Next-generation sequencing has transformed cancer care by providing essential insights for diagnosis, prognosis, and treatment. However, variability in testing timing, reporting practices, and interpretation challenges limits its clinical impact. This article highlights key opportunities to optimize somatic reporting, emphasizing the importance of timely testing throughout the cancer care continuum to maximize the diagnostic and therapeutic relevance of findings. Technical factors such as test design, sequencing depth, and the use of liquid biopsy substantially influence result accuracy and interpretation, underscoring the need for careful integration with clinical history. Standardized reporting practices that clearly delineate diagnostic, prognostic, and therapeutic findings can enhance the clinical utility of next-generation sequencing results. Streamlined formats and curated clinical trial data further support actionable decision making. Additionally, direct patient engagement and education are essential for empowering patients to navigate genomic testing and make informed decisions about their care. By leveraging multidisciplinary tumor boards, decision-support tools, and emerging artificial intelligence technologies, clinicians can better navigate the complexities of somatic reports. Standardization and clarity in reporting are critical to advancing precision oncology, empowering providers and patients to make informed treatment decisions and improve outcomes.

Purpose Aberrant alternative splicing (AS) events have been implicated in cancer progression; however, their role in metastatic renal cell carcinoma (mRCC) remains underexplored. This study aims to identify AS events associated with clinical benefits from immune checkpoint inhibitors and targeted therapies in mRCC. Materials and methods We conducted a retrospective analysis on 101 patients with mRCC who received systemic therapy and underwent RNA sequencing. Patients were divided into subgroups based on ICIs (alone or in combination) and targeted therapies. Responders and non-responders were classified according to Response Evaluation Criteria in Solid Tumors V.1.1 criteria. Differential gene expression and splicing analyses were performed between responders and non-responders in each cohort. Novel AS events were analyzed for their potential to generate peptide neoantigens through major histocompatibility complex (MHC) class I binding predictions. Results Outlier splicing analysis identified 10 aberrant splice events specific to mRCC. AS analysis revealed 461 differentially spliced events between responders and non-responders in the ICI cohort and 253 in the targeted therapy cohort, with intron retention as the predominant motif. Thirteen unique AS events were enriched in responders, including PTPN6 and ACTN1. Predictive neoantigen analysis identified high MHC class I binding potential in peptides from AS events in IFFO1 and ZNF692. High splice burden was linked to an immunogenic tumor microenvironment, characterized by enriched antigen processing and adaptive immune responses. Conclusions This study provides a comprehensive analysis of AS events in mRCC, highlighting intron retention as potential biomarkers for treatment response. Identified AS-derived neoantigens may serve as potential targets for adoptive cell therapy strategies.

Abstract Waiting for test results is a primary cause of delay in the diagnostic classification and risk stratification of patients with AML. With conventional cytogenetic, FISH, and targeted NGS approaches taking a median turnaround time (TAT) of 7-15 days, there is a significant unmet need to deliver these results faster using a more comprehensive testing platform. We have very recently developed, and demonstrated Analytical Validity (AV), Clinical Validity (CV) and Clinical Utility (CU) in accordance with MolDX L38047, for a rapid Whole Genome Sequencing (WGS) approach for AML (DEX Z-Code Z04C0). Importantly, this test (termed ALTseq) was specifically designed to deliver clinically actionable genomic results that encompass those from cytogenetics, FISH, and targeted NGS in under 48 hours (TAT mean = 33 hours). This accelerated turnaround time was enabled by streamlining laboratory workflows, enhancing bioinformatic pipelines, and expediting variant approval for reporting. The assay captures single nucleotide variants, indels (including FLT3-ITDs and KMT2A-PTDs), and 155 distinct structural variants including KMT2A rearrangements, and genome-wide copy number alterations. Additionally, we have recently developed a method to measure monosomal and complex karyotypes from WGS sequencing data. By deploying WGS we are able to gain insight in all genes in the human exome, with the curated clinical reporting covering all current key AML-related aberrations. These include mutations in NPM1, TP53, RUNX1, IDH1/2, FLT3, MEN1, rearrangements involving KMT2A, MECOM, NUP98, and canonical translocations such as PML::RARA, RUNX1::RUNX1T1, and BCR::ABL1. ALTseq has a limit of detection of 9%, 8%, 10%, and 7% for SNVs, indels, CNAs, and SVs, respectively, with sensitivities of 96%, 96.4%, 95.7%, and 100%, respectively. The positive predictive value for all variant types is ≥99.5%. Since implementation, ALTseq has been used in 66 AML cases, achieving a mean TAT of 33 hours from sample receipt to report delivery. Recent evidence of clinical utility includes the incorporation of Mylotarg in induction therapy based on the identification of CBFB::MYH11 fusion gene, and the inclusion of Revumenib for a KMT2A rearrangement that could not be identified with standard breakaway FISH probes. In summary, we will describe the clinical deployment of a high-throughput, fast-turnaround WGS platform for AML, capable of delivering comprehensive genomic profiling in <48 hours from sample receipt to clinical reporting enabling earlier, more informed treatment decisions. Citation Format: Wayne M. Jepsen, Jonathan J. Keats, Sara A. Byron, Cherie Wesley, Bryce Turner, Christophe Legendre, Tyler Izatt, Tracey White, Amy Stouffer, Lucy Ghoda, Yeneka Campana, Courtney Holden, Jonathan Beteran, Michelle Afkhami, Anthony Stein, Tibor Kovacsovics, Guido Marcucci, Jeffrey Trent. Rapid clinical diagnostic classification and risk stratification in acute myelogenous leukemia (AML) using whole genome sequencing (WGS) [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 2495.

