Spontaneously occurring canine cancer as a relevant animal model for developing novel treatments for human cancers

Mizuno, Takuya

doi:10.33611/trs.2021-007

Cited by 3 publications

(3 citation statements)

References 98 publications

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“…In recent years, the life expectancy of dogs has increased and cancer is becoming more common. Canine cancer is now a major cause of death in dogs, accounting for approximately one-third to half of all deaths in older dogs [ 1 , 2 , 3 ]. The current first-line treatment for canine cancer is surgery, followed by chemotherapy, radiation therapy, and immunotherapy, including immune checkpoint inhibitors [ 1 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

“…Canine cancer is now a major cause of death in dogs, accounting for approximately one-third to half of all deaths in older dogs [ 1 , 2 , 3 ]. The current first-line treatment for canine cancer is surgery, followed by chemotherapy, radiation therapy, and immunotherapy, including immune checkpoint inhibitors [ 1 , 3 ]. However, there are still several concerns in treating canine cancers, including the lack of experience in treating dogs compared with humans, the diversity of dog breeds, and the limited medical facilities available for dogs.…”

Section: Introductionmentioning

confidence: 99%

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Targeted Suicide Gene Therapy with Retroviral Replicating Vectors for Experimental Canine Cancers

Sonoda-Fukuda,

Takeuchi,

Ogawa

et al. 2024

IJMS

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Cancer in dogs has increased in recent years and is a leading cause of death. We have developed a retroviral replicating vector (RRV) that specifically targets cancer cells for infection and replication. RRV carrying a suicide gene induced synchronized killing of cancer cells when administered with a prodrug after infection. In this study, we evaluated two distinct RRVs derived from amphotropic murine leukemia virus (AMLV) and gibbon ape leukemia virus (GALV) in canine tumor models both in vitro and in vivo. Despite low infection rates in normal canine cells, both RRVs efficiently infected and replicated within all the canine tumor cells tested. The efficient intratumoral spread of the RRVs after their intratumoral injection was also demonstrated in nude mouse models of subcutaneous canine tumor xenografts. When both RRVs encoded a yeast cytosine deaminase suicide gene, which converts the prodrug 5-fluorocytosine (5-FC) to the active drug 5-fluorouracil, they caused tumor-cell-specific 5-FC-induced killing of the canine tumor cells in vitro. Furthermore, in the AZACF- and AZACH-cell subcutaneous tumor xenograft models, both RRVs exerted significant antitumor effects. These results suggest that RRV-mediated suicide gene therapy is a novel therapeutic approach to canine cancers.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Targeted Suicide Gene Therapy with Retroviral Replicating Vectors for Experimental Canine Cancers

Sonoda-Fukuda,

Takeuchi,

Ogawa

et al. 2024

IJMS

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show abstract

“…Third, such pets live in similar environments as humans but the accelerated progress of animal cancers allow for rapid testing and results. A further argument is that the biological and treatment responses to tumors in pets are better models of human tissue reactions than tiny rodent bodies [ 77 ]. Thus, when feasible, these kinds of studies are a key intermediate step for testing BNCT technologies for clinical development.…”

Section: Introductionmentioning

confidence: 99%

In Vivo Accelerator-Based Boron Neutron Capture Therapy for Spontaneous Tumors in Large Animals: Case Series

Kanygin

Кичигин

Zaboronok

et al. 2022

Biology

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(1) Background: accelerator-based neutron sources are a new frontier for BNCT but many technical issues remain. We aimed to study such issues and results in larger-animal BNCT (cats and dogs) with naturally occurring, malignant tumors in different locations as an intermediate step in translating current research into clinical practice. (2) Methods: 10 pet cats and dogs with incurable, malignant tumors that had no treatment alternatives were included in this study. A tandem accelerator with vacuum insulation was used as a neutron source. As a boron-containing agent, 10B-enriched sodium borocaptate (BSH) was used at a dose of 100 mg/kg. Animal condition as well as tumor progression/regression were monitored. (3) Results: regression of tumors in response to treatment, improvements in the overall clinical picture, and an increase in the estimated duration and quality of life were observed. Treatment-related toxicity was mild and reversible. (4) Conclusions: our study contributes to preparations for human BNCT clinical trials and suggests utility for veterinary oncology.

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Comprehensive Analysis of the Tumour Immune Microenvironment in Canine Urothelial Carcinoma Reveals Immunosuppressive Mechanisms Induced by the COX–Prostanoid Cascade

Eto,

Kato,

Saeki

et al. 2024

Vet Comparative Oncology

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A comprehensive understanding of the tumour immune microenvironment (TIME) is essential for advancing precision medicine and identifying potential therapeutic targets. This study focused on canine urothelial carcinoma (cUC) recognised for its high sensitivity to cyclooxygenase (COX) inhibitors. Using immunohistochemical techniques, we quantified the infiltration of seven immune cell populations within cUC tumour tissue to identify clinicopathological features that characterise the TIME in cUC. Our results revealed several notable factors, including the significantly higher levels of CD3+ T cells and CD8+ T cells within tumour cell nests in cases treated with preoperative COX inhibitors compared to untreated cases. Based on the immunohistochemistry data, we further performed a comparative analysis using publicly available RNA‐seq data from untreated cUC tissues (n = 29) and normal bladder tissues (n = 4) to explore the link between COX–prostanoid pathways and the immune response to tumours. We observed increased expression of COX‐2, microsomal prostaglandin E2 synthase‐1 (mPGES‐1) and mPGES‐2 in cUC tissues. However, only mPGES‐2 showed a negative correlation with the cytotoxic T‐cell (CTL)–related genes CD8A and granzyme B (GZMB). In addition, a broader analysis of solid tumours using The Cancer Genome Atlas (TCGA) database revealed similar patterns in several human tumours, suggesting a common mechanism in dogs and humans. Our results suggest that the COX‐2/mPGES‐2 pathway may act as a cross‐species tumour‐intrinsic factor that weakens anti‐tumour immunity, and that COX inhibitors may convert TIME from a ‘cold tumour’ to a ‘hot tumour’ state by counteracting COX/mPGES‐2–mediated immunosuppression.

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Spontaneously occurring canine cancer as a relevant animal model for developing novel treatments for human cancers

Cited by 3 publications

References 98 publications

Targeted Suicide Gene Therapy with Retroviral Replicating Vectors for Experimental Canine Cancers

Targeted Suicide Gene Therapy with Retroviral Replicating Vectors for Experimental Canine Cancers

In Vivo Accelerator-Based Boron Neutron Capture Therapy for Spontaneous Tumors in Large Animals: Case Series

Comprehensive Analysis of the Tumour Immune Microenvironment in Canine Urothelial Carcinoma Reveals Immunosuppressive Mechanisms Induced by the COX–Prostanoid Cascade

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