Table S6: Cell migration simulator parameter values

Figure S4. Quantification of single cell migration and cell morphology. A, B, & C) Ex vivo migration and morphology data from each individual animal. D, E, & F) Migration and morphology data for each individual mouse primary tumor line in mouse organotypic brain slice. G, H, & I) Migration and morphology data for each individual PDX line in mouse organotypic brain slice.

Figure S1. Unsupervised clustering of mouse tumor and healthy brain tissue transcriptomic profiles and pathway enrichment analysis. A) Heatmap showing expression profile of NRAS and PDGF tumors and healthy mouse brain tissues. Heatmap shows existence of three gene clusters: Tumor-specific cluster, normal brain tissue specific cluster and NRAS tumor-specific cluster. B,C&D) Gene ontology analysis of gene clusters was performed using EnrichR.

Table S5: Characteristics of patient-derived xenograft (PDX) lines used in this study

Soft-tissue sarcoma (STS) are rare and heterogeneous mesenchymal tumours with over 100 recognized human subtypes. Despite advances in cytogenetic and molecular characterization, diagnostic precision and therapeutic options remain limited for most subtypes. Spontaneously occurring canine STS could represent valuable translational models, due to their higher incidence and clinical similarity to human counterparts. However, molecular cross-species comparisons of specific subtypes are largely missing. Here, we performed a tissue-resolved, cross-species analysis of tumour and matched adjacent normal tissue (NT) in human and canine fibrosarcoma (FSA) and myxofibrosarcoma (MFS) by laser-capture microdissection of FFPE specimens combined with RNAseq and LC-MS/MS. Multimodal profiling revealed FSA and MFS to represent a molecular continuum rather than distinct entities in both species, resulted in identification of clinically relevant subgroups based on immune activation, proliferative activity and copy number alterations, and identified a novel canine STS subtype associated with a gene fusion. Moreover, our analyses revealed cross-species conserved transcriptomic and proteomic alterations distinguishing tumour from NT, including pathways linked to extracellular matrix remodelling, immune modulation, and cell proliferation. These data establish the first comprehensive molecular comparison of canine and human FSA and MFS, highlight the translational relevance of canine models, and identify candidate biomarkers for diagnostic refinement and development of targeted therapeutic modalities.

Figure S2. Clustering analysis of mouse and human tumors using gene signatures associated with classical, mesenchymal, and proneural subtypes. A) Heatmap shows the clustering of human GBM samples using subtype-specific gene signatures. B) Heatmap shows the clustering of mouse tumors using subtype-specific gene signatures. C&D) Quantification of subtype gene signatures within human GBM subtypes and NRAS and PDGF mouse tumors. Solid and dashed lines represent mean and median values respectively. Error bars are S.E.M. +p <0.05, * p <0.01, ** p<0.001, *** p<0.0001, **** p<0.00001.