Abstract Background: KRAS mutations are among the most prevalent oncogenic drivers across solid tumors, with particularly high incidence in Pancreatic Ductal Adenocarcinoma (PDAC). Despite their clinical relevance, direct targeting of KRAS has historically been difficult. The advent of KRAS G12C-specific inhibitors has marked a breakthrough in targeted therapy, yet acquired resistance remains a major challenge. RMC-6236 (daraxonrasib), a noncovalent RAS(ON) inhibitor, targets the active GTP-bound form of both mutant and wild-type RAS isoforms and has shown potent antitumor activity, especially in codon 12 KRAS-mutant cancers. In a Phase 1 trial for metastatic PDAC, RMC-6236 extended progression-free survival to approximately eight months. Recent studies suggest that KRAS inhibition may sustain focal adhesion kinase (FAK) activation, implicating the FAK-YAP axis and tumor-associated fibrosis in resistance. FAK, a key regulator of survival and DNA damage repair, has emerged as a promising co-target, with evidence of synergy between FAK inhibition and KRAS blockade, as well as enhanced sensitivity to PD-1 checkpoint inhibitors and radiation. We hypothesize that dual targeting of KRAS and FAK pathways will yield synergistic therapeutic effects in PDAC by disrupting oncogenic signaling and promoting cell death. To test this, we employ patient-derived organoid (PDO) cultures that preserve tumor architecture, heterogeneity, and stromal structure, enabling physiologically relevant evaluation of drug combinations. Methods: Patient-derived cells were treated with RMC-6236, defactinib, and ifebemtinib, alone and in combination, in 2D and 3D viability assays. Organoids were generated by co-culturing tumor cells and fibroblasts (1:1) for 72 hours, then treated with an 8-point, 2-fold serial dilution of drugs for another 72 hours. Synergy was assessed using Bliss analysis via Combenefit, and 2D dose responses were analyzed in GraphPad Prism using Student’s t-test. Western blotting was performed to evaluate RAS-MAPK pathway inhibition and apoptosis markers. Results: Preliminary data from four KRAS-mutant PDOs (G12D, G12V, G12R) revealed robust synergy between RMC-6236 and either FAK inhibitor, with up to 10-fold and 100-fold increases in efficacy for defactinib or ifebemtinib and RMC-6236, respectively. Western blot analysis confirmed suppression of RAS-MAPK signaling, downregulation of c-MYC, and increased apoptotic markers including cleaved PARP and activated Caspase-3. These findings support the potential of KRAS-FAK co-targeting strategies in PDAC and lay the groundwork for future clinical development. These findings underscore a mechanistic interplay between KRAS and FAK signaling pathways, suggesting that dual targeting may overcome resistance and enhance cell death in KRAS-mutant PDAC, to improve outcomes in KRAS-driven pancreatic cancers. Citation Format: Jaeger Moore, Taylor Bargenquast, Tithi Ghosh Halder, Serina Ng, Erkut Borazanci, Sara A. Byron, Cherie Wesley, Raffaella Soldi, Sunil Sharma. Synergistic disruption of KRAS and FAK pathways: A preclinical pipeline for PDAC therapy optimization [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 6497.

