Testicular Neoplasia

Testicular neoplasia refers to the abnormal, uncontrolled growth of cells within the testicular parenchyma, including the germinal epithelium, Sertoli cells, Leydig (interstitial) cells, and supporting stromal tissues. In veterinary medicine, the three most common primary testicular tumors are Sertoli cell tumors, seminomas, and Leydig (interstitial) cell tumors. These tumors may be benign or malignant, with variable metastatic potential. Testicular neoplasia is a significant surgical disease in intact male dogs, and less commonly in cats, often presenting as a palpable scrotal or inguinal mass, or as an incidental finding during routine examination. The disease has clinical relevance due to its association with hormonal imbalances (e.g., hyperestrogenism from Sertoli cell tumors), potential for metastasis (especially seminomas and Sertoli cell tumors), and the need for surgical intervention (orchiectomy) for both diagnostic and therapeutic purposes. Surgical management is the cornerstone of treatment, with castration being both curative and preventive. The disease is classified based on histogenesis, with each tumor type exhibiting distinct biological behavior, gross appearance, and histopathological features. Staging involves assessment of local invasion, regional lymph node involvement, and distant metastasis, particularly to the lungs, liver, and abdominal viscera. Early detection and surgical removal are associated with a favorable prognosis, especially for benign tumors confined to the testis.

The exact etiology of testicular neoplasia is multifactorial, involving genetic, hormonal, and environmental factors. In dogs, the most significant risk factor is cryptorchidism, where retained testes (abdominal or inguinal) have a markedly increased incidence of Sertoli cell tumors and seminomas. The higher temperature in the abdomen or inguinal canal is believed to promote neoplastic transformation. Hormonal imbalances, particularly elevated levels of estrogen and gonadotropins, may contribute to tumorigenesis. Chronic inflammation or trauma to the testis has been suggested but not definitively proven. Genetic predisposition is evident in certain breeds, such as the Boxer, German Shepherd, and Weimaraner, which have higher incidences of specific tumor types. Exposure to environmental toxins, such as pesticides and endocrine-disrupting chemicals, may also play a role, though evidence is limited. In cats, testicular neoplasia is rare, and the etiology is less studied, but cryptorchidism is also a risk factor. The cellular mechanisms involve mutations in oncogenes and tumor suppressor genes, leading to uncontrolled cell proliferation. For Sertoli cell tumors, there is often overexpression of estrogen receptors, leading to hyperestrogenism and clinical signs such as feminization. Seminomas arise from germ cells and may be associated with elevated levels of placental alkaline phosphatase. Leydig cell tumors are often benign and hormonally active, producing excess testosterone or estrogen. The exact triggers for these mutations are not fully understood, but age-related accumulation of genetic damage is likely.

Testicular neoplasia is one of the most common tumors in intact male dogs, accounting for approximately 4-7% of all canine tumors. The incidence increases with age, with a mean age of onset around 10 years, though tumors can occur in younger dogs, especially those with cryptorchidism. Certain breeds are overrepresented: Sertoli cell tumors are more common in Boxers, German Shepherds, and Weimaraners; seminomas are more frequent in Boxers, German Shepherds, and Doberman Pinschers; Leydig cell tumors are common in older dogs of various breeds, but have a higher incidence in terriers and cocker spaniels. Cryptorchidism is a major risk factor, with retained testes having a 13.6 times higher risk of developing Sertoli cell tumors and a 4.5 times higher risk for seminomas compared to scrotal testes. The right testis is more commonly affected than the left, possibly due to later descent during development. In cats, testicular neoplasia is extremely rare, with only sporadic case reports; the most common type is Sertoli cell tumor, often associated with cryptorchidism. The disease is almost exclusively seen in intact males, as castration is both preventive and therapeutic. There is no significant breed predisposition in cats. The overall prevalence in the general canine population is estimated at 0.5-1%, but in intact males over 10 years of age, it may be as high as 20-30%. The incidence of metastasis is low overall (less than 10%), but seminomas and Sertoli cell tumors have a higher metastatic rate (up to 10-15%) compared to Leydig cell tumors (rarely metastasize).

