849 Background: Expression of the L-type amino acid transporter 1 (LAT1; gene symbol: SLC7A5 ) is significantly enriched across a wide variety of cancers, and has been associated with cancer progression and poor prognosis. Yet the relationship between LAT1 and known prognostic genomic alterations in genes such as TP53 , KRAS , and BRAF remains understudied. We evaluated SLC7A5 expression within gastrointestinal (GI) tumors in the cBioPortal database and characterized its correlation to known genomic/transcriptomic markers of cancer prognosis. Methods: We used 30,993 samples to analyze expression of SLC7A5 expression z-scores relative to diploid samples (RNA Seq V2 RSEM) across malignancies, excluding overlapping samples, from 88 cancer studies within cBioPortal. Sub-analysis were performed in hepatobiliary (HPB), colorectal (CRC), esophagogastric (EGC), and pancreatic cancers (PDAC), along with a combination of these cancer types (pan-GI-cancer). mRNA expression z-scores relative to diploid samples were stratified by SLC7A5 expression quartiles for each sub-analysis. The log2 ratio (L2R) alteration frequency of genomic/transcriptomic markers between quartiles was evaluated within the pan-GI-cancer cohort and each subgroup using a one-way ANOVA test with FDR correction. Results: SLC7A5 enrichment was significantly associated with worsened overall survival across all cancers (Hazard Ratio (HR) 1.361 95% Confidence Interval (CI) 1.282 - 1.445; p < 0.001). In the pan-GI-cancer cohort, tumors with high SLC7A5 expression were enriched for genomic alterations in TP53 (L2R 0.38), APC (L2R 0.98) and KRAS (L2R 0.61; q < 0.001 for all). In particular, KRAS alterations were enriched in CRCs and HPBs with high SLC7A5 (L2R 0.38 and 3.05; q < 0.001), while TP53 alterations were enriched in EGCs and HPBs (L2R 0.33 and 0.81; q < 0.001). Within KRAS mutant GI tumors, SLC7A5 -high expression status trended towards worsened disease free survival (HR 1.143 95% CI 0.745 - 1.753; p = 0.527). Conversely, alterations in CDH1 and SMAD4 were significantly depleted in SLC7A5 -high EGCs (L2R -2.69; q < 0.001) and PDACs (L2R -0.96, q < 0.001), respectively. Neither ERBB2 (HER2) nor CD274 (PD-L1) expression was correlated with SLC7A5 expression status in any GI cancer. Conclusions: SLC7A5 expression levels are correlated with mutations in poor prognostic genomic markers, such as TP53 , KRAS , and APC , in GI malignancies. For KRAS , SLC7A5 -high status appears to be an independent poor prognostic indicator, though larger data sets are necessary to confirm these findings. Future prospective analyses may provide further insight into the mechanisms by which LAT1 expression impacts GI cancer outcomes.

Human papillomavirus (HPV) is a well-established oncogenic virus implicated in the development of several epithelial cancers, most notably cervical, anogenital, and oropharyngeal carcinomas. In contrast, neuroendocrine neoplasms (NENs)—a heterogeneous group of malignancies arising from neuroendocrine cells across various organ systems—have not traditionally been linked to HPV infection. In this study, we performed extensive genomic and transcriptomic profiling to compare HPV-positive NENs to HPV-positive non-NENs across anatomical sites, aiming to uncover biologically and clinically actionable differences. HPV16- and HPV18-positive tumors were identified from 101,343 solid tumors profiled at Caris Life Sciences (Phoenix, AZ) with DNA and RNA sequencing. Prevalence of pathogenic mutations and copy number amplifications were calculated. Fisher’s exact/χ2 tests were applied appropriately with p-values adjusted for multiple comparisons (p < 0.05). HPV positivity was most frequent in cervical carcinomas (70

Over the past decade, Immuno-Oncology has largely focused on blocking inhibitory surface receptors like PD-1 to enhance T cell anti-tumor activity. However, intracellular immune checkpoints such as CISH, which function independently of tumor-expressed ligands, offer powerful and previously untapped therapeutic potential. As a downstream regulator of TCR signaling, CISH controls T cell activation, expansion, and neoantigen reactivity. Though historically considered undruggable, recent advances in CRISPR engineering have enabled functional interrogation of these targets. We demonstrate that CISH deletion enhances T cell activation and anti-cancer functions more effectively than other emerging intracellular checkpoints. In CAR-T cells, CISH inactivation significantly increased sensitivity to tumor antigen, enabling robust recognition and killing even at low antigen levels, conditions that often lead to treatment failure with conventional T cell therapies, mirroring antigen escape scenarios seen in solid tumors. Our findings further validate CISH as a potent and druggable intracellular checkpoint capable of boosting anti-tumor T cell responses across diverse cancer types, independent of PD-L1 status. The underlying mechanisms of CISH inhibition may help explain the positive outcomes reported in recent clinical studies of this approach in solid tumor immunotherapy.

