Surgical removal of tumors amenable to wide resection is typically the treatment of choice for cutaneous and subcutaneous canine MCTs. In dogs with large, ulcerated tumors, incisional biopsy can be considered for grading and treatment prior to definitive therapy. Lateral surgical margins of 2 to 3 cm and a fascial plane underlying the tumor are typically recommended when possible.39-44 Incompletely excised tumors can be treated with scar revision surgery or definitive radiation therapy to address microscopic residual disease. Marginal excision of small, low- to intermediate-grade tumors with margins of 3 to 4 mm may be adequate in preventing local recurrence.40-44 High-grade MCTs have a higher risk for recurrence as compared with low-grade tumors (≈36% vs ≈4%), regardless of the histologic tumor-free margin.44 Nonsurgical and/or recurrent tumors can be treated with palliative radiation.45,46 Neoadjuvant radiation can also be used to shrink MCTs prior to surgical removal.
Chemotherapy can be considered for neoadjuvant therapy, postoperatively for incompletely excised tumors in which additional surgery or radiation is not elected or feasible, and for any high-grade or metastatic tumors. Various chemotherapeutic agents have been used alone or in combination in the treatment of MCTs, with overall response rates between ≈20% to 90%. The average response rate to chemotherapy in dogs with MCTs is ≈40%.47-60
For dogs with primary tumors <3 cm3, electrochemotherapy may be considered if surgery is not elected; a subset of these dogs may experience outcomes comparable with dogs treated surgically.61-63
Novel therapies, including tyrosine kinase inhibitors (TKIs), are available for the treatment of MCTs. Approximately 25% to 30% of canine MCTs have activating mutations in the c-Kit gene that can cause unregulated downstream signal transduction that promotes tumorigenesis.64-67 Activating mutations in the c-Kit gene have been shown to correlate with increased local tumor recurrence, metastasis, and poorer prognosis.68,69 Toceranib phosphate is a veterinary-approved TKI with an overall biologic response rate of 60% and a median time to tumor progression of 4.5 months.70 Dogs with an activating mutation in the c-Kit gene have increased response rates (up to ≈69%) to TKI therapy as compared with traditional injectable and oral chemotherapeutics used in the treatment of MCTs.69-74
In general, dogs that have nonmetastatic, low-grade MCTs may experience long-term tumor control or cure with surgery ± radiation therapy. Patients with several (regardless of grade), nonsurgical, recurrent, high-grade, and/or metastatic tumors may benefit from local therapy in combination with chemotherapy or TKI therapy.
Therapies that can help mitigate the effects of MCT degranulation in dogs with bulky tumors include H1 and H2 antagonists, proton-pump inhibitors, steroid therapy, and other medications (eg, sucralfate, misoprostol) to treat active or suspected gastric/duodenal ulceration secondary to MCTs.
In cats, a chemotherapeutic standard of care for MCTs has not been definitively established. Positive responses to predniso(lo)ne, lomustine, vinblastine, TKIs (eg, imatinib, toceranib), and chlorambucil have been reported.75-81 Although cats with the c-Kit gene mutation may have an increased chance for response to TKI therapy, the impact of mutation status on overall prognosis does not appear to be significant as compared with dogs.75,76,82