About

Steven Suter is associated with the College of Veterinary Medicine at NC State University, which is dedicated to shaping the future of veterinary medicine and supporting the next generation of veterinary professionals. The college emphasizes a collaborative and caring culture, fostering student achievement, well-being, and extracurricular growth through research, international programs, and community engagement. While specific details about Dr. Suter's research focus, background, or key contributions are not provided in the page text, his association with the college suggests involvement in advancing veterinary education and research initiatives.

Research topics

• Surgery
• Internal medicine
• Medicine
• Pathology
• Oncology
• Biology
• Gastroenterology

Selected publications

• Genomic Evaluation of Canine Prostatic Carcinomas as a Model for the Human Disease: or ‘UC or not UC – that is the question’

  Veterinary and Comparative Oncology · 2025-07-23 · 4 citations

  articleOpen access

  Spontaneous canine prostate cancer (PC) is widely considered a pertinent clinical model for the human disease. While over 95% of PC in men are adenocarcinomas, arising from prostatic glandular epithelium, it is increasingly recognised that many canine PC are of urothelial origin, arising within the prostatic urethra or ducts, or through invasion from a primary urinary bladder tumour. At diagnosis, canine prostatic tumours are often poorly differentiated and widely disseminated, masking the primary site and limiting the sensitivity of cellular biomarkers. Consequently, published studies of canine PC show varying representation of glandular versus urothelial tumours, yielding conflicting observations regarding their molecular pathogenesis and clinical behaviour. We characterised DNA sequence mutations and copy number aberrations in 31 canine PC, seeking evidence supporting relevance as a disease model. Only three tumours resembled adenocarcinomas. The remainder were either histologically consistent with urothelial carcinoma (n = 15), showed mixed glandular and urothelial morphology (n = 4), or were carcinomas of undetermined cell type (n = 9). BRAF V588E mutation was detected in 87% of tumours, including all three adenocarcinomas. Urinary bladder involvement was evident in 46% of cases, but none of the adenocarcinomas. Genome-wide DNA copy number instability was apparent throughout the cohort, with chromosome 36 gain significantly associated with urothelial tumours. Hallmark alterations of human PC, such as defects within PI3K and androgen receptor signalling pathways, were not detected. Improved molecular subclassification of canine PC is needed to direct selection of relevant cases for modelling the human disease and to ensure appropriate extrapolation between canine and human studies.

  PublisherOA PDFDOI

• Genomic Evaluation of Canine Prostatic Carcinomas as a Model for the Human Disease

  UNC Libraries · 2025-12-12

  articleOpen access

  Spontaneous canine prostate cancer (PC) is widely considered a pertinent clinical model for the human disease. While over 95% of PC in men are adenocarcinomas, arising from prostatic glandular epithelium, it is increasingly recognised that many canine PC are of urothelial origin, arising within the prostatic urethra or ducts, or through invasion from a primary urinary bladder tumour. At diagnosis, canine prostatic tumours are often poorly differentiated and widely disseminated, masking the primary site and limiting the sensitivity of cellular biomarkers. Consequently, published studies of canine PC show varying representation of glandular versus urothelial tumours, yielding conflicting observations regarding their molecular pathogenesis and clinical behaviour. We characterised DNA sequence mutations and copy number aberrations in 31 canine PC, seeking evidence supporting relevance as a disease model. Only three tumours resembled adenocarcinomas. The remainder were either histologically consistent with urothelial carcinoma (n = 15), showed mixed glandular and urothelial morphology (n = 4), or were carcinomas of undetermined cell type (n = 9). BRAF V588E mutation was detected in 87% of tumours, including all three adenocarcinomas. Urinary bladder involvement was evident in 46% of cases, but none of the adenocarcinomas. Genome-wide DNA copy number instability was apparent throughout the cohort, with chromosome 36 gain significantly associated with urothelial tumours. Hallmark alterations of human PC, such as defects within PI3K and androgen receptor signalling pathways, were not detected. Improved molecular subclassification of canine PC is needed to direct selection of relevant cases for modelling the human disease and to ensure appropriate extrapolation between canine and human studies.

