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.

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.

A three year old male neutered mixed breed dog presented with a mass on the right carpus and accompanying lameness. A Jamshidi bone biopsy was performed, and histopathology results were consistent with a sarcoma. The dog received oncolytic virotherapy (OV) with vesicular stomatitis virus (VSV) as part of a clinical trial in dogs with osteosarcoma (OSA). Ten days after VSV treatment, the affected limb was amputated, and histopathology was consistent with intramedullary HSA. Considering the new diagnosis, standard doxorubicin chemotherapy was prescribed. With this combination of therapies, the dog had an extended survival of more than seven years and remains alive at the time of writing. This is the first case report documenting OV given in conjunction with the standard of care for canine appendicular HSA.

Abstract Angiosarcomas are rare (fewer than 300 cases each year), highly aggressive sarcomas of blood vessel-forming cells with an unfavorable prognosis. We and others have previously reported that propranolol, a beta adrenergic receptor antagonist commonly used to treat heart disease and anxiety, increased the overall survival of patients with advanced angiosarcoma when used alone or incorporated into chemotherapy regimens. Treatment of angiosarcoma has been hampered by the relative lack of suitable models to analyze molecular responses to treatment. To overcome this hurdle and understand the vulnerability of angiosarcoma to propranolol, we capitalized on the similar morphological and clinical characteristics between human angiosarcoma and canine hemangiosarcoma, which occurs in thousands of dogs each year. The objectives for the PRO-DOX clinical trial were to assess tolerability and clinical benefit of propranolol in dogs with hemangiosarcoma when given as an adjunct to chemotherapy. We conducted a phase I study using a continuous reassessment model with three dose cohorts (0.8, 1.0, and 1.3 mg/kg PO q 8 hrs) in dogs diagnosed with stage 1 or stage 2 splenic hemangiosarcoma. Following splenectomy, propranolol was onboarded using a dose escalation strategy over 12 days prior to the start of doxorubicin (30 mg/m2 intravenously every three weeks, five rounds). Twenty dogs were enrolled and distributed across the dose cohorts based on the study design. One dog in the highest cohort experienced acute hypotension after six months on propranolol, which resolved with dose reduction. Although a statistically significant survival benefit was not seen in this study when compared to historic controls, a subset of dogs (n=8 or 40%) exceeded the expected survival of 4-6 months. Notably, three dogs diagnosed at or below age five survived over two years. Gene expression analysis of tumors obtained from the short-, mid-, and long-term survivors revealed sets of genes associated with immune responses (e.g. lymphocyte activation, positive regulation of T cell activation), antigen processing, cell adhesion, and mitochondrial metabolism in the long-term survivor group. Our findings suggest that age (< 6 years) may predict a favorable outcome, and immune mediated responses differ between the short and long-term survivors. Ongoing experiments seek to define the specific molecular properties and immune responses contributing to these outcomes, with potential implications for human angiosarcoma. Citation Format: Erin B. Dickerson, Jeremy Chacón, Brian D. Husbands, Michael S. Henson, Jaime F. Modiano, Kathleen M. Stuebner, Amber Winter, Sara Pracht, Andrea Chehadeh, Kelly Bergsrud, Caitlin Feiock, Julia Medland, Heather Scavello, Pascale C. Salah, Jennifer Mahoney, Michael O. Childress, David R. Brown, Antonella Borgatti. Propranolol may enhance long term survivorship in a subset of dogs with hemangiosarcoma when combined with doxorubicin chemotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(7_Suppl):Abstract nr LB407.

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.