RAS mutations, particularly KRASG12X, are critical oncogenic drivers in pancreatic cancer, with existing KRASG12C inhibitors unable to target other mutations and often leading to resistance. RMC-6236, a multi-selective RAS(ON) inhibitor, demonstrates potent activity in KRASG12X models, but resistance mechanisms that increase mutant RAS(ON) may reduce its effectiveness. The fibrotic tumor microenvironment in pancreatic cancer exacerbates therapy resistance, and combining RMC-6236 with other therapies could overcome both intrinsic and acquired resistances. This study evaluates RMC-6236 efficacy in patient-derived pancreatic tumors harboring KRAS mutations, and the impact of cancer-associated fibroblasts (CAFs) on its potency as a single agent and in combination with other therapies. We also assess its impact on downstream RAS signaling and apoptosis using pro-apoptotic markers. Patient-derived tumor cells and fibroblasts were treated with RMC-6236 in 2D and 3D viability assays. Patient-derived organoids (PDOs) were generated by combining tumor and fibroblasts in a 1:1 ratio and allowing them to form in media for 72 hours. Synergy studies explored combinations of RMC-6236 with gemcitabine and abraxane chemotherapies, along with other targeted therapies, including CDK7, WNT, and mTOR pathway inhibitors. Samples were stained for α-SMA via immunofluorescence for CAF detection. Western blot analysis assessed RAS pathway inhibition and apoptotic markers. These results demonstrate the efficacy of RMC-6236 in a pancreatic cancer PDO model when combined with other therapeutic agents. Sensitivity to RMC-6236 was assessed in tumor cells, fibroblasts, and tumor-fibroblast co-cultures, yielding IC50 values ranging from 0.1 to 11 nM, 1 to 3.5 nM, and 0.2 to 5 nM, respectively. These results highlight that the presence of CAFs in KRAS-mutated pancreatic cancer PDOs does not affect sensitivity to RMC-6236 treatment. Notably, synergy studies assessing RMC-6236 in combination with chemotherapy agents (gemcitabine and abraxane), as well as WNT inhibitors (WNTi) and CDK7 inhibitors (CDK7i), revealed a significant reduction in IC50 values, with a more than 100-fold decrease (ranging from 0.0001 nM to 0.001 nM). This substantial enhancement in drug potency underscores the synergistic effects of combining RMC-6236 with these agents, particularly with WNTi. The combination of RMC-6236 with standard chemotherapy and targeted therapies enhances its antitumor activity, suggesting a promising strategy for improving therapeutic outcomes in pancreatic cancer. The observed synergistic interactions, especially with WNTi, warrant further investigation in clinical trials to evaluate the potential of this combination approach in improving treatment responses. Taylor Bargenquast, Cherie Wesley, Janith Don, Guangfa Zhang, Tithi Ghosh Halder, Serina Ng, Alexis Weston, Trason Thode, Erkut Borazanci, Mohan Kaadige, Sara A. Byron, Nicholas Schork, Raffaella Soldi, Sunil Sharma. Evaluating the efficacy of RAS(ON) inhibitor RMC-6236 combined with chemotherapy and other targeted therapies in 3D models involving patients with KRAS-mutated pancreatic cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 4706.

The recent trial Pediatric Neuro-Oncology Consortium 003 (PNOC003) utilized a molecular tumor board to recommend personalized treatment regimens based on tumor sequencing results in children with DIPG. We separately developed the Central Nervous System Targeted Agent Prediction (CNS-TAP) tool, which numerically scores targeted anticancer agents using preclinical, clinical, and patient-specific data. We hypothesized that highly scored agents from CNS-TAP would overlap with the PNOC003 tumor board’s recommendations. For each of the 28 participants, actionable genetic alterations were derived from PNOC003 genomic reports and input to CNS-TAP to identify the highest scoring agents. These agents were then compared with PNOC003 recommendations, with a resultant concordance percentage calculated. Overall, 38% of the total agents recommended by the tumor board were also selected by CNS-TAP, with higher concordance (63%) in a subanalysis including only targeted anticancer agents. Furthermore, nearly all patients (93%) had at least 1 drug chosen by both methods. We demonstrate overlap between agents recommended by CNS-TAP and PNOC003 tumor board, though this does not appear to improve survival. We do observe some discordance, highlighting strengths and limitations of each method. We propose that a combination of expert opinion and data-driven tools may improve targeted treatment recommendations for children with DIPG.