Abstract Introduction: Lymphomas are among the most common malignancies in dogs, and their morphologic and biological similarities to human counterparts have established them as widely accepted models of human disease. However, emerging molecular data suggest that conservation varies by subtype, and that many common lymphoma subtypes are principally convergent rather than homologous conditions, requiring a critical reassessment of when and how canine lymphomas provide relevant models of human disease. Methods: We employed conventional pathology, immunohistochemistry, and next generation sequencing platforms, including single-cell sequencing and spatial genomics, to characterize the transcriptional landscape and cellular organization of canine lymphomas, complemented by population metadata. Results: Our analysis revealed that canine DLBCL lacks the traditional GCB/ABC bifurcation seen in humans. While activation of NFκB pathways is seen commonly in these tumors, a germinal center-like DLBCL subtype is not apparent in dogs, and the transcriptional signatures are distinct from those of activated B-cell like DLBCL. Instead, we identified a novel canine-specific DLBCL subset driven by an AP-1-associated transcriptional signature, mirroring advanced human follicular lymphoma rather than human DLBCL. In contrast, emerging data suggest that downregulation of quiescence programs might be a shared feature of both human and canine MZLs, making this subtype a candidate for conserved disease mechanisms. While canine T-cell lymphomas exhibited extensive transcriptional heterogeneity, the samples in our dataset did not align with established human T-cell subgroups, suggesting that high incidence in dogs might not equate to molecular similarity. Conclusions: Our results suggest canine and human lymphomas are principally convergent rather than homologous diseases whose evolution and topological organization are constrained by developmental programs. The distinct transcriptional programs of canine and human DLBCLs reveal informative biological divergence, while potential shared features of MZL suggest contexts where comparative oncology may illuminate conserved disease mechanisms. Canine T-cell lymphomas exhibit extensive transcriptional heterogeneity that, at present, defies simple classification, mirroring challenges in their human counterparts and underscoring the need for larger studies to establish molecular patterns that inform causation, prognosis, and treatment. These findings highlight contexts where distinct and conserved molecular features between canine and human lymphoma can reveal shared and divergent disease mechanisms, ultimately underscoring the need for subtype-specific validation as canine lymphomas are adopted as models of human disease. Use of AI: Generative AI was used to improve clarity and readability of the abstract. AI was not used to conduct the study or to produce new text or material. Citation Format: Jaime F. Modiano, Amy E . Treeful, Grace E. Walker, Davis M. Seelig, Caitlyn M. Callaghan, Timothy D. O'Brien, Shruthi Naik, Aaron L. Sarver. Different paths to the same destination: Molecular divergence and functional convergence in human and canine lymphomas [abstract]. In: Proceedings of the Fifth AACR International Meeting on Advances in Malignant Lymphoma: From Discovery to Clinical Impact; 2026 Jun 24-27; Philadelphia, PA. Philadelphia (PA): AACR; Blood Cancer Discov 2026;7(3_Suppl):Abstract nr A023.

Glioblastoma (GBM) remains a deadly cancer driven in part by invasion of tumor cells into the brain. Transcriptomic analyses have identified distinct molecular subtypes, but mechanistic differences that account for clinical differences are not clear. In this study, we show that, as predicted by the motor-clutch model of cell migration, mesenchymal glioma cells are more spread, generate larger traction forces, and migrate faster in brain tissue compared with proneural cells. Despite their rapid migration and comparable proliferation rates in vitro, mice with mesenchymal tumors survive longer than those with proneural tumors. This improved survival correlated with an immune response in mesenchymal tumors, including T cell-mediated. Consistently, inducing mesenchymal tumors in immunodeficient mice resulted in shorter survival, supporting a protective immune role in mesenchymal tumors. Thus, mesenchymal tumors have aggressive migration but are immunologically "hot," which suppresses net proliferation. These two features counteract each other and may explain the lack of a strong survival difference between subtypes clinically, while also opening up new opportunities for subtype-specific therapies. SIGNIFICANCE:This study highlights new mechanical and immunologic insights into GBM molecular subtypes using an integrated modeling-genome engineering strategy, which can potentially facilitate GBM subtype-specific therapeutic strategies.

Osteosarcoma is a heterogeneous malignancy, exhibiting significant variability among patients, individual cancer cells within a tumor, and the stromal cells that compose primary and metastatic lesions. To facilitate the study of this complex disease, we compiled a unique cross-species single-cell transcriptomic dataset totaling over a million cells/nuclei from human specimens, canine specimens, patient-derived xenografts/PDX, and syngeneic mouse models at both primary (bone) and metastatic (lung) sites. Using a rigorous process for multi-species alignment and annotation, we identified six conserved tumor cell transcriptional states organized along hierarchical differentiation trajectories from progenitor to differentiated phenotypes. Parallel analysis of tumor-associated cells identified conserved macrophage, fibroblast, and endothelial populations that exhibit species- and site-specific reprogramming. Validation by mapping cell types using spatial transcriptomics revealed structured neighborhood architectures that were reproduced across multiple samples. Cell-cell interaction analysis revealed similarities and differences in tumor-host networks across primary and metastatic sites and across species. This analysis enabled pathway-specific assessment of tumor-host communication fidelity across osteosarcoma model systems relative to humans, revealing canine osteosarcoma as a more faithful model. Metastatic lung lesions, counterintuitively, exhibited more intense and complex extracellular matrix (ECM) signaling than primary bone tumors. A key example was tumor-derived fibronectin (FN1), which engages integrin and syndecan receptors on lung epithelial cells, driving a pathological mesenchymal and profibrotic state that promotes fibrotic niche formation and metastatic lung colonization. Together, this cross-species resource delineates both conserved and divergent tumor microenvironment programs, demonstrates how model-aware analyses uncover previously unrecognized tumor-host interactions, and underscores the need for therapies that co-target tumor heterogeneity and its supportive metastatic niche.