Abstract Background: Osteosarcoma a common cancer in dogs that can serve as a translational model for certain aspects of human osteosarcoma. We previously developed a serum exosome gene signature in dogs with osteosarcoma capable of detecting minimal residual disease and predicting prognosis after therapy. Our goal is to continue expanding our understanding of exosomes for liquid biopsy applications in dogs with cancer, and to leverage this information in the design of liquid biopsy tests to address risk, early detection, and management of human cancer patients. For this study, we hypothesized that dogs with cancer would have higher plasma exosome concentrations compared with healthy control dogs. Methods: Plasma exosomes were enriched from 29 dogs with cancer, including 8 dogs with osteosarcoma, and 26 healthy control dogs. Exosome size and concentration in the plasma samples were characterized with nanoparticle tracking analysis. Wilcoxon rank sum tests were performed to assess differences between groups. Results: Dogs with cancer had a higher mean exosome concentration at 1.4 x 1012 (+/- 1.1 x 1012) particles/ml, compared with 5.0 x 1011 (+/- 2.7 x 1011) particles/ml in healthy control dogs (p = 0.0046). There was no difference in exosome size between dogs with cancer (mean diameter = 99.9 nm) and healthy control dogs (107.8 nm; p = 0.16) when all cancer types were included. However, exosomes enriched from healthy control samples were found to be significantly larger when compared to the exosomes enriched from the subset of cancer dogs that had osteosarcoma (mean exosome diameter = 83.9 nm; p = 0.0065). Similarly, when comparing exosome size between dogs with osteosarcoma and dogs with other cancers, plasma exosomes were larger in the dogs with other cancers (107.4 nm; p = 0.023). Conclusions: In this population, dogs with cancer have higher plasma exosome concentrations compared with healthy control dogs. Interestingly, we also found that dogs with osteosarcoma had significantly smaller exosome size than dogs with other cancers and healthy control dogs. Though the size of exosomes from dogs with osteosarcoma was found to be smaller, it is possible that the larger exosome concentration in dogs with osteosarcoma results in a similar total exosomal mass. Ongoing work includes analysis of exosomal cargo to develop a liquid biopsy test capable of assessing risk of osteosarcoma development in dogs, and applying similar methodology to determine exosomal genes associated with prognosis in pediatric osteosarcoma. The higher exosome concentrations in dogs with cancer suggests that this feature, combined with analysis of exosomal cargo, may have utility in development of a liquid biopsy cancer test in dogs. Citation Format: Kelly M. Makielski, Jaron M. Magstadt, Courtney H. Labe, Ali Khammanivong, Meagan Wojtysiak, Kyle Duval, Mitzi Lewellen, Amber Winter, Kelly Reid, Andrea Chehadeh, Michelle Buettner, Caitlin Feiock, Aaron K. Rendahl, Gary R. Cutter, Logan G. Spector, Brenda J. Weigel, Jaime F. Modiano. Dogs with cancer have higher plasma exosome concentrations compared with healthy dogs in the COED (canine osteosarcoma early detection) study [abstract]. In: Proceedings of the AACR Special Conference: Liquid Biopsy: From Discovery to Clinical Implementation; 2024 Nov 13-16; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2024;30(21_Suppl):Abstract nr B003.

Abstract Background: Nonrandom patterns of cell-free DNA (cfDNA) are closely associated with malignancy. We hypothesize that they are also found in the systemic microenvironment that gives rise to cancer, and that such signatures can inform a risk stratification test. To achieve this, we have initiated the Lymphoma Risk Assessment (LyRA) study, using machine learning on a training set of dogs with known health status and a test set of otherwise healthy adult pet dogs to identify cfDNA signatures that are associated with elevated risk of developing diffuse large B- cell lymphoma (DLBCL). We will validate the predictive accuracy of these signatures, including the persistence of the risk environment and the interval between risk detection and development of clinical disease. Since cfDNA is the primary input of the LyRA test, we first performed a pilot study to assess how sample characteristics affect cfDNA quality and subsequent low-pass whole genome sequencing (WGS) data. Methods: Blood samples were collected from pet dogs with the owner’s informed consent. Paired samples were collected into potassium (K3)EDTA tubes and additive-free red top tubes (n = 5 dogs) or K3EDTA tubes and Cell-free DNA BCT® Streck Tubes (n = 6 dogs). Additional serum samples (n=3) were generously provided by the Morris Animal Foundation Golden Retriever Lifetime Study. cfDNA was isolated using the QIAamp® Circulating Nucleic Acid kit. Total cfDNA concentration was measured by PicoGreen™ and fragment distribution by Agilent High Sensitivity D500 ScreenTape® Assay, with comparisons made by starting material (plasma vs. serum) and collection tubes. Results: Serum had both higher total concentrations of cfDNA (PicoGreen™) and calibrated concentrations of long fragment cfDNA (515-658 bp Agilent traces) compared to plasma. In addition, total cfDNA concentrations increased with malignancy, following the pattern: no cancer < cancer < hematological cancer. Median fragment lengths of Agilent peaks also increased with malignancy for short (125-181 bp) and medium (340-425 bp) fragments, in both serum and plasma, but decreased for long fragments. In these pilot data the trends seen were consistent with our hypothesis and with prior studies, although due to sample size, no statistical testing was performed. Conclusions: The pilot study demonstrated that the effects of sample parameters on cfDNA quality are consistent with existing literature, validating our methods and supporting the rationale for the LyRA study. These features may prove valuable when integrated with genomic data to identify high-risk microenvironments. Recent research has shown that a majority of cfDNA in tumor patients originates from non-malignant cells and current methods often overlook potentially important patterns in this so-called 'discard cfDNA.' By focusing on these overlooked patterns, with an emphasis on risk stratification, the LyRA test could shift clinical management to a prevention-focused approach, serving as a model of testing and interception for DLBCL and other cancers in dogs, and potentially in humans. Citation Format: Lauren E Burt, Amy E Treeful, Mitzi Lewellen, Kimberly Demos-Davies, Andrea Chehadeh, Sara Pracht, Ashley J Schulte, Caitlin Feiock, Julia Medland, Davis Seelig, Kelly M Makielski, Ali Khammanivong, Antonella Borgatti, Michael S Henson, Michael Linden, Daniel Vallera, Gary R Cutter, Aaron L Sarver, Jaime F Modiano. Identifying patterns of cell-free DNA associated with elevated risk of diffuse large B-cell lymphoma in adult dogs [abstract]. In: Proceedings of the AACR Special Conference: Liquid Biopsy: From Discovery to Clinical Implementation; 2024 Nov 13-16; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2024;30(21_Suppl):Abstract nr A051.