PURPOSE:Age and sex are known to influence outcomes in neuroendocrine neoplasms (NENs), yet their molecular determinants remain poorly defined. We queried a real-world dataset of gastrointestinal (GI) tract and pancreatic (P) NENs and characterized their clinical, molecular, and immune profiles. METHODS:One thousand nine hundred thirty-five cases (GI: n = 1431, P: n = 504) of NENs were analyzed using Next Generation or Whole Exome Sequencing of DNA, and 1211/1935 cases (GI: n = 917, P: n = 294) underwent Whole Transcriptome Sequencing. We compared the molecular and immune profile with respect to age and sex. RESULTS:Older age at diagnosis was associated with worse survival in both GI- and P-NENs. In patients with GI-NENs, there was decreased survival in males compared to females. In GI-NENs, TP53, RB1, FAT1, and KMT2D mutations, as well as immune checkpoint gene (ICG) expressions of LAG3, CD80, and HAVCR2 and M1 macrophages increased with increasing age while APC mutations and M2 macrophages decreased with increasing age. In P-NENs, TP53, RB1, KRAS, and SMAD4 mutations and CD4+ T cells increased with increasing age while MUTYH and NTHL1 mutations and M2 macrophages decreased with increasing age. In GI-NENs, TP53, FBXW7, and TERT (promoter) mutations and genomic loss of heterozygosity (gLOH) were increased in males. In P-NENs, PIK3CA mutations and dMMR/MSI-H were increased in females. CONCLUSION:Our study queries one of the largest datasets of GI- and P-NENs to date and highlights distinct age- and sex-specific molecular and immune profiles. Given the exploratory nature of these analyses and borderline significance, these results remain hypothesis-generating, providing an initial framework for future validation studies.

Histone-lysine N-methyltransferase 2 (KMT2) family proteins methylate lysine 4 on the histone H3 tail at important regulatory regions in the genome and thereby impart crucial functions through modulating chromatin structures and DNA accessibility. We aimed to identify the molecular profile of KMT2-MT oesophageal cancer (EC) and associations with patient outcomes. In our study, KMT2 mutations were significantly associated with longer immunotherapy-related overall survival (OS) in the esophageal adenocarcinoma (EA) (21.42 vs 13.42 months, HR = 0.66, 95% CI: 0.50-0.88, P = 0.004), but not in the esophageal squamous cell carcinoma (ESCC). KMT2 mutations were significantly associated with microsatellite instability-high and higher tumor mutation burden in both EA and ESCC. KMT2-MT EA showed significantly higher mutation rates in CIC (13% vs 1.1%), NF1 (12.5% vs 2.2%), FBXW7 (12% vs 3.4%), ATM (11.5% vs 2.6%) and BRCA1 (11.5% vs 1%, all q < 0.05), compared to KMT2-wildtype (WT) tumors. Meanwhile, no significant mutational differences were observed between KMT2-MT and WT ESCC. Fat digestion and absorption, cholesterol metabolism and the infiltration of activated B cells were significantly enriched in KMT2-MT EA compared to KMT2-WT EA, but these results were not observed in the ESCC. This is the largest study to investigate the distinct molecular landscapes in KMT2-MT EC, characterized by higher tumor mutational burden, an increased frequency of microsatellite instability-high, and gene mutations involved in DNA damage repair and epigenetic regulation.

