Testicular Tumors in Dogs: Classification, Epidemiology, and Clinical Insights

Testicular tumors are among the most frequently diagnosed neoplasms in intact male dogs, yet their true incidence is often underestimated due to widespread neutering practices. These tumors present a diverse spectrum of histological types and biological behaviors, making their understanding essential for effective clinical management¹. 

Classification and Histological Diversity 

Testicular tumors are classified based on their cell of origin into germ cell tumors and stromal tumors. Germ cell tumors include seminomas and non-seminomatous variants, while stromal tumors comprise Sertoli cell tumors (SCTs) and interstitial (Leydig) cell tumors (ICTs)¹. Mixed germ cell-sex cord stromal tumors are also recognized, particularly in canine cases. 

Recent evidence suggests that many tumors historically classified as seminomas in dogs may actually correspond to spermatocytic tumors, based on their morphological and molecular characteristics¹. This distinction is important, as spermatocytic tumors have different pathogenesis and clinical behavior compared to classical seminomas. 

Epidemiology and Age Distribution 

Testicular tumors account for approximately 6.2–7.1% of all tumors in male dogs. The average age of onset is around 10 years, although Sertoli cell tumors may occur earlier, with a reported mean age of 8.6 years^1,2,3. 

Among tumor types, seminomas and interstitial cell tumors are the most prevalent, followed by Sertoli cell tumors and mixed tumors^1,2,3. However, these proportions can vary significantly depending on study populations and classification criteria. 

Influence of Cryptorchidism on Tumor Patterns 

Cryptorchidism plays a major role in altering the distribution of testicular tumor types. In cryptorchid dogs, Sertoli cell tumors become the predominant neoplasm, accounting for up to 21–62% of cases^1,2,3. Seminomas follow, while interstitial cell tumors are relatively rare in retained testes. 

The risk of developing specific tumor types is also markedly increased. Cryptorchid dogs have been reported to have a 23-fold higher risk of Sertoli cell tumors and a 16-fold higher risk of seminomas compared to normal dogs¹. 

Pathogenesis and Cellular Origin 

The development of testicular tumors is closely linked to abnormalities in cell differentiation. Seminomas are believed to originate from germ cells that fail to differentiate properly, leading to the persistence of gonocyte-like cells. These cells may evolve into germ cell neoplasia in situ and eventually malignant tumors^1,4. 

Sertoli cell tumors, on the other hand, are associated with the persistence of immature Sertoli cells. These tumors often express markers such as AMH and inhibin alpha, which are typically found in immature cells^1,5. The persistence of these markers in adult dogs suggests a failure of normal cellular maturation. 

Clinical Presentation and Systemic Effects 

The clinical presentation of testicular tumors varies depending on tumor type. Sertoli cell tumors are particularly significant due to their endocrine activity. They are associated with increased estrogen production, leading to feminization syndrome characterized by gynecomastia, alopecia, hyperpigmentation, and bone marrow suppression^1,6. 

Seminomas are often asymptomatic and may be detected incidentally during routine examinations. Interstitial cell tumors are generally benign and less clinically significant. 

Diagnostic Approach¹ 

Diagnosis relies on physical examination, imaging, and histopathology. Ultrasonography is useful for identifying intra-abdominal tumors, while histopathological examination remains the gold standard for definitive diagnosis. 

Hormonal assays can also provide valuable information. Elevated AMH levels are indicative of Sertoli cell tumors, while alterations in testosterone and estradiol levels may reflect tumor activity. 

Conclusion 

Testicular tumors in dogs represent a complex and clinically significant group of neoplasms. Their diverse histological types, association with cryptorchidism, and potential systemic effects necessitate a thorough understanding among veterinarians. Early detection and appropriate management are essential to ensure optimal clinical outcomes. 

Reference 

1. Soto-Heras S, Reinacher L, Wang B, Oh JE, Bunnell M, Park CJ, Hess RA, Ko CJ. Cryptorchidism and testicular cancer in the dog: unresolved questions and challenges in translating insights from human studies. Biology of reproduction. 2024 Aug;111(2):269-91. https://academic.oup.com/biolreprod/article-pdf/111/2/269/58824383/ioae075.pdf 

2. Manuali E, Forte C, Porcellato I, Brachelente C, Sforna M, Pavone S, Ranciati S, Morgante R, Crescio IM, Ru G, Mechelli L. A fiveyear cohort study on testicular tumors from a population-based canine cancer registry in Central Italy (Umbria). Prev Vet Med 2020; 185:105201. https://cris.unibo.it/bitstream/11585/819159/5/Manuscript_IP_EM160420.pdf 

3. Gazin AA, Vatnikov YA, Sturov NV, Kulikov EV, Grishin V, Krotova EA, Varentsova AAR, Sapego NYR, Troshina NI, Byakhova VM, Lisitskaya KV. Canine testicular tumors: an 11-year retrospective study of 358 cases in Moscow region. Russia Vet World 2022; 15:483–487. https://pmc.ncbi.nlm.nih.gov/articles/PMC8980386/pdf/Vetworld-15-483.pdf 

4. Baroni T, Arato I, Mancuso F, Calafiore R, Luca G. On the origin of testicular germ cell tumors: from gonocytes to testicular cancer. Frontiers in endocrinology. 2019 Jun 6;10:343. https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2019.00343/pdf 

5. Pecile A, Groppetti D, Pizzi G, Banco B, Bronzo V, Giudice C, Grieco V. Immunohistochemical insights into a hidden pathology: canine cryptorchidism. Theriogenology 2021; 176:43–53. https://air.unimi.it/bitstream/2434/887422/5/ManuscriptREV-draft.pdf 

6. Marshall H. Estrogen-induced myelotoxicity in a 4-year-old golden retriever dog due to a Sertoli cell tumor. Can Vet J 2018; 59:425–427. https://pmc.ncbi.nlm.nih.gov/articles/PMC5855222/pdf/cvj_04_425.pdf