EGFR-targeted therapies are efficacious, but toxicity is common and can be severe. Urokinase type plasminogen activator receptor (uPAR)-targeted drugs are only emerging, so neither their efficacy nor toxicity is fully established. Recombinant eBAT was created by combining cytokines EGF and uPA on the same single-chain molecule with truncated Pseudomonas toxin. Its purpose was to simultaneously target tumors and their vasculature in the tumor microenvironment. In prior studies on mice and dogs, the drug proved efficacious. Here, we report the safety of eBAT in normal wildtype, uPAR knockout, and immunoreplete and immunodeficient tumor-bearing mice, as well as in dogs with spontaneous sarcoma that more closely mirror human cancer onset. In immunocompetent mice, tumor-bearing mice, uPAR knockout mice, and mice receiving species-optimized eBAT, toxicities were mild and self-limiting. Likewise, in dogs with life-threatening sarcoma given dosages found to be biologically active, eBAT was well tolerated. In mice receiving higher doses, eBAT was associated with dose-dependent evidence of liver injury, including portal biliary hyperplasia, oval cell proliferation, lymphoplasmacytic inflammation, periportal hepatocellular microvesicular change, hemorrhage, necrosis, and apoptosis. The results support continuing the clinical development of eBAT as a therapeutic agent for individuals with sarcoma and other cancers.

Abstract 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 eBAT, a novel bispecific ligand-targeted toxin that targets emerging cancer cells and the inflammatory niche to disrupt cancer formation. The Shine On Study used machine- learning algorithms to determine cancer risk based on a training set of 97 dogs with known conditions and a test set of 209 adult dogs with no evidence of cancer or other chronic diseases. Dogs assigned to the low-risk category had a less than 4% chance of developing cancer within 400 days after testing, whereas dogs assigned to the high-risk category had a nearly 25% chance of developing cancer in that timeframe. By 1,450 days, more than 50% of dogs assigned to the high-risk category developed cancer. Surprisingly, the SOS test’s specificity varied by breed. In Boxers and Portuguese Water Dogs the test accurately predicted the risk of hemangiosarcoma and other malignancies, whereas for Golden Retrievers, the test accurately predicted the risk for hemangiosarcoma, but no significant difference in the development of other cancers was observed between high-risk and low-risk groups. This suggests that the contribution of the cancer-permissive environment detected by the SOS test interacts with heritable factors, i.e., those defined by ancestry in creating the overall cancer risk state. To date, eBAT interception has been administered to 9 dogs, with only 1 potentially developing cancer 2 years after treatment. The drug is well-tolerated and shows promising outcomes. Future research aims to refine the SOS test, understand breed-specific responses, and explore the identity and function of niche- forming cells to improve cancer prevention strategies and their applicability to humans. Citation Format: Ashley J Schulte, Taylor A DePauw, Ali Khammanivong, Mitzi Lewellen, Lauren Burt, Rose Dicovitsky, Amber L Winter, Kathleen M Stuebner, Andrea Chehadeh, Sara Pracht, Christopher Ober, Kari L Anderson, Esther Nell, Antonella Borgatti, Michael S Henson, Erin B Dickerson, Aaron L Sarver, Daniel A Vallera, Gary R Cutter, Jaime F Modiano. Could ancestry play a role in cancer development? Insights from a risk assessment and early detection test of naturally occurring cancers in companion dogs [abstract]. In: Proceedings of the AACR Special Conference: Liquid Biopsy: From Discovery to Clinical Implementation; 2024 Nov 13-16; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2024;30(21_Suppl):Abstract nr A066.