Endocytosis regulates receptor trafficking and signaling, yet its role in colorectal cancer (CRC) remains unclear. We analyzed transcriptomic data from 15,025 CRC tumors to evaluate gene expression in clathrin-mediated endocytosis (CME) and the endosomal sorting complexes required for transport (ESCRT) pathway. Pathway-level signatures were compared across consensus molecular subtypes (CMS) and examined in relation to oncogenic signaling programs, while individual endocytosis-related genes were evaluated for associations with clinical outcomes in an independent randomized trial cohort. Expression of CME and ESCRT pathways varied by CMS, with the highest expression in CMS4 and the lowest in CMS3. Endocytosis signatures correlated with multiple oncogenic signaling pathways, including MAPK, TGF-β, WNT, PI3K, NOTCH, and angiogenesis, suggesting broad links between endocytic activity and tumor biology. In the randomized phase III CALGB/SWOG 80405 trial, low expression of AP2M1 —a core adaptor in the CME complex—was significantly associated with longer overall survival and progression-free survival in patients treated with anti-EGFR agents, but not in those receiving anti-VEGF agents. These findings suggest that endocytic trafficking may be associated with oncogenic signaling and differential therapeutic benefit in patients with metastatic CRC. The endocytosis pathway reflects biologically relevant heterogeneity in CRC and may help guide therapeutic stratification.

There remains a critical need for prognostic biomarkers of treatment response in epithelial ovarian cancer (EOC). The KELIM score, derived from the rate of CA-125 elimination during the first 100 days of treatment, is a clinically available biomarker of treatment response to platinum-based chemotherapy, its utility is limited by the need for post-treatment data. Tumor–stroma proportion (TSP) has emerged as a prognostic biomarker across several malignancies. Studies from our group have shown that high TSP (≥50% stroma content assessed by pathologist evaluation, TSPmanual) is associated with platinum resistance and poor survival in EOC at diagnosis and before treatment. We compared the prognostic value of TSP and KELIM by analyzing manual pathologist (TSPmanual) and artificial intelligence–derived assessments (TSPauto) on digitized images from a cohort of EOC specimens. In this cohort, we showed the prognostic significance of TSPmanual, confirming prior findings. Furthermore, TSPauto and TSPmanual assessments were highly concordant (94% agreement, Cohen’s Kappa 0.89, p<0.001), providing a highly reproducible, automated approach. Unlike KELIM, which was only associated with platinum resistance, high TSPauto was significantly associated with poor survival (HR 1.99, p = 0.02). These findings support AI-derived TSP as a pre-treatment prognostic biomarker for EOC that complements KELIM.

Violin plots depicting somatic TMB

Purpose The TEM8 receptor (coded by ANTXR1) plays several roles in oncogenesis and novel oncolytic therapies, such as the SVV-01 virus, uniquely bind this protein in neuroendocrine tumor (NET) histologies, such as small-cell lung cancer (SCLC). Emerging pre-clinical data suggest that TEM8-targeting therapies may convert immunologically “cold” tumor microenvironments (TME) into “hot” milieu with greater responses to immune checkpoint inhibitors (ICIs). Methods NextGen sequencing of DNA (592 genes or whole exome)/RNA (whole transcriptome) was performed on SCLC (N=1404) and other NET (N=1668) samples submitted to Caris Life Sciences (Phoenix, AZ). Samples were stratified by ANTXR1 expression quartiles (Q1 low, Q4 high). TME cell fractions were estimated by RNA deconvolution using quanTIseq. Real-world overall survival (OS) was assessed from insurance claim data. Results The landscape of pathogenic gene mutations was similar among ANTXR1 Q1 vs Q4 tumors among SCLC and NET cohorts. The TME of SCLC and NET Q4 tumors comprised a greater fraction of B cells and M1/M2 macrophages and were more frequently classified as ‘T cell-inflamed’ based on a transcriptional signature predictive of response to ICI. However, OS from the start of ICI was similar between ANTXR1 Q1 and Q4 cohorts. Conclusions Increased B cell and M1/M2 macrophage infiltrate, along with T-cell inflamed status, associated with ANTXR1 Q4 TMEs suggest these patients with SCLC and NET may respond preferentially to ICI. A Phase 1 trial incorporating SVV-01 along with ICI is underway. Prospective investigation of molecular associations and clinical outcomes related to ANTXR1 expression in SCLC is warranted.