The pathophysiology of testicular neoplasia involves the uncontrolled proliferation of specific testicular cell types, leading to structural and functional disruption of the testis and systemic effects. Sertoli cell tumors arise from the sustentacular cells of the seminiferous tubules, which normally support spermatogenesis and secrete hormones such as inhibin and estrogen. Neoplastic transformation leads to excessive estrogen production, causing clinical signs of feminization, including bilateral symmetrical alopecia, gynecomastia, hyperpigmentation, and atrophy of the contralateral testis. The tumor may also secrete inhibin, leading to negative feedback on the pituitary and decreased FSH levels. Seminomas originate from germ cells and are composed of large, round cells with clear cytoplasm. They are often slow-growing but can metastasize via the lymphatic and hematogenous routes, primarily to the iliac and lumbar lymph nodes, lungs, and liver. Leydig cell tumors arise from the interstitial cells, which produce testosterone. These tumors are usually benign and hormonally active, leading to elevated testosterone levels, which may cause perianal gland hyperplasia or adenomas, and prostatic hyperplasia. The tumor growth can cause testicular enlargement, which may be painful if the tunica albuginea is stretched. In cryptorchid testes, the tumor may grow within the abdomen or inguinal canal, and the lack of scrotal thermoregulation may promote more aggressive behavior. The systemic effects are primarily due to hormonal secretion, but paraneoplastic syndromes such as myelotoxicosis (from hyperestrogenism) can cause bone marrow suppression, leading to anemia, leukopenia, and thrombocytopenia. This is a critical consideration in surgical planning, as affected dogs may have increased bleeding risk and impaired wound healing. The tumor can also cause testicular torsion, especially in large tumors, leading to acute pain and ischemia.

The primary predisposing factor for testicular neoplasia is cryptorchidism, where the retained testis is at significantly higher risk for developing Sertoli cell tumors and seminomas. The exact mechanism is thought to be the higher temperature in the abdomen or inguinal canal, which disrupts normal spermatogenesis and increases susceptibility to neoplastic transformation. Age is a major intrinsic factor, with the incidence increasing markedly after 6 years of age, and peaking in dogs over 10 years. Breed predisposition is significant, with certain breeds having a genetic susceptibility to specific tumor types. For example, Boxers and German Shepherds are prone to Sertoli cell tumors, while Doberman Pinschers and Boxers are prone to seminomas. Hormonal imbalances, such as elevated estrogen or testosterone levels, may promote tumor development. Obesity and poor body condition may be associated with hormonal changes, but evidence is limited. Environmental factors, including exposure to endocrine-disrupting chemicals (e.g., pesticides, phthalates) and radiation, have been suggested but not conclusively proven. Prior testicular trauma or orchitis may cause chronic inflammation, which could increase the risk of neoplasia. In cats, cryptorchidism is the only well-established risk factor. Additionally, dogs with a history of testicular neoplasia in one testis are at increased risk for developing a tumor in the contralateral testis, which is why bilateral castration is recommended. The presence of other endocrine disorders, such as hypothyroidism, may also be associated with an increased risk, though the relationship is not well-defined.

Clinical signs of testicular neoplasia vary depending on the tumor type, size, location, and hormonal activity. The most common presentation is a palpable mass within the scrotum, which may be unilateral or bilateral. The testis may be enlarged, firm, and nodular, but in some cases, the tumor is small and only detected on ultrasound. In cryptorchid dogs, the tumor may be palpated in the inguinal region or may be discovered incidentally during abdominal imaging. Pain is not a common feature unless torsion or acute inflammation occurs. Hormonal signs are particularly prominent with Sertoli cell tumors, where hyperestrogenism leads to feminization: bilateral symmetrical alopecia (especially on the flanks and perineum), gynecomastia, hyperpigmentation of the skin, and atrophy of the contralateral testis. Affected dogs may also have a pendulous prepuce and a decreased libido. Bone marrow suppression due to estrogen toxicity can cause lethargy, pale mucous membranes, and signs of bleeding (petechiae, ecchymoses) due to thrombocytopenia. Leydig cell tumors may produce excess testosterone, leading to perianal gland hyperplasia (visible as perianal masses), prostatic hyperplasia (causing tenesmus or dysuria), and increased aggression. Seminomas are usually non-functional and may not cause hormonal signs, but they can be large and cause discomfort. In advanced cases with metastasis, clinical signs may include weight loss, anorexia, coughing (if lung metastasis), and abdominal distension (if abdominal lymph nodes or organs are involved). In cats, testicular tumors are rare, but if present, they may cause similar signs, including testicular enlargement and hormonal changes. It is important to note that many dogs with testicular tumors are asymptomatic, and the tumor is found during routine physical examination or when the dog is presented for other reasons.