Abstract Background: Canine nodal marginal zone lymphoma (MZL) is the second most common histologic diagnosis of diffuse B-cell lymphomas in dogs, but a molecular profile that can distinguish this condition from the more common canine diffuse large B-cell lymphoma (DLBCL) has been elusive. Here, we use single-cell sequencing to define the transcriptomic signatures of canine MZL before and after oncolytic virotherapy followed by traditional chemotherapy. Objective: The aims of this study were to define the canine MZL transcriptome at single cell resolution and to evaluate its changes in the face of selective pressures introduced by therapy. Methods: Longitudinal biopsies and fine needle aspirates were collected from a dog with MZL enrolled in an immunotherapy trial. Peripheral blood B-cells from healthy dogs served as reference controls. Single-cell sequencing was done using the 10x Genomics Chromium GEM X platform (v3.1), and data was aligned to the canFam4_Y genome. Quality control, clustering, and cell annotation were performed using Seurat in R (v4.4.0). Differential gene expression analysis (DGEA) was performed on 500 randomized MZL B-cells and 500 healthy canine B-cells. InferCNV was deployed on the longitudinal MZL samples for prediction of tumor B-cell CNV profiles. Results: When compared to normal peripheral blood B-cells, the tumor cells were characterized by downregulation of quiescence-associated genes, including KLF2. Copy number analysis uncovered loss on canine chromosome 20 (CFA20) encoding KLF2, gain on CFA13, and gains on CFA32 and CFA36. While an anti-viral T-cell response was identified after VSV treatment, the B-cell subpopulations retained stable transcriptomes, with a disappearance of proliferating B-cells after chemotherapy. Conclusion: This is the first report describing the molecular properties of canine MZL at single cell resolution. Clonal diversity was apparent in the tumor, with copy number loss on CFA20, presumably leading to loss of KLF2. The transcriptional features of the tumor cells remained stable even in the face of a T-cell response to an oncolytic virus. Taken together, the results document silencing of KLF2 as a key phenotypic homology between canine and human MZL, supporting the potential for comparative approaches to enhance our understanding of the significance of KLF2 silencing in this disease. Citation Format: Elise Weir, Grace Walker, Jaime F. Modiano, Aaron L. Sarver, Shruthi Naik, Amy Treeful. Reduced KLF2 expression in canine marginal zone lymphoma mirrors human disease [abstract]. In: Proceedings of the Fifth AACR International Meeting on Advances in Malignant Lymphoma: From Discovery to Clinical Impact; 2026 Jun 24-27; Philadelphia, PA. Philadelphia (PA): AACR; Blood Cancer Discov 2026;7(3_Suppl):Abstract nr A043.

Companion dogs have a lifetime cancer risk similar to that of humans. This excess risk, as compared to what is seen in other species, seems to be due to our recent success in outliving our evolutionarily adapted lifespan. For cancers to develop, a cancer-permissive environment must be present, which may exist months or even years before a tumor becomes detectable. We have developed the Shine On Suspicion (SOS) test, a flow cytometry based test to detect these changes that lead to a cancer-permissive environment. To make this test actionable, we combined it with a novel agent for cancer interception (secondary prevention) called eBAT. eBAT is a bispecific ligand targeted toxin consisting of truncated, deimmunized Pseudomonas exotoxin fused to epidermal growth factor (EGF) and the amino terminal fragment of urokinase. This drug was designed to use epidermal growth factor receptors (EGFR) and urokinase-type plasminogen receptors (uPAR) as baits to deliver the lethal toxin into the cells, rather than disrupting receptor signaling. eBAT has self-limiting, well-tolerated side effects and is safe enough for administration to otherwise healthy individuals. To date, eBAT has been administered to 11 healthy dogs that were determined to have elevated cancer risk based on the SOS test, with only 1 of the 11 dogs developing cancer more than 2 years after treatment. A hazard ratio calculated with a 95% confidence interval shows that dogs receiving eBAT interception had nearly 4 times reduction in risk of a cancer diagnosis compared to controls. Ongoing research aims to explore the identity and function of niche-forming cells to improve cancer prevention strategies and their applicability to humans. Ashley J. Schulte, Rose Dicovitsky, Taylor A. DePauw, Amber L. Winter, Kathleen L. Stuebner, Andrea Chehadeh, Sara Pracht, Antonella Borgatti, Ali Khammanivong, Mitzi Lewellen, Lauren E. Burt, Daniel A. Vallera, Michael S. Henson, Erin B. Dickerson, Christopher Ober, Kari L. Anderson, Esther Nell, Aaron L. Sarver, Gary R. Cutter, Jaime F. Modiano. Active interception to modulate the systemic cancer-permissive microenvironment and reduce cancer incidence in companion dogs with elevated cancer risk [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 1041.