707 Background: Due to insufficient data, therapy for unresectable, locally advanced pancreatic adenocarcinoma (LAPAC) is based on trials in metastatic disease, and outcomes remain poor. TTFields disrupt cancer cell division using alternating low-frequency electric fields delivered externally by a portable device. In the phase 3 PANOVA-3 trial (NCT03377491), TTFields with gemcitabine/nab-paclitaxel (GnP) significantly improved overall survival (OS; HR 0.82) and pain-free survival (HR 0.74) vs GnP in patients with unresectable LAPAC. Methods: In PANOVA-3, patients with newly diagnosed LAPAC were randomized 1:1 to receive GnP with or without concomitant TTFields. Kaplan-Meier methodology was used for time-to-event analyses. Response evaluations were based on RECIST V1.1. OS, pain-free survival, and safety were analyzed post-hoc in subgroups based on sex (male, female), age ( < 65, ≥65 years), and BMI (<25, ≥25 kg/m 2 for efficacy; ≤20, 20–25, 25–30, ≥30 kg/m 2 for safety). Differences between treatment arms were compared using the log-rank test. Results: Efficacy outcomes are shown in the table. TTFields significantly extended pain-free survival in females and patients ≥65 years. Device-related adverse events (AEs) were comparable between sexes, older and younger patients, and across BMI ranges. Some device-related skin adverse events occurred more frequently in females (e.g. dermatitis, 33.1% vs 22.7%; rash 21.8% vs 13.5%, females vs males, respectively); others occurred more often in males (e.g. maculo-papular rash, 9.8% vs 14.2%; erythema, 9% vs 12.1%, females vs males, respectively). Dermatitis and pruritus had a higher incidence in the BMI ≥30 kg/m 2 subgroup (38.5%), whereas patients with BMI <30 kg/m 2 did not show noticeable differences in device-related AEs. Skin irritation (11.5% vs 5.5%) and skin reactions (8.5% vs 2.8%) were more common in patients ≥65 years than patients <65 years. Conclusions: Median OS and pain-free survival in these post-hoc subgroup analyses are generally consistent with the overall analysis, supporting use of TTFields with GnP in unresectable LAPAC. No new safety concerns were noted; observations were consistent with the general PANOVA-3 population. Clinical trial information: NCT03377491 . Survival outcomes for the subgroup analyses. Median OS, months TTFields + GnP GnP P value Age<65 years≥65 years 18.6 (n=113)15.4 (n=172) 16.0 (n=114)12.9 (n=172) 0.2060.061 SexFemaleMale 16.8 (n=138)15.7 (n=147) 14.5 (n=161)13.4 (n=125) 0.1140.145 BMI<25≥25 16.7 (n=166)16.2 (n=117) 14.2 (n=174)14.5 (n=108) 0.1550.105 Median pain-free survival, months Age<65 years≥65 years 16.5 (n=113)13.1 (n=172) 9.2 (n=114)8.3 (n=172) 0.4070.035 SexFemaleMale 16.5 (n=138)15.2 (n=147) 8.3 (n=161)9.3 (n=125) 0.0260.478 BMI<25≥25 16.6 (n=166)14.7 (n=117) 9.1 (n=174)8.3 (n=108) 0.1170.088

Although the tissue-agnostic FDA approval of pembrolizumab for tumor mutational burden (TMB)-high tumors has provided meaningful clinical benefit to patients, there remains a need to optimize TMB assessment. In this cohort study, we investigated the discordance between whole-exome sequencing (WES) and panel-based methods and evaluated their relative clinical utility in identifying patients likely to benefit from pembrolizumab. Molecularly-profiled tumors from patients treated with pembrolizumab were analyzed (N = 26,756). TMB was calculated using WES data or panels of genes (324, 523, and 648) from commercially available assays (TMB-High ≥ 10 mutations/Mb). Pembrolizumab-specific overall survival (OS) was calculated from insurance claims data (treatment start to last contact). Targeted gene panels tended to overestimate TMB and demonstrated 10–15