  PublisherDOI

• Novel niclosamide stearate prodrug therapeutic shows potential efficacy against naturally occurring canine osteosarcoma in a clinical feasibility study

  American Journal of Veterinary Research · 2025-10-27

  articleOpen accessSenior author

  Objective: To manufacture and characterize a modified niclosamide stearate (NS) prodrug therapeutic (mNSPT) for use in a small clinical trial in a metastatic canine osteosarcoma (OS) model. Animals: 10 dogs that presented for treatment of nondetectable metastatic OS underwent resection of primary tumors prior to systemic therapy. Four cycles of IV carboplatin (300 mg/m2, IV, q 3 wk) followed by 4 cycles of the experimental mNSPT (10 mg/kg, IV, weekly). Posttreatment surveillance included physical examination and thoracic radiographs every 3 months for 2 years. Samples for pharmacokinetic analysis were taken at the end of the 0.5- to 1-hour IV infusion of the mNSPTs and followed for 2 hours. Clinical Presentation: The NS average concentration at the end of infusion was 134.88 ± 13.32 μg/mL; the average area under the curve was 211.62 ± 27.89 h·µg/mL. The niclosamide concentration at the end of infusion was 23.11 μg/mL ± 3.77 μg/mL, and the area under the curve was 27.52 ± 5.92 h·µg/mL, well above the NSPT 0.75 μg/mL (1.27 μM) cell-effective concentrations for OS cells in culture. The average terminal half-life was 4.57 hours for NS and 3.23 hours for niclosamide. Three dogs developed metastatic disease on carboplatin and did not receive mNSPT. The median time to tumor progression and OS of the 7 treated dogs was 510 and 632 days, respectively, with 3 dogs living > 4 years. Results: The results support further translational investigation of this novel therapeutic approach to OS treatment in a randomized, prospective phase III study in dogs and, if successful, ultimately in OS patients. Clinical Relevance: These results suggest that niclosamide-when transformed into the highly bioavailable NSPT-may have potential as a novel therapeutic agent for treating OS.

  PublisherDOI

• Postmortem pathologic findings in dogs that underwent total body irradiation and hematopoietic cell transplant: A case series of five dogs with B-cell multicentric lymphoma

  Veterinary Pathology · 2024-05-02 · 2 citations

  article

  Alternative therapies that can help achieve complete remission in dogs with lymphoma include total body irradiation and hematopoietic cell transplant, though there are few reports describing successes and pathologic sequelae of these procedures. During a 10-year period, 94 dogs with multicentric lymphoma received a hematopoietic cell transplant following total body irradiation at North Carolina State University College of Veterinary Medicine. Seven of these 94 dogs (7%) died prior to discharge, five (5%) of which presented for postmortem examination. Of these dogs, four received an autologous hematopoietic cell transplant, while one received a haploidentical allogeneic hematopoietic cell transplant. All five dogs had bone marrow depletion with all hematopoietic lines affected. Three had systemic candidiasis, while two had bacterial infections. To the authors' knowledge, this is the first report to document pathologic findings and development of systemic mycoses in dogs post total-body irradiation therapy and hematopoietic cell transplant.

  PublisherDOI

• Supplementary Figure 1 from Gene Profiling of Canine B-Cell Lymphoma Reveals Germinal Center and Postgerminal Center Subtypes with Different Survival Times, Modeling Human DLBCL

  2023-03-30

  preprintOpen accessSenior author

  <p>PDF file - 2708K, Immunohistochemistry of cBCLs.</p>

  PublisherDOI

• Supplementary Table 2 from Gene Profiling of Canine B-Cell Lymphoma Reveals Germinal Center and Postgerminal Center Subtypes with Different Survival Times, Modeling Human DLBCL

  2023-03-30

  supplementary-materialsOpen accessSenior author

  <p>XLSX file - 40K, Canine genes identified by Ingenuity Pathway Analysis as part of the NF-kB or B-cell receptor signaling pathways (Fig. 5).</p>

  PublisherDOI

• Supplementary Table 2 from Adjuvant Sirolimus Does Not Improve Outcome in Pet Dogs Receiving Standard-of-Care Therapy for Appendicular Osteosarcoma: A Prospective, Randomized Trial of 324 Dogs