SUMMARY Glioblastoma remains a deadly cancer driven by invasion of tumor cells into the brain. Transcriptomic analyses have revealed distinct molecular subtypes, but mechanistic differences that explain clinical differences are not clear. Here, we show that, as predicted by the motor-clutch model for cell migration, mesenchymal glioma cells are more spread, generate larger traction forces, and migrate faster in brain tissue compared to proneural cells. Despite their fast migration and comparable proliferation rate in vitro, mice with mesenchymal tumors live longer than mice with proneural tumors, which was correlated with an immune response in the mesenchymal mice that included T cell-mediated killing of cancer cells, similar to human tumors. Thus, mesenchymal tumors have aggressive migration, but are relatively immunologically ‘hot’ which suppresses net proliferation. These two features counteract each other and may explain the lack of a strong survival difference between subtypes clinically, while also opening up new opportunities for subtype-specific therapies.

Canine hemangiosarcoma is a common and aggressive vascular malignancy predominantly affecting dogs over six years of age. Despite surgical resection followed by adjuvant chemotherapy, median survival remains around 4–6 months. Propranolol, a beta-adrenergic receptor (β-AR) antagonist, has shown efficacy in human angiosarcoma, a tumor with similar clinical and morphological characteristics, when combined with chemotherapy. To determine if propranolol could be repurposed as an effective adjunct to chemotherapy, we conducted a phase I clinical study evaluating the safety and efficacy of propranolol combined with doxorubicin (PRO-DOX) in 20 dogs with stage 1 or stage 2 splenic hemangiosarcoma.Plasma from 19 dogs was analyzed for propranolol pharmacokinetics and RNA was extracted from tumors from 13 of the dogs for transcriptional profiling. Although propranolol did not appear to influence treatment outcomes, our results revealed long-term survival in young adult dogs (less than 6 years of age), suggesting the possibility of a better response to doxorubicin. Faster clearance of 4-OH propranolol also correlated with long-term survival in younger dogs, but this appeared to be associated with drug metabolism due to age rather than effects of the drug on survival outcomes. Gene expression analysis identified distinct age-associated tumor signatures, with young dogs exhibiting increased immune-related gene expression and older dogs showing elevated expression of genes associated with the cell cycle and the DNA damage response and repair. These findings highlight several hallmarks of cellular aging in hemangiosarcoma that may influence treatment responses and long-term survival. Our findings suggest that young adult dogs with splenic hemangiosarcoma treated with doxorubicin have a better prognosis and underscore the need for further research into age-related molecular mechanisms of disease. These insights could refine therapeutic strategies and clinical decision-making in hemangiosarcoma management.

