Nine months ago my eleven-year-old dog underwent a massive surgery when a soccer-ball-sized tumor ruptured on his spleen (The x-ray is difficult to see). While his veterinarian showed me the x-ray of his chest cavity, the veterinarian explained that he suspected my dog had a visceral hemangiosarcoma. With my dog rapidly internally bleeding, my family and I made the decision to have the tumor removed. The one condition, however, was that my dog would be euthanized if the veterinarian saw signs of metastasis during surgery.
Miracle number one: my dog survived the surgery even after going into cardiac arrest. Miracle number two: the veterinarian saw no signs of metastasis. The statistics were as follows according to the veterinarian. 85% of spleenic tumors are malignant. While the lack of additional tumors gave us hope that my dog’s tumor was non-cancerous, the statistics showed a long battle ahead for my dog. Miracle number three: one week later, the biopsy results revealed a benign tumor.
While I would like to believe that my dog was given a miracle, I do not understand how a tumor so large and life threatening could be benign. If 85% of spleenic tumors are cancerous, what genetically made my dog’s cells different?
The soccer-ball-sized mass provides evidence for two hallmarks of cancer. Foremost, the tumor showed insensitivity to growth inhibitory signals. The size of the mass indicates that tumor suppressor genes were unable to signal the cells to stop dividing. Rather than lying side by side cohesively, the tumor cells formed a large mass. The tumor also had sustained angiogenesis. Blood vessels became incorporated into the tumor and it was the rupturing of a vessel that led the veterinarian to discover the tumor.
Other hallmarks are possible as well, but there isn’t hard evidence that they were present in this particular tumor. It is very possible that this tumor grew independently of growth signals. However, it is difficult to know if this hallmark of cancer was present in the tumor because it is also possible that my dog’s cells produced excess growth signals and that the cells were multiplying in response. The tumor cells could have evaded programmed cell death. A mutation in the p53 pathway may have contributed to the large mass formation. Another mutation also could have activated telomerase, giving cells limitless replicative potential.
If all these hallmarks could have been potentially satisfied in my dog’s tumor, why was it still non-cancerous?
The tumor had not metastasized. By definition, a tumor is not cancerous until it has invaded surrounding cells, crossing the basal lamina. I am still curious as to how a tumor can become so large and not cross the basal lamia. Was my dog just lucky? Or is there a deciding factor within cells that change the cell from being benign to malignant? All five other hallmarks could have been present. These hallmarks still require mutations and uncontrolled growth. I am still curious.