Osteosarcoma is a devastating bone cancer that disproportionally afflicts children, adolescents, and young adults. Standard therapy includes surgical tumor resection combined with multiagent chemotherapy, but many patients still suffer from metastatic disease progression. Neoadjuvant systemic oncolytic virus (OV) therapy has the potential to improve clinical outcomes by targeting primary and metastatic tumor sites and inducing durable antitumor immune responses. Here we described the first evaluation of neoadjuvant systemic therapy with a clinical-stage recombinant oncolytic Vesicular stomatitis virus (VSV), VSV-IFNβ-NIS, in naturally occurring cancer, specifically appendicular osteosarcoma in companion dogs. Canine osteosarcoma has a similar natural disease history as its human counterpart. VSV-IFNβ-NIS was administered prior to standard of care surgical resection, permitting microscopic and genomic analysis of tumors. Treatment was well-tolerated and a 'tail' of long-term survivors (~35%) was apparent in the VSV-treated group, a greater proportion than observed in two contemporary control cohorts. An increase in tumor inflammation was observed in VSV-treated tumors and RNAseq analysis showed that all the long-term responders had increased expression of a T-cell anchored immune gene cluster. We conclude that neoadjuvant VSV-IFNβ-NIS is safe and may increase long-term survivorship in dogs with naturally occurring osteosarcoma, particularly those that exhibit pre-existing antitumor immunity.

Abstract The goal of this study was to evaluate safety, efficacy, and immunological activity of Vesicular Stomatitis Virus (VSV) expressing a species relevant (canine) interferon-beta (IFN-β) and the sodium iodide symporter (NIS), henceforth called VSV, in companion dogs with naturally occurring appendicular osteosarcoma. The hypothesis was that VSV would track to the tumor, induce oncolysis, and lead to enhanced infiltration of immune cells, expansion of virus- and tumor specific T-cell clones, and improved survival outcomes.The first 15 dogs enrolled in the VSV Immunotherapy and Genomics of Osteosarcoma Research (VIGOR) study received a single iv dose of VSV (1x109 TCID50/kg) 10 days before amputation and adjuvant carboplatin chemotherapy. The final 13 dogs were randomized in a double-blinded fashion to receive either a single dose of VSV or placebo. Outcome data were compared to those from an historical control group of 57 dogs with appendicular osteosarcoma treated between 2006 and 2018 using the standard of care of alone. VSV treatment was associated with mild systemic effects (fever and inflammation), which were self-limiting and caused no symptomatology. Alterations in the tumor microenvironment (micronecrosis, increased fibrosis, and increased inflammation) were more common and more pronounced in VSV treated dogs than in placebo-treated dogs.Reduction in the expression of co-regulated cell cycle gene clusters in tumors after VSV-treatment was observed in dogs with longer survival. Conversely, increased expression of co-regulated immune/inflammatory gene clusters was observed in both VSV-treated dogs and in placebo-treated dogs, suggesting this might be, at least partly, due to the biopsy procedures. Assessment of changes in the clonal composition of T cells within the tumors, draining lymph nodes, and systemic circulation is in progress. No differences were evident in median event-free or overall survival times among the different groups, although aspects of the study design and sample size could obscure differences. Intriguingly, a “tail” of nine dogs (41%) that were long-term survivors (>450 days) was apparent in the VSV-treated group. All but one of these long-term survivors had evidence of inflammation in the pre-treatment tumor samples or showed increased inflammation in the post-treatment samples. We conclude that neoadjuvant VSV has an excellent safety profile and provides a survival benefit for a subset of dogs with spontaneous bone cancer. Ongoing work seeks to establish distinguishing characteristics that identify those individuals most likely to benefit from this therapy, as well as to evaluate the potential to enhance this benefit through the addition of novel immunomodulatory agents as part of our efforts to translate this approach to human cancer patients. Citation Format: Kelly M. Makielski, Aaron L. Sarver, Aishwarya Sathyanarayan, Michael S. Henson, Kathleen M. Stuebner, Alexandru-Flaviu Tabaran, Ingrid Cornax, Gerard O'Sullivan, Andrea Chehadeh, Donna Groschen, Kelly Bergsrud, Lauren J. Mills, Amber L. Winter, Sara Pracht, Milcah C. Scott, Michael A. Farrar, Gary R. Cutter, Joseph S. Koopmeiners, Stephen J. Russell, Shruthi Naik, Jaime F. Modiano. Oncolytic Vesicular Stomatitis Virus expressing a species relevant interferon-beta is safe and provides a survival benefit when added as neoadjuvant to the standard of care for dogs with naturally occurring bone cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1747.