Eastern Cooperative Oncology Group performance status of 0 or 1. Patients with ACC must have measurable disease per Response Evaluation Criteria in Solid Tumours, version 1.1 (RECIST 1.1) that is not amenable to radical surgical resection or definitive radiotherapy. Further inclusion criteria for patients with mCRPC include prior treatment with ≥1 line of ARPI therapy for castration-sensitive or -resistant prostate cancer for ≥12 weeks and with ≥1 line of chemotherapy (or not amenable to chemotherapy). These patients must also have ≥1 of the following criteria: prostate-specific antigen (PSA) progression per Prostate Cancer Working Group 3 (PCWG3) criteria, bone disease progression per PCWG3 criteria, or soft tissue disease progression per RECIST 1.1. Patients will receive DS9051 orally at escalating doses. The primary objective is to assess the safety and tolerability of DS9051 and to determine the maximum tolerated dose and/or recommended dose for expansion. Safety endpoints include dose-limiting toxicities and treatment-emergent adverse events. Secondary endpoints for both tumor types include objective response rate, disease control rate, clinical benefit rate, and duration of response (all assessed by the investigator, per RECIST 1.1 for ACC and per PCWG3 criteria for mCRPC); for ACC, progression-free survival (PFS) will be assessed by the investigator per RECIST 1.1, and for mCRPC, radiographic PFS and PSA decline will be assessed by the investigator per PCWG3 criteria. Enrollment is ongoing. Clinical trial information: NCT07189403 .

Risk factors for relapse in patients with stage I testicular seminoma.

e17011 Background: The relapse rate for patients with clinical stage I seminoma is approximately 20% and surveillance is strongly preferred. Risk- adapted management with adjuvant carboplatin chemotherapy is another option for those at high risk of relapse but no consensus on high risk factors has yet been determined. Tumour size &gt; 4 cm, lymphovascular and rete testis invasion have been inconsistently associated with the risk of relapse. In our centre all patients with stage I seminoma are managed with surveillance wich gives us the opportunity to investigate risk factors for relapse. The aim of this study was to investigate the association of tumour size, lymphovascular invasion and rete testis invasion with the risk of relapse in patients with stage I seminoma. Methods: We identified patients with clinical stage I seminoma diagnosed between 2010 and 2020 who had tumour size, lymphovascular invasion and rete testis invasion reported in their medical record. Relapse rate was rhe primary outcome and the variables for relapse were tumour size &gt; 4, lymphovascular invasion and rete testis invasion. To evaluate this variables The Cox proportional hazard model was built. Results: In total, 97 patients were evaluated. Median age of the population was 36 years (range 22- 56 years). 29 patients (29.8 %) relapsed and the median relapse time was 16 months (range 3 -57 months). Median follow- up time for patients without relapse was 9.3 years. Lymphovascular invasion and tumour size &gt; 4 were statistically significant and independent risk factors for relapse. Lymphovascular invasion was associated with approximately 2,38 times higher risk of relapse. Tumour size &gt; 4 cm was associated with 2,6 times higher risk of relapse and was the strongest predictor of relapse. Rete testis invasion slightly increased the risk of relapse but this was not statistically significant. Results are shown in Table 1. Conclusions: Tumour size and lymhpovascular invasion were independent factors associated with increased risk of relapse while rete testis invasion was not. The strongest risk factor for relapse was tumour size &gt; 4 cm which is consistent with previous studies. Since the risk of relapse for stage I seminoma is acceptably low and disease specific- survival high surveillance is the preferred option. For patients not suitable for surveillance risk-adapted management with well defined risk factors can be useful in clinical practice. Results. Variable coef HR (exp(coef)) SE(coef) z p-value Lower 95% CI Upper 95% CI Lymphovascular invasion 0,8665 2,3785 0,3848 2,25 0,0245 1,1187 5,0645 Tumour size &gt; 4 cm 0,9498 2,5852 0,3807 2,49 0,0128 1,2227 5,4627 Rete testis invasion 0,2002 1,2217 0,4087 0,49 0,6234 0,5516 2,7061 HR = hazard ratio; CI = confidence interval.

A comparative socio-ecological analysis of psychosocial barriers to breast and cervical cancer screening across three Nigerian states: Significance of location.

e13624 Background: Community-based screening programs and the availability of community cancer care facilities are vital to improving cancer outcomes in Nigeria. However, the uptake of these services remains low despite the rising disease burden. While some studies in Low and Middle Income Countries (LMICs) have cited fear as a strong barrier, the underlying dimensions of this fear are rarely examined comparatively across diverse settings. The main objective is to explore how fear is experienced, perceived, and articulated within communities, and how it shapes participation in screening programs and by association, community care facilities. Methods: A qualitative, multi-site study was conducted across three purposively selected Nigerian states. The Federal Capital Territory (FCT), Nasarawa, and Rivers, between September and November 2024. The study was implemented in collaboration with the community leaders and local health authorities. Data was collected through 12 semi-structured focus group discussions and 60 in-depth interviews with community women and key stakeholders (community leaders, community influencers, and traditional healers). Transcripts were analyzed using Dedoose software and findings interpreted using the Socio-Ecological Model (SEM) to explore context specific, fear related themes shaping behavior. Results: The analysis identified multiple, interrelated domains of fear. In the FCT, the predominant SEM domains were interpersonal and organizational. The domains centered around social and institutional stigma, fear of discrimination by providers, concerns regarding privacy, distrust with sterility of screening process and procedural discomfort. On the other hand, in Nasarawa State, the societal/structural domain was at the fore. Economic vulnerability was the primary driver, with hospital-based care perceived as more expensive than traditional and herbal alternatives. In Rivers State, the community domain was most prevalent, characterized by experiential and observational fears stemming from community members witnessing the morbid effects of the disease on fellow community members. Conclusions: Fear is a multidimensional barrier to breast and cervical cancer screening. Whether rooted in social neglect, economic hardship, or situational trauma, these fears influence how communities engage with screening services. Interventions must move beyond "one-size-fits-all" approaches, prioritizing context adapted strategies, and culturally responsive communication to improve screening uptake and care-seeking behavior in Nigeria.