The immune system plays a critical role in defending against pathogens and surveilling tumors. Understanding immune cell behavior in both health and disease is essential for advancing therapeutic strategies, particularly in oncology. However, there remains a gap in knowledge regarding how immune cell profiles differ across species and how these differences might impact cancer immunology. In this study, we conduct a comparative analysis of single-cell transcriptional profiles of immune cells from three mammalian species—humans, mice, and dogs—under both normal and tumor-bearing conditions. Using high-throughput single-cell RNA sequencing (scRNA-seq), we aim to identify both conserved and species-specific transcriptional signatures that define immune cell function in health and cancer, with the ultimate goal of enhancing translational research and therapeutic development. To generate a comprehensive dataset, we analyzed immune cell samples from both normal and tumor tissues across humans, mice, and dogs. These species were selected for their distinct immunological and clinical features: humans as the primary model for clinical oncology, mice as the standard laboratory model for cancer research, and dogs as a naturally occurring cancer model with genetic and environmental similarities to humans. Immune cells from canine samples were isolated and analyzed using scRNA-seq. Publicly available human, mouse and canine datasets were also incorporated into the analysis. Analyses of these datasets enabled high-resolution characterization of the immune landscape in each species. We developed a pipeline to systematically identify both commonalities and species-specific differences in immune cell transcriptional profiles. In tumor free samples, immune cell profiles were broadly similar across species, with T cells, B cells, macrophages, and dendritic cells as the dominant populations. However, we also observed notable species-specific variations in the transcriptional features of immune cells in normal and tumor tissue. This study provides a comprehensive cross-species analysis of immune cell transcriptional profiles in both normal and tumor states. Our findings highlight the importance of considering species-specific differences when translating preclinical results to human cancer research, emphasizing the value of utilizing multiple animal models, including canines, to enhance our understanding of cancer immunology. These insights are critical for the design of immunotherapies and the optimization of preclinical cancer models. Aaron L. Sarver, Caitlyn M. Callaghan, Marissa Macchietto, Lauren Burt, Meagan Wojtysiak, Courtney H. Labé, Taylor DePauw, Ashley Schulte, Kelly M. Makielski, Julia E. Medland, Jaime F. Modiano. Comparative analysis of single-cell immune cell transcriptional profiles in humans, mice, and dogs: insights from normal and tumor states [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 5871.

11544 Background: The mTOR pathway is a central signaling circuit that contributes to cancer cell proliferation, angiogenesis, metabolism, and other pivotal processes. The phase III SUCCEED trial showed marginal benefit of mTOR inhibition (mTORi) in chemo-responsive sarcomas, despite promising foundational phase II data. Since these trials did not account for mTOR-related physiology, we sought to identify sarcoma subgroups that display mTORC1 activated/activation phenotypes (mTORC1-act) that might derive more benefit from mTORi. Methods: DNA (592-gene or whole exome; N=7028) and RNA (whole transcriptome; N=3757) sequencing was performed from sarcoma patient samples, representing 49 histologic subtypes, submitted to Caris Life Sciences (Phoenix, AZ). A transcriptomic signature associated with up-regulation of mTORC1 complex activity (HALLMARK_MTORC1_SIGNALING, mSigDB) was analyzed by single-sample Gene Set Enrichment Analysis (ssGSEA). Real-world overall survival (OS) was obtained from insurance claims data and calculated from date of biopsy to last contact, with hazard ratio calculated using Cox proportional hazards model (p-values calculated by log-rank test). Results: Among the most mTORC1-act subtypes were PEComa (n=49, median ssGSEA score=0.114) and osteosarcoma (n=163, median score=0.084). Novel findings included high degrees of mTORC1-act in UPS (n=225, median score=0.132), IMT (n=36, median score=0.167), and epithelioid sarcoma (n=26, median score=0.155). Histologic subtype was a strong predictor of mTORC1-act (p<0.00001); other predictors were alterations in TSC2 (p<0.0001), TSC1 (p=0.0019), PTEN (p=0.0126), and PIK3R1 (p=0.0223). In PEComa, TSC2 alterations were associated with mTORC1-act (p=0.036), but TSC1 alterations were not (p=0.63). In a pan-sarcoma population, high ssGSEA mTORC1-act scores were associated with lower median OS of 15.4 months (m) compared to intermediate (24.2 m) and low (36.8 m) mTORC1-act scores (p<0.000001). Similar findings were observed for LMS (16.2 v 30.6 v 45.9 m, p<0.0001) and LPS (11.2 v 30.1 v 46.8 m, p<0.0001), but not all subtypes. Conclusions: The high levels of mTORC1-act in PEComa and osteosarcoma are consistent with prior reports. Increased mTORC1-act among TSC2-mutant, but not TSC1-mutant, PEComa aligns with lower responses to mTORi observed in non- TSC2-mutant patients in the AMPECT trial. Together, these findings support the use of ssGSEA to identify histologic subtypes (UPS, IMT, epithelioid) and genetic factors ( TSC2 variants > others) associated with increased mTORC1 activity that may predict for better responses to mTORi, and they suggest a clinical trial to further pursue this pathway in sarcomas. These data provide additional valuable prognostic information for patients with a wide range of sarcoma subtypes.