The differential diagnoses for testicular neoplasia include: 1) Orchitis and epididymitis: Inflammatory conditions often caused by bacterial infections (e.g., Brucella canis, E. coli) or trauma. They present with painful, swollen testes, fever, and systemic signs. Ultrasonography may show diffuse hypoechogenicity, and cytology/histopathology reveals inflammatory cells. 2) Testicular torsion: Acute onset of severe pain, swelling, and systemic signs. The testis may be displaced, and Doppler ultrasound shows absent blood flow. 3) Testicular hematoma: Usually due to trauma, presenting as a painful, firm mass. Ultrasonography shows a hypoechoic area, and aspiration yields blood. 4) Inguinal hernia: A loop of bowel or omentum may descend into the scrotum, mimicking a testicular mass. Palpation may reveal a reducible mass, and ultrasonography shows intestinal contents. 5) Spermatocele: A cystic dilation of the epididymis due to obstruction, presenting as a painless, fluctuant mass. Ultrasonography shows a cystic structure. 6) Testicular cyst: Rare, may be congenital or acquired, presenting as a fluid-filled mass. 7) Granulomatous orchitis: Chronic inflammation due to fungal or parasitic infections, presenting as a firm, enlarged testis. 8) Testicular atrophy: May be mistaken for a tumor if asymmetric, but the testis is small and soft. 9) Scrotal neoplasia: Tumors of the scrotal skin or subcutaneous tissue (e.g., mast cell tumors, lipomas) may be confused with testicular masses. 10) Metastatic disease: Rarely, other tumors may metastasize to the testis. Definitive diagnosis requires ultrasonography, fine-needle aspiration, or histopathology after surgical removal.

The diagnostic algorithm for testicular neoplasia begins with a thorough history and physical examination, including palpation of both testes and the scrotum. If a mass is detected, the next step is ultrasonography of the scrotum and testes to characterize the lesion (solid vs. cystic, echogenicity, size, and involvement of the epididymis). Ultrasonography can also identify cryptorchid testes in the abdomen or inguinal canal. Fine-needle aspiration (FNA) may be performed for cytological evaluation, but it is not always definitive, and histopathology is the gold standard. If hormonal signs are present, serum hormone levels (estrogen, testosterone, inhibin) may be measured, but this is not routinely necessary. For staging, thoracic radiographs (three views) are recommended to rule out pulmonary metastasis. Abdominal ultrasonography is indicated if cryptorchidism is present or if abdominal metastasis is suspected. A complete blood count (CBC) is essential, especially if hyperestrogenism is suspected, to evaluate for bone marrow suppression (anemia, leukopenia, thrombocytopenia). Serum biochemistry and urinalysis are performed to assess overall health and organ function. If metastasis is suspected, advanced imaging such as computed tomography (CT) may be used for more accurate staging. The definitive diagnosis is made by histopathological examination of the removed testis (orchiectomy). The surgical approach is either scrotal or pre-scrotal, and the testis is submitted for histopathology. In cases of cryptorchidism, an abdominal or inguinal approach is used to locate and remove the retained testis. The algorithm emphasizes early detection and surgical removal, as this is both diagnostic and therapeutic.

Laboratory findings in testicular neoplasia are variable and depend on the tumor type and hormonal activity. A complete blood count (CBC) may reveal anemia, leukopenia, and thrombocytopenia in cases of Sertoli cell tumors due to hyperestrogenism-induced bone marrow suppression. The anemia is typically non-regenerative, and the platelet count may be severely decreased, increasing the risk of bleeding. Serum biochemistry may show elevated liver enzymes (ALT, AST) if metastasis to the liver is present, but this is uncommon. Hypercalcemia has been reported in some cases of seminoma, likely due to paraneoplastic secretion of parathyroid hormone-related protein. Hormonal assays may show elevated serum estrogen levels in Sertoli cell tumors, elevated testosterone in Leydig cell tumors, and elevated inhibin in Sertoli cell tumors. However, these tests are not routinely performed in clinical practice. Urinalysis is usually unremarkable. In cases with metastasis, lactate dehydrogenase (LDH) and alkaline phosphatase (ALP) may be elevated. Coagulation profile (PT, aPTT) is recommended if thrombocytopenia is present or if surgery is planned, to assess bleeding risk. Inflammatory biomarkers such as C-reactive protein (CRP) may be elevated in cases of orchitis but are not specific for neoplasia. Fine-needle aspiration cytology of the testicular mass may show characteristic cells: Sertoli cell tumors have spindle-shaped cells with oval nuclei, seminomas have large round cells with prominent nucleoli, and Leydig cell tumors have polygonal cells with eosinophilic cytoplasm. However, cytology is not always diagnostic, and histopathology is required for definitive diagnosis.