Evaluating genomic signatures may improve prognostic information and outcomes for patients with lung cancer. To determine if homologous recombination deficiency (HRD) is associated with clinical features or overall survival in patients with lung cancer. This is a retrospective cohort study derived from City of Hope’s Implementing Next-Generation Sequencing for Precision Intervention and Risk Evaluation (INSPIRE) study. Study participants with histologically confirmed lung cancer and adequate tissue for comprehensive paired tumor-normal whole exome sequencing were eligible for analysis. 197 patients were sequenced, excluding 14 with rare histologies. Clinical and treatment variables were obtained from cancer registries and the electronic medical record and were recorded by experienced data curation and abstraction specialists. HRD scores were calculated using the scarHRD R package. Mutational signatures were analyzed using SigProfiler and SigEstimation. Associations between clinical variables and HRD status were measured using univariate and multivariate methods. Unsupervised analysis was performed to identify genes in HRD-high (sum score greater than or equal to 42) and HRD-low samples (sum score less than 42). Overall survival was quantified using non-parametric Kaplan-Meier statistics and multivariate Cox-proportional hazards models. Of the 183 lung cancer samples analyzed, 63 (34.4%) samples were HRD-high. Of these, 43 had a TP53 alteration and 20 did not; 120 (65.6%) samples were HRD-low, 50 with a TP53 alteration and 70 without (OR 3.01 (95%CI 1.58, 5.72), p=0.0008). TP53 alterations were strongly associated with high HRD scores. Overall survival was improved in patients with HRD-high tumors treated with platinum therapy, although this difference did not reach statistical significance. Katherine G. Roth, Kevin J. McDonnell, Ernest Nadal, Joseph D. Bonner, Arman Seuylemezian, Suravi Nahar, Lawrence Shaktah, Jonathan Salazar, Sidney Lindsey, Xiaoyu Xia, Sara A. Byron, Jonathan J. Keats, Allen Mao, Adrien Larsen, Bryce Turner, Ravi Salgia, Stacy W. Gray, Stephen B. Gruber. Homologous recombination deficiency in lung cancer in the INSPIRE study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 2047.

Background Children with relapsed central nervous system (CNS tumors), neuroblastoma, sarcomas, and other rare solid tumors face poor outcomes. This prospective clinical trial examined the feasibility of combining genomic and transcriptomic profiling of tumor samples with a molecular tumor board (MTB) approach to make real‑time treatment decisions for children with relapsed/refractory solid tumors. Methods Subjects were divided into three strata: stratum 1—relapsed/refractory neuroblastoma; stratum 2—relapsed/refractory CNS tumors; and stratum 3—relapsed/refractory rare solid tumors. Tumor samples were sent for tumor/normal whole-exome (WES) and tumor whole-transcriptome (WTS) sequencing, and the genomic data were used in a multi-institutional MTB to make real‑time treatment decisions. The MTB recommended plan allowed for a combination of up to 4 agents. Feasibility was measured by time to completion of genomic sequencing, MTB review and initiation of treatment. Response was assessed after every two cycles using Response Evaluation Criteria in Solid Tumors (RECIST). Patient clinical benefit was calculated by the sum of the CR, PR, SD, and NED subjects divided by the sum of complete response (CR), partial response (PR), stable disease (SD), no evidence of disease (NED), and progressive disease (PD) subjects. Grade 3 and higher related and unexpected adverse events (AEs) were tabulated for safety evaluation. Results A total of 186 eligible patients were enrolled with 144 evaluable for safety and 124 evaluable for response. The average number of days from biopsy to initiation of the MTB-recommended combination therapy was 38 days. Patient benefit was exhibited in 65% of all subjects, 67% of neuroblastoma subjects, 73% of CNS tumor subjects, and 60% of rare tumor subjects. There was little associated toxicity above that expected for the MGT drugs used during this trial, suggestive of the safety of utilizing this method of selecting combination targeted therapy. Conclusions This trial demonstrated the feasibility, safety, and efficacy of a comprehensive sequencing model to guide personalized therapy for patients with any relapsed/refractory solid malignancy. Personalized therapy was well tolerated, and the clinical benefit rate of 65% in these heavily pretreated populations suggests that this treatment strategy could be an effective option for relapsed and refractory pediatric cancers. Trial registration ClinicalTrials.gov, NCT02162732. Prospectively registered on June 11, 2014.