Immune cell infiltration and comparative immune signatures between canine hemangiosarcoma and human angiosarcoma. A, A total of 461 upregulated genes were identified in immune-high (N = 8) compared with immune-low (N = 5) groups in human angiosarcomas (FDR P value < 0.05). B, 567 immune gene signatures were identified among three molecular subtypes of canine hemangiosarcomas (N = 76; FDR P value < 0.001; fold change > 3). The heat maps show upregulated (red) and downregulated (green) genes by unsupervised hierarchical clustering (average linkage; mean-centered; log2 transformed). C, Venn diagram shows 58 common genes associated with signaling pathways of immune cell functions between human and canine tumors. Representative photomicrographs of H&E and IHC staining showing histologic morphology and immune cell infiltration in canine hemangiosarcoma (D) and human angiosarcoma tissues (E) using anti-CD3, anti-PAX5, anti-MAC387, and anti-Iba1 (for canine) or anti-CD163 (for human) antibodies for detecting T cell, B cell, and macrophages. Horseradish peroxidase (counterstain = hematoxylin) or alkaline phosphate (for Iba1; counterstain = methylene blue). Bar = 50 µm. Scatter plots display correlation between transcriptional and IHC immune score in canine hemangiosarcoma (F) and human angiosarcoma (G). Spearman correlation coefficient (R) was calculated.

Abstract Our research is (focused) on delineating the relationship of aging and cancer with the goal to develop prevention and intervention therapies. Our success towards this end is based on the ability to employ companion dogs in clinical studies, particularly given the similarities of aging and cancer in dogs and people. Here, we report results of the development of both a companion diagnostic and a potential therapeutic intervention from the canine clinical Shine On study. The Shine On study included a training set of 97 dogs in four groups, consisting of (1) healthy 2-4 year-old dogs that were skeletally mature but had not reached the age boundary where cancer risk is apparent, and three groups where dogs had pathologically confirmed (2) hemangiosarcomas, (3) other malignant cancers, or (4) benign splenic masses. It also included a test set of 209 dogs over 6 years of age with no evidence of cancer or other chronic diseases. Using the Shine On Suspicion (SOS) test, dogs could be assigned to a low-risk category, where the probability of developing cancer over the next 400 days (approximately 1/10th of a modern domestic dog’s lifespan) was less than 4%, or to a high-risk category, where the probability of developing cancer over the same time period was almost 25%, and it increased to more than 50% by 1,450 days. Not surprisingly, the relative risk of cancer in dogs that were originally assigned to the low-risk category increased in a fashion that was comparable to that seen in dogs assigned to the high-risk category within 400-600 days after testing. We have used the bispecific ligand targeted toxin, eBAT, as a strategic preventative in seven dogs to date. The drug is well tolerated and associated with favorable outcomes (extended lifespan with no cancer deaths). Ongoing experiments seek to define the identity and functional properties of putative-niche forming cells and mechanisms through which we can modify the permissive environment to delay or prevent cancer in dogs - and eventually in humans. Citation Format: Jaime F. Modiano, Ashley J. Schulte, Rose Dicovitsky, Taylor A. DePauw, Ali Khammanivong, Mitzi Lewellen, Lauren E. Burt, Daniel A. Vallera, Gary R. Cutter, Amber L. Winter, Kathleen M. Stuebner, Andrea Chehadeh, Sara Pracht, Antonella Borgatti, Michael S. Henson, Erin B. Dickerson, Christopher Ober, Kari L. Anderson, Esther Nell, Aaron L. Sarver. Risk assessment, early detection, and strategic prevention of naturally occurring cancers in companion dogs [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 7313.