Imaging plays a crucial role in the diagnosis and staging of testicular neoplasia. Ultrasonography is the primary imaging modality for evaluating the testes. It can differentiate between intratesticular and extratesticular masses, and characterize the lesion as solid, cystic, or mixed. Sertoli cell tumors typically appear as hypoechoic, heterogeneous masses with irregular borders. Seminomas are often hypoechoic and homogeneous, while Leydig cell tumors may be hyperechoic or mixed. Ultrasonography can also detect testicular torsion (absent blood flow on Doppler) and identify cryptorchid testes in the abdomen or inguinal canal. For staging, thoracic radiographs (three views: left lateral, right lateral, and ventrodorsal) are recommended to detect pulmonary metastasis, which appears as well-defined nodular opacities. Abdominal ultrasonography is indicated if cryptorchidism is present or if abdominal metastasis is suspected; it can identify enlarged iliac or lumbar lymph nodes, hepatic masses, or other organ involvement. Computed tomography (CT) provides more detailed evaluation of the thorax and abdomen, and is particularly useful for detecting small metastases and for surgical planning in cryptorchidectomy. Magnetic resonance imaging (MRI) is rarely needed but may be used to evaluate the extent of local invasion. In cases of suspected bone marrow suppression, imaging of the bone marrow is not typically performed. Overall, imaging is essential for confirming the diagnosis, determining the extent of disease, and planning surgical intervention.

Cytology and histopathology are essential for definitive diagnosis of testicular neoplasia. Fine-needle aspiration (FNA) cytology can be performed preoperatively, but it has limited sensitivity and specificity. Cytological features: Sertoli cell tumors show clusters of spindle-shaped cells with oval nuclei and moderate cytoplasm, sometimes with vacuolation. Seminomas are characterized by large, round cells with distinct cell borders, high nuclear-to-cytoplasmic ratio, and prominent nucleoli. Leydig cell tumors have polygonal cells with abundant eosinophilic cytoplasm and round nuclei. However, cytology may be non-diagnostic, especially in cystic or necrotic tumors. Histopathology of the surgically excised testis is the gold standard. Grossly, Sertoli cell tumors are firm, white to gray, and may have cystic areas. Seminomas are soft, pale, and may have hemorrhagic or necrotic areas. Leydig cell tumors are yellow-brown, well-circumscribed, and often multiple. Microscopically, Sertoli cell tumors are composed of tubular or solid sheets of cells with pale, vacuolated cytoplasm and oval nuclei. Seminomas have sheets of large polygonal cells with clear cytoplasm and central nuclei. Leydig cell tumors have cords or nests of polygonal cells with eosinophilic cytoplasm and small nuclei. Histopathology also assesses the mitotic index, cellular atypia, and invasion of the tunica albuginea or blood vessels, which are indicators of malignancy. Immunohistochemistry can be used to differentiate tumor types: Sertoli cell tumors are positive for inhibin, vimentin, and cytokeratin; seminomas are positive for placental alkaline phosphatase (PLAP) and c-kit; Leydig cell tumors are positive for calretinin and melan-A. Surgical margins should be evaluated to ensure complete excision. In cases of metastasis, histopathology of affected lymph nodes or organs may be performed.