A genomic understanding of the oncogenic processes and individual variability of human cancer has steadily fueled improvement in patient outcomes over the past 20 years. Mutations within tumour tissues are routinely assessed through clinical genomic diagnostic assays by academic and commercial laboratories to facilitate diagnosis, prognosis and effective treatment stratification. The application of genomics has unveiled a wealth of mutation-based biomarkers in canine cancers, suggesting that the transformative principles that have revolutionized human cancer medicine can be brought to bear in veterinary oncology. To advance clinical genomics and genomics-guided medicine in canine oncology, we have developed and validated a canine cancer next-generation sequencing gene panel for the identification of multiple mutation types in clinical specimens. With this panel, we examined the genomic landscapes of 828 tumours from 813 dogs, spanning 53 cancer types. We identified 7856 alterations, encompassing copy number variants, single nucleotide variants, indels and internal tandem duplications. Additionally, we evaluated the clinical utility of these alterations by incorporating a biomarker framework from comprehensive curation of primary canine literature and inferences from human cancer genomic biomarker literature and clinical diagnostics. Remarkably, nearly 90% of the cases exhibited mutations with diagnostic, prognostic or therapeutic implications. Our work represents a thorough assessment of genomic landscapes in a large cohort of canine cancers, the first of its kind for its comprehensive inclusion of multiple mutation types and structured annotation of biomarkers, demonstrating the clinical potential of leveraging mutation-based biomarkers in veterinary oncology.

1037 Background: AURKA is a key regulator of the mitotic spindle, G2/M transition and epithelial-mesenchymal transition. AURKA is amplified and/or overexpressed in breast cancer and is associated with therapy resistance and worse survival. A randomized phase II trial in hormone receptor (HR)-positive, HER2-negative and triple negative (TN) MBC pts showed that addition of A to weekly P significantly improved progression-free survival (PFS) compared with P alone (O’Shaughnessy J et al. JAMA N etwork Open, 2021). Pts’ primary or metastatic disease tissues were analyzed for biomarkers associated with clinical benefit from A. Methods: Retrospective analysis of tumor whole exome and whole transcriptome sequencing of formalin-fixed paraffin embedded pre-treatment tissues from 96 pts (77 HR+, 19 TN) was performed. Clinical benefit from A+P or P was defined as having PFS of at least 6 mos and lack of benefit as PFS less than 6 mos. Enrichment for cancer gene mutations was assessed using Fisher's exact test. Transcriptome data were evaluated for differential expression with DeSeq2 and gene set enrichment analysis (GSEA) and compared to cancer hallmark gene sets. Molecular features were compared between A+P responders and non-responders, P responders and non-responders, and A+P and P responders. P-values <0.05 were considered significant. Results: PIK3CA, TP53, and CDH1 were altered in 41%, 39%, and 13% of tumors, respectively, and these and other known cancer genes were not associated with A+P benefit. Alterations in AKT1, PIK3CA, ERBB2, CDH1, TP53, and KMT2C/ KMT2D, as well as amplifications of CCND1, MYB, and MDM2, did not preclude benefit from A+P. RNA expression of AURKA, or its upstream regulator, FOXM1, was not significantly different based on treatment group or benefit from A+P or P. Increased C-MYC RNA expression (p=0.008), and enrichment for MYC targets and UPR by GSEA were enriched in pts with lack of benefit from P compared to those with benefit from P (p<0.05), but not in pts with lack of benefit from A+P. Wnt/Beta-catenin signaling was enriched in pts with lack of benefit from P compared to those with benefit from P (p=0.03), and with lack of benefit from A+P compared to those with benefit from A+P (p=0.086). Benefit from A+P was associated with enrichment for MYC targets and UPR compared with benefit from P (p=0.024), suggesting activity of A+P, but not P, with high MYC activation and UPR. Conclusions: A added to P improved PFS in HR+ HER2- and TN MBC pts compared with P alone. Pts whose breast cancers had increased C-MYC expression, high MYC activation and increased UPR on RNA expression derived greater clinical benefit from A+P than from P alone. Clinical trial information: NCT02187991 .