e16367 Background: Outcomes of unresectable, locally advanced pancreatic adenocarcinoma (LAPAC) remain poor, with therapy based mainly on data from trials in metastatic disease. TTFields use alternating electric fields to disrupt cancer cell proliferation. The phase 3 PANOVA-3 trial (NCT03377491) demonstrated that TTFields with gemcitabine/nab-paclitaxel (GnP) significantly improved overall survival (OS; HR 0.82) and pain-free survival (HR 0.74) vs GnP in patients with unresectable LAPAC. We report an analysis of efficacy and safety in PANOVA-3 by tumor location. Methods: Patients with newly diagnosed LAPAC were randomized 1:1 to receive GnP with or without concomitant TTFields. Kaplan-Meier methodology was used for time-to-event analyses. Response evaluations were based on RECIST V1.1. OS and pain-free survival were analyzed post-hoc without stratification in patient subgroups with tumors in the head, body, and tail of pancreas. Differences between treatment arms were compared using a 2-sided log-rank test. Results: Tumors were located in: head of pancreas, n=163 and 158 in the TTFields + GnP and GnP arms, respectively; body of pancreas, n=81 and 79; tail of pancreas, n=9 and 19. Baseline characteristics were generally similar in the TTFields + GnP and GnP arms in each subgroup, with the exception of gender (male: head 51.5% vs 41.1%; body 45.7% vs 48.1%; tail 88.9% vs 52.6%). Median OS was 15.8 (12.7, 18.0) vs 12.9 (11.5, 15.4) months in the TTFields + GnP and GnP arms in the head of pancreas subgroup; 18.6 (95% CI: 15.7, 22.5) vs 16.4 (13.1, 20.1) months in the body of pancreas subgroup; and 13.9 (3.0, 17.1) vs 14.9 (11.5, 18.7) months in the tail of pancreas subgroup (all P>0.05). Median pain-free survival was 10.2 (6.6, 16.5) vs 7.6 (5.9, 9.5) months, 18.7 (11.0, NE) vs 9.3 (6.6, 16.3) months (P=0.041), and 5.4 (1.2, NE) vs NE (4.5, NE) months, respectively, in these subgroups (P>0.05 unless otherwise stated). The type and incidence of device-related adverse events (AEs) were comparable. Conclusions: In this post-hoc subgroup analysis with small sample sizes, median OS and pain-free survival were consistent with the primary analysis of the overall population. These data support the use of TTFields with GnP in unresectable LAPAC regardless of tumor location. Clinical trial information: NCT03377491 .

Class II and III BRAF mutations are uncommon events, with limited data on their clinical and biological characteristics. We investigated clinical and molecular features of BRAF mutation classes in a total of 24,402 patients with mismatch repair proficient CRC (MMRp). Samples collected between 2006 and 2023 were profiled using next-generation sequencing and whole-transcriptome sequencing. We identified 1268 (5.2%), 132 (0.54%), and 323 (1.3%) patients with class I, II, and III BRAF-mutated CRC. Patients with class III mutations had significantly better median overall survival (OS) than those with class I mutations (23.6 vs 17.4 months; HR = 1.26, CI: 1.08-1.47, p = 0.004). Transcriptomic analyses revealed that the MAPK pathway score was significantly lower for class II and III BRAF mutations without concurrent RAS mutations than for those with RAS co-mutations. The cetuximab score, an RNA expression-based predictor of EGFR therapy response, was significantly better for class II and III BRAF mutations than for class I. The cetuximab score significantly improved for only class III BRAF mutations when those with concurrent RAS mutations were excluded. The results of this large multi-institutional analysis of BRAF mutation classes reveal the prognostic value of class II and III BRAF mutations, and their distinct clinical and molecular features.

177 Background: The phase 3 ATOMIC trial (NCT02912559) demonstrated the addition of an immune checkpoint inhibitor (ICI) to adjuvant chemotherapy (CT) significantly improved disease-free survival in stage 3 resected deficient mismatch repair/microsatellite instability-high (dMMR/MSI-H) colon cancer. The clinical impact of CT on ICI efficacy in dMMR/MSI-H colorectal cancer (CRC) adjuvant therapy is not well characterized. Methods: This IRB-approved retrospective study included patients diagnosed between 2009-2025 with dMMR/MSI-H and/or TMB-H stage II (T4 only) or stage III CRC pts identified from multi-institutional electronic health records. Microsatellite status and genomic testing were performed in CLIA-certified, CAP-accredited labs. Pt characteristics, genomics and in-depth clinical treatment history were analyzed. Disease-free survival (DFS) and overall survival (OS) were determined by Kaplan-Meier method. Survival curves were compared using the log-rank test. Results: The 90 CRC pts included T4N0 (n = 15) and TxN + (n = 75), and 77 were MSI-H and 13 MSS/TMB-H. These pts received surgery alone (n = 33), or surgery with CT (n = 42), or ICI ± CT (n = 15). Pts who received surgery alone (median 83yo [44 – 92]) were much older than those had received additional CT (median 69yo [32 - 88]) or ICI ± CT (median 67yo [35 - 86]). The median DFS (3.3yr and 4.5yr; p = 0.36) and 5yrs OS rate (74.1% vs 62.2% p = 0.34) were not significantly improved in pts who received adjuvant CT compared to surgery alone, and only 16% of these pts received ICI subsequently. Pts who received ICI after prior CT had significantly decreased median DFS compared to those who received treatment-naive immunotherapy (median DFS of 8.9 mo vs NR; p = 0.043), although both 5y OS rate were ≥ 90% and not significantly different. Of the 16 pts who received ICI, only 1 had tumor progression and 11 developed no evidence of disease. Pts who had received ICI compared to CT alone showed trend toward higher rate of 5yr OS (0.93 vs 0.70; p = 0.27). Conclusions: This study supports the use of adjuvant immunotherapy alone in dMMR/MSI-H and TMB-H colorectal cancer (CRC) ), with possible detriment including shorter DFS when ICI is administered following upfront CT. Clinical trial investigation comparing adjuvant ICI alone to CT + ICI is warranted in T4 stage 2 and stage 3 MSI-H CRC.