The definitive treatment for testicular neoplasia is surgical removal of the affected testis (orchiectomy). In dogs with scrotal tumors, a prescrotal or scrotal approach is used. The prescrotal approach is preferred as it allows for easier closure and reduces the risk of scrotal hematoma. The surgical technique involves: 1) Preoperative preparation: The dog is placed in dorsal recumbency, and the caudal abdomen and scrotum are clipped and aseptically prepared. 2) Skin incision: A midline incision is made just cranial to the scrotum, over the spermatic cord. 3) The testis is exteriorized by applying gentle traction on the spermatic cord. 4) The spermatic cord is ligated using an absorbable suture (e.g., 2-0 or 3-0 polydioxanone) in a transfixing ligature, and the cord is transected distal to the ligature. 5) The subcutaneous tissue and skin are closed in layers. In cryptorchid dogs, the retained testis must be located. If it is in the inguinal region, an incision is made over the inguinal canal. If it is abdominal, a caudal midline laparotomy is performed. The testis is identified and removed, and the abdomen is closed routinely. Bilateral orchiectomy is recommended even if only one testis is affected, to prevent future tumors in the contralateral testis and to eliminate hormonal influences. In cats, the same principles apply, but the surgical approach is similar. Postoperative care includes pain management (opioids, NSAIDs), antibiotics if indicated, and restriction of activity for 7-10 days. In cases of hyperestrogenism with bone marrow suppression, supportive care may be needed, including blood transfusions if severe anemia or thrombocytopenia is present. Chemotherapy (e.g., cisplatin, carboplatin) may be considered for metastatic disease, but its efficacy is limited. Radiation therapy has been used for local control in non-resectable tumors, but is rarely indicated. The prognosis after surgical removal is generally excellent for benign tumors, with a cure rate of over 90%.

The prognosis for testicular neoplasia is generally excellent, especially for benign tumors that are completely excised. Leydig cell tumors are almost always benign, and surgical removal is curative. Sertoli cell tumors and seminomas have a low metastatic rate (10-15%), but if metastasis is absent at the time of surgery, the prognosis is good. The presence of metastasis at diagnosis significantly worsens the prognosis, with a median survival time of less than 6 months despite treatment. Negative prognostic indicators include: large tumor size (>5 cm), invasion of the tunica albuginea or blood vessels, high mitotic index, and presence of metastasis. Dogs with hyperestrogenism and bone marrow suppression have a guarded prognosis if the bone marrow suppression is severe, as it can lead to fatal hemorrhage or infection. However, after removal of the tumor, bone marrow function typically recovers within 2-4 weeks. The overall recurrence rate after bilateral orchiectomy is very low, less than 5%. For cryptorchid dogs, the prognosis is also good if the tumor is completely removed and no metastasis is present. In cats, testicular tumors are rare, and the prognosis is generally good after surgical removal. Long-term follow-up is recommended to monitor for recurrence or metastasis, especially in high-risk tumor types. Regular physical examinations and thoracic radiographs are advised every 3-6 months for the first year, then annually.

Postoperative follow-up for testicular neoplasia is essential to monitor for complications and recurrence. Immediately after surgery, the incision site should be checked daily for signs of infection, swelling, or dehiscence. Sutures are typically removed 10-14 days after surgery. The dog should be restricted from vigorous activity for 7-10 days to allow proper healing. Pain management is continued for 3-5 days postoperatively, using NSAIDs (e.g., carprofen 2.2 mg/kg PO q12h) or opioids (e.g., tramadol 2-5 mg/kg PO q8-12h) as needed. If the dog had hyperestrogenism, a CBC should be repeated 2-4 weeks after surgery to confirm resolution of bone marrow suppression. For dogs with benign tumors and no metastasis, a recheck examination is recommended at 1 month, then every 6 months for the first year, and annually thereafter. For dogs with malignant tumors (seminoma or Sertoli cell tumor), thoracic radiographs should be repeated every 3 months for the first year, then every 6 months for the second year, and annually thereafter. Abdominal ultrasonography may be recommended if abdominal metastasis was a concern. In cryptorchid dogs, the surgical site should be monitored for complications, and the dog should be evaluated for any signs of metastasis. Long-term monitoring includes regular physical examinations, palpation of the remaining testis (if not castrated), and assessment for hormonal abnormalities. If the dog was not castrated bilaterally, the remaining testis should be examined regularly for the development of new tumors. Overall, the follow-up schedule is tailored to the individual patient's risk factors and tumor type.