Proportion of patients with mutation/activation of the PIK3CA-AKT-mTOR pathway in liver metastases compared to other organ sites and primary tumors of the breast.

AKT S473 distribution based on ER, HER2 expression measured by IHC in for primary and metastatic lesions included in the validation set.

Introduction: Tumor mutation burden (TMB), defined as the number of somatic gene mutations per megabase in a tumor genome, is used clinically to identify cancer patients that may respond to immune checkpoint inhibitors. Recent studies suggest that patient ancestry can influence TMB, where individuals of African ancestry were found to have elevated TMB values based on tumor-only sequencing analysis. However, the impact of patient ancestry on germline mutational burden and implications for interpretation of tumor-only mutational burden data is largely unexplored. Methods: We examined the influence of patient ancestry on germline and tumor mutation burden using tumor-normal whole exome sequencing (WES) data from a pan-cancer cohort of 1228 individuals from a single institution. Genetic ancestry was estimated from constitutional WES data using single nucleotide polymorphism weights from external reference panels. Variant calling was performed using constitutional, tumor-only, and paired tumor-normal workflows. Total and loss-of-function burden scores were calculated for each participant from each workflow based on the total number of mutations detected in each sample and the total number of predicted loss-of-function mutations, based on snpEff annotations, respectively. Results: Genetic ancestry analysis found that one-third of this pan-cancer cohort was of non-European ancestry. 9.4% of individuals were of Eastern Asian ancestry, 5.3% of African ancestry, 1.0% of South Asian ancestry, 0.2% of Native American ancestry, and 17.1% of admixed ancestry, predominantly European and Native American admixed ancestry (15.6%). Total and loss-of-function germline burden scores varied across ancestral groups, with individuals of African ancestry showing significantly increased germline burden scores compared to other ancestral groups (p<0.0001). Tumor-only analysis also showed increased mutation burden for individuals of African ancestry. However, when private and rare germline variation was taken into account using paired tumor-normal analysis, tumor mutation burden did not differ based on patient ancestry, suggesting the differences seen in tumor-only analysis are due to germline variation rather than differences in true somatic mutation burden. Conclusion: Our study reveals that the paucity of knowledge of ancestry-specific reference genomes leads to unacceptable health disparities in cancer, specifically in patients with African ancestry. We show that germline mutational burden varies by ancestral background, with individuals of African ancestry displaying increased genetic variation compared to other ancestral populations. These results suggest that patient ancestry should be considered when interpreting tumor mutational burden values, particularly from tumor-only analysis. Approaches utilizing paired tumor-normal analysis or ancestry-specific reference genomes can aid in more accurate assessment of TMB, thereby avoiding futile treatments targeted at presumed high mutational burden tumors specifically in African American populations. Citation Format: Janith Don, Sara A. Byron, Guangfa Zhang, Tyler Izatt, Jiaming Zhang, Bethany Davis, Bryce Turner, Jonathan J. Keats, Jeffrey M. Trent, Lorna Rodriguez-Rodriguez, Nicholas J. Schork. Increased germline mutational burden in individuals of African ancestry: Implications for interpretation of tumor mutation burden [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr A006.

AKT S473 distribution based on ER expression measured by IHC for 31 lesions included of the discovery set. ER was measured in a binary scale (Panel A) and in continuous scale using the H-Score (Panel B).

Study Workflow Diagram. Key steps in the study are outlined, including the number of patients at each stage. BEV: bevacizumab.

Consensus Matrix of the GSVA Enrichment Scores Computed for 50 Hallmark Gene Sets. xCell Immune Score Values by GSVA Cluster.

Additional Longitudinal Analysis of Relapsed and Refractory Childhood Solid Tumors.

Pathway diagram of genes/proteins that were measured for this analyses and found altered across the 32 breast cancer metastases evaluated of the discovery set.