  2023-03-31

  supplementary-materialsOpen access

  <p>Supplementary Table 2 contains the summary comparison of both the Intent-to-treat and Per-protocol analyses of clinical outcomes for dogs enrolled in Standard of Care (SOC) and Standard of Care + sirolimus</p>

  PublisherDOI

• Supplementary Table 3 from Gene Profiling of Canine B-Cell Lymphoma Reveals Germinal Center and Postgerminal Center Subtypes with Different Survival Times, Modeling Human DLBCL

  2023-03-30

  supplementary-materialsOpen accessSenior author

  <p>PDF file - 41K, Distribution of lymphoma samples into "Ongoing" or "Static" categories based on the proportion of IGHV subclones that are identical at the CDR3 region for each sample.</p>

  PublisherOA PDFDOI

• Supplementary Figure 2 from Adjuvant Sirolimus Does Not Improve Outcome in Pet Dogs Receiving Standard-of-Care Therapy for Appendicular Osteosarcoma: A Prospective, Randomized Trial of 324 Dogs

  2023-03-31

  preprintOpen access

  <p>Supplementary Fig. 2 shows the walk-in pharmacokinetics, both measured results and simulated values, for dogs treated with oral sirolimus in preparation for the definitive adjuvant trial.</p>

  PublisherDOI

• Data from Adjuvant Sirolimus Does Not Improve Outcome in Pet Dogs Receiving Standard-of-Care Therapy for Appendicular Osteosarcoma: A Prospective, Randomized Trial of 324 Dogs

  2023-03-31

  preprintOpen access

  <div>AbstractPurpose:<p>The mTOR pathway has been identified as a key nutrient signaling hub that participates in metastatic progression of high-grade osteosarcoma. Inhibition of mTOR signaling is biologically achievable with sirolimus, and might slow the outgrowth of distant metastases. In this study, pet dogs with appendicular osteosarcoma were leveraged as high-value biologic models for pediatric osteosarcoma, to assess mTOR inhibition as a therapeutic strategy for attenuating metastatic disease progression.</p>Patients and Methods:<p>A total of 324 pet dogs diagnosed with treatment-naïve appendicular osteosarcoma were randomized into a two-arm, multicenter, parallel superiority trial whereby dogs received amputation of the affected limb, followed by adjuvant carboplatin chemotherapy ± oral sirolimus therapy. The primary outcome measure was disease-free interval (DFI), as assessed by serial physical and radiologic detection of emergent macroscopic metastases; secondary outcomes included overall 1- and 2-year survival rates, and sirolimus pharmacokinetic variables and their correlative relationship to adverse events and clinical outcomes.</p>Results:<p>There was no significant difference in the median DFI or overall survival between the two arms of this trial; the median DFI and survival for standard-of-care (SOC; defined as amputation and carboplatin therapy) dogs was 180 days [95% confidence interval (CI), 144–237] and 282 days (95% CI, 224–383) and for SOC + sirolimus dogs, it was 204 days (95% CI, 157–217) and 280 days (95% CI, 252–332), respectively.</p>Conclusions:<p>In a population of pet dogs nongenomically segmented for predicted mTOR inhibition response, sequentially administered adjuvant sirolimus, although well tolerated when added to a backbone of therapy, did not extend DFI or survival in dogs with appendicular osteosarcoma.</p></div>

  PublisherDOI

Frequent coauthors

• Kristy L. Richards

  89 shared

• Alison A. Motsinger‐Reif

  National Institute of Environmental Health Sciences

  76 shared

• Matthew Breen

  Cancer Genetics (United States)

  75 shared

• George W. Small

  University of North Carolina at Chapel Hill

  68 shared

• Rachael Thomas

  North Carolina State University

  67 shared

• Luke B. Borst

  64 shared

• Dahlia M. Nielsen

  North Carolina State University

  63 shared

• Sandeep S. Davé

  University College London

  61 shared

Education

• PhD, Section of Medical Genetics

  University of Pennsylvania

• VMD, Veterinary

  University of Pennsylvania

Awards & honors

• Associate Member, Lineberger Comprehensive Cancer Center, UN…
• Member, Comparative Medicine Institute, NC State
• Member, Veterinary Cancer Society
• Member, North Carolina Veterinary Medical Association