Summarized broad trends observed across cancer types

The intratumoral microbiome is increasingly recognized as a regulator of cancer biology, yet sex-specific patterns and their relevance to cancer disparities remain poorly understood. We perform a multi-kingdom analysis of more than 5,000 tumors from seven datasets to identify sex-differential microbial taxa across aerodigestive and gastrointestinal cancers. We identify and validate 22 taxa with consistent sex-biased abundance, including in real-world cohort. These microbes show cancer-type- and microbe-specific associations with tumor transcriptomes, oncogenic pathways, and immune cell infiltration. Female-enriched microbes are linked to increased estrogen signaling and interferon responses, whereas male-enriched taxa show opposing patterns. In gastric cancer, intratumoral Epstein-Barr virus is enriched in males and associated with higher CD8+ T cell infiltration and improved survival. Functional co-culture experiments demonstrate that sex-biased microbes modulate chemotherapy sensitivity. Together, these findings reveal a sex-biased intratumoral microbiome axis that shapes tumor phenotypes and disease outcomes, highlighting opportunities for microbiota-guided, sex-aware approaches in oncology.

Abstract Neutrophils (polymorphonuclear cells, PMNs) have been shown to directly induce necrosis through the formation of neutrophil extracellular traps (NETs) in murine models of breast and lung cancer. Although necrosis is a well-recognized predictor of poor outcomes in cancer, it is typically regarded as a passive and non-targetable process. To determine whether NETs actively drive necrosis in colorectal cancer (CRC), we evaluated the pathogenic impact of NET formation in human CRC specimens and complementary preclinical models.In blood samples from patients with CRC, we identified elevated populations of neutrophils primed for NET formation, including an expanded CD177Low subset that retained strong NET-forming capacity with reduced extravasation ability. Histologic and immunofluorescent analyses of human CRC and colorectal liver metastases demonstrated abundant NET accumulation within necrotic regions, forming intravascular deposits. The extent of necrosis correlated with metastatic disease, independent of tumor size. Single-cell RNA sequencing and spatial transcriptomic profiling of human primary CRC and liver metastases showed that NET-rich necrotic tumors activate transcriptional programs associated with myelopoiesis (CSF1, CXCL2, CXCL12), hypoxia signaling, migration, and epithelial-to-mesenchymal transition—features linked to increased metastatic potential. In a mismatch-repair-proficient orthotopic CRC model using AKPS (APCKO KRASG12D P53KO SMAD4KO) organoids implanted via colonoscopic injection, tumor progression was marked by rising circulating PMNs, bone marrow skewing toward myelopoiesis, and increasing NET deposition within necrotic tumor regions. Genetic and pharmacologic inhibition of NET formation reduced intratumoral necrosis and significantly decreased metastatic burden. Collectively, these findings demonstrate that NETs are active drivers of necrosis and metastatic evolution in CRC, reframing necrosis as an immunopathologic process rather than an unavoidable consequence of tumor growth. Targeting NET formation represents a promising translational strategy to improve disease control and oncologic outcomes for patients with CRC. Citation Format: Emma Gazzara, Adrover Jose, Sebastian Dziadowicz, Song Han, Alex Liu, Zakeria Aminzada, Nischal Bhandari, Venktesh Shirue, Bhupinder Shergill, Matthew Curtis, Steven C. George, Alexander Cicala, Arvind Rishi, Craig Devoe, Hai Huang, Matthew Weiss, Emil Lou, David A. Tuveson, Semir Beyaz, Peter Maxwell Kienitz Westcott, Mikala Egeblad, Sepideh Gholami. Neutrophil extracellular trap inhibition mitigates tumor necrosis and metastasis in colorectal cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 6786.

Assessing the Prevalence of TP53 Mutations Based on the Site of Tumor Sequenced