Telangiectatic Osteosarcoma Case Study: Scout
With a combination approach that included FidoCure® therapy, Scout has lived for 1.5 years after his initial diagnosis of telangiectatic osteosarcoma.History and Initial Therapy
Scout Shiratori, an almost 9-year-old male neutered Golden Retriever mix as seen on June 3, 2020 for a mass found under his right forelimb. Physical examination and radiographs confirmed a mass possibly associated with the fifth rib. Cytology was diagnostic for a sarcoma, likely osteosarcoma or chondrosarcoma. CT scan confirmed the osteolytic lesion on the distal aspect of the right fifth rib, and there was no evidence of pulmonary metastasis. Scout had surgery to remove the mass and associated rib. Histopathology was diagnostic for a telangiectactic osteosarcoma removed with clean margins.
Following surgery, Scout completed a course of Carboplatin on August 31, 2020. At that visit, a metastic pulmonary nodule was found on radiographs. He then received the Yale vaccine and was started on metronomic cyclophosphanide on September 21, 2020. At that time, tissue was submitted for FidoCure analysis.
FidoCure Analysis
Genomic analysis of Scout’s tumor revealed 8 mutations, 4 of which were considered actionable. These alterations included CDK4, P53 (2), and SETD2. CDK4 is the gene encoding cyclin-dependent kinase 4. CDKs are kinases that regulate progression through the cell cycle. CDK4 is specifically involved in the transition from G1 to S phase. Loss of G1 control in the cell cycle appears to be an important contributor to tumorigenesis.
TP53 encodes a protein called tumor protein p53 which has become one of the most well published tumor suppressor genes in both human and canine cancer. This protein helps to regulate cell growth and damaged cells by controlling signals for pausing the cell cycle and cell death.
SETD2 is a gene that encodes a lysine methyltransferase which has been described for tumor suppressor properties in human cancer literature. Mutations in SETD2 contribute to epigenetic regulation and interact with or modify the activity of histone deacetylases (HDAC).
