Abstract
Hemangiosarcomas (HSA) are common neoplasms of dogs that often metastasize and are typically fatal. Recently it was demonstrated that thalidomide extends the survival time of dogs with HSA, potentially due to thalidomide-induced inhibition of vascular endothelial growth factor (VEGF) production by the neoplastic cells. To investigate this, immunostaining was used to evaluate VEGF within HSA metastases that developed after thalidomide treatment. The immunostaining was then compared to VEGF immunostaining in primary tumors from the same dogs prior to treatment with thalidomide and in metastatic tumors from untreated dogs with splenic HSA. Immunostaining was scored from 1 to 4 for each sample. Immunostaining in the metastatic lesions that had been treated with thalidomide had a mean immunostaining score of 1.4 which was significantly lower than the mean score in the corresponding primary splenic HSA (3.8, p = 0.02) and in metastases from untreated dogs (3.5, p = 0.02). This supports the hypothesis that thalidomide prolongs survival time in dogs with HSA due to inhibition of VEGF production by the neoplastic cells. As VEGF remained visible within HSAs exposed to thalidomide, additional treatments to inhibit VEGF production may further prolong survival times of dogs with these common canine neoplasms.
Highlights
Hemangiosarcomas (HSA) are common neoplasms of dogs that most frequently develop in the spleen and the right atrium of the heart [1]
A role of thalidomide in reducing the presence of vascular endothelial growth factor (VEGF) in a neoplasm was supported by previous research done in human neoplasms that demonstrated thalidomide reduced the production of VEGF by colonic [5], multiple myeloma [6], and prostatic neoplastic cells [7]
The study included five dogs that had been diagnosed with splenic HSA and did not have any evidence of metastases prior to treatment with thalidomide
Summary
Hemangiosarcomas (HSA) are common neoplasms of dogs that most frequently develop in the spleen and the right atrium of the heart [1]. As these neoplasms develop from the endothelial cells of blood vessels, they typically rapidly metastasize and canine HSA have a poor prognosis and affected dogs typically have short survival times [1]. As thalidomide is known to suppress vascular endothelial growth factor (VEGF) [3,4], it was hypothesized that the increased survival times observed in the treated dogs were due to inhibition of VEGF production by the neoplastic cells.
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