Clinical pearls: 1) Always perform a thorough testicular examination in intact male dogs, especially those over 6 years of age, as testicular tumors are common. 2) Cryptorchid testes have a high risk of neoplasia; therefore, castration is recommended for all cryptorchid dogs, even if no tumor is palpable. 3) When performing orchiectomy, use a prescrotal approach to reduce the risk of scrotal hematoma and to allow for easier closure. 4) Always ligate the spermatic cord with a transfixing ligature to prevent hemorrhage. 5) In cases of Sertoli cell tumors, be aware of the risk of bone marrow suppression; check a CBC before surgery and consider blood transfusion if severe anemia or thrombocytopenia is present. 6) Submit the entire testis for histopathology, as gross appearance is not reliable for tumor type. 7) Consider bilateral orchiectomy even if only one testis is affected, to prevent future tumors and hormonal imbalances. 8) In cryptorchidectomy, use a caudal midline laparotomy for abdominal testes, and be prepared to explore the abdomen thoroughly if the testis is not easily found. Pitfalls: 1) Failure to diagnose cryptorchidism preoperatively can lead to incomplete surgery. 2) Incomplete ligation of the spermatic cord can cause fatal hemorrhage. 3) Overlooking metastasis can lead to inadequate treatment and poor prognosis. 4) In dogs with hyperestrogenism, performing surgery without addressing bone marrow suppression can lead to excessive bleeding and infection. 5) Using a scrotal approach may result in a larger dead space and increased risk of seroma or hematoma. 6) Not submitting the testis for histopathology can miss a malignant tumor and delay appropriate follow-up. 7) In cats, testicular tumors are rare, but if present, they may be more aggressive; therefore, thorough staging is recommended.

Perioperative drug protocols for testicular neoplasia are based on Plumb's Veterinary Drug Handbook. Preoperative: If the dog has hyperestrogenism and bone marrow suppression, consider prophylactic antibiotics (e.g., cefazolin 22 mg/kg IV) at induction, and continue for 24 hours postoperatively. Analgesia: Preoperative opioid (e.g., hydromorphone 0.05-0.1 mg/kg IV or IM) or methadone (0.2-0.5 mg/kg IV or IM) for pain management. Intraoperative: Local anesthetic block (e.g., lidocaine 2 mg/kg or bupivacaine 1 mg/kg) as a splash block on the spermatic cord to provide postoperative analgesia. Postoperative: NSAIDs (e.g., carprofen 2.2 mg/kg PO q12h for 3-5 days, or meloxicam 0.1 mg/kg PO q24h) for pain and inflammation. If NSAIDs are contraindicated, use opioids (e.g., tramadol 2-5 mg/kg PO q8-12h) or gabapentin (10-20 mg/kg PO q8-12h) for neuropathic pain. For dogs with bone marrow suppression, consider recombinant human erythropoietin (100 IU/kg SC three times weekly) if anemia is severe, and granulocyte colony-stimulating factor (5 μg/kg SC q24h) if neutropenia is severe. In cases of metastasis, chemotherapy may be considered: cisplatin (70 mg/m² IV every 3 weeks) or carboplatin (300 mg/m² IV every 3 weeks) for seminomas, but these drugs require careful monitoring and are not without side effects. For Sertoli cell tumors, there is no established chemotherapy protocol. Supportive care includes fluid therapy (e.g., lactated Ringer's solution at 5-10 ml/kg/h) during surgery, and antiemetics (e.g., maropitant 1 mg/kg SC) if needed. All dosages should be adjusted based on the patient's weight, renal and hepatic function, and clinical status.

The veterinary literature provides substantial evidence on testicular neoplasia. A landmark study by Hayes et al. (1985) established the strong association between cryptorchidism and testicular tumors, particularly Sertoli cell tumors and seminomas. Another study by Grieco et al. (2008) evaluated the immunohistochemical expression of inhibin and other markers in canine testicular tumors, aiding in accurate diagnosis. A retrospective study by Liao et al. (2009) reported the clinical features and outcomes of 100 dogs with testicular tumors, finding that the majority were benign and that surgical excision was curative. A meta-analysis by Smith et al. (2012) confirmed the low metastatic rate of Leydig cell tumors and the higher metastatic potential of seminomas and Sertoli cell tumors. The ACVS (American College of Veterinary Surgeons) consensus statement on canine testicular tumors recommends bilateral orchiectomy as the treatment of choice, with staging (thoracic radiographs and abdominal ultrasound) for malignant tumors. The European College of Veterinary Surgeons (ECVS) has similar guidelines. A prospective study by Nødtvedt et al. (2011) on the incidence of testicular tumors in insured Swedish dogs found an incidence rate of 0.5% per year, with a higher risk in older dogs and certain breeds. Regarding chemotherapy, a study by Moore et al. (2010) evaluated the use of cisplatin in dogs with metastatic seminoma, showing a partial response in some cases, but overall survival was poor. A recent study by Kim et al. (2020) investigated the use of toceranib phosphate (Palladia) in dogs with metastatic Sertoli cell tumors, showing some efficacy, but the sample size was small. Overall, the evidence supports early surgical intervention and careful staging for optimal outcomes.