Abstract
This study investigated the role of mast cells in canine cutaneous vascular tumors, and is the first such study to distinguish between tumors arising in the dermis versus the subcutis. Mast cell numbers in canine cutaneous hemangiomas (HA) and hemangiosarcomas (HSA) were evaluated to identify a relationship between mast cells, tumor type (HA, HSA), histologic location (dermis, subcutis) and tumor recurrence. One hundred and sixty-seven biopsies from 148 dogs were evaluated. Using only one biopsy from each dog, mast cell counts (MCC) for each tumor (n = 148) were obtained by averaging the number of mast cells counted in ten 400× fields. A significant difference in mean MCC was found only between tumor types, with HA having more mast cells than HSA (4.2 ± 4.2 vs. 2.2 ± 2.6; p < 0.001). No significant difference in mean MCC existed between tumors that recurred and those that did not. There was no difference in recurrence rate between tumor type or histologic location. Our results indicate that benign HA contain more mast cells than malignant endothelial cell tumors, regardless of histologic location; whether this is a cause or effect relationship remains to be determined.
Highlights
Mast cells are derived from CD34+ pluripotent bone marrow hematopoietic stem cells
This study investigated the role of mast cells in canine cutaneous vascular tumors, and is the first such study to distinguish between tumors arising in the dermis versus the subcutis
Assessing mast cell numbers in various tumor types is an early step in understanding their role in carcinogenesis
Summary
Mast cells are derived from CD34+ pluripotent bone marrow hematopoietic stem cells. Undifferentiated, but committed mast cell precursors from the bone marrow enter the blood and travel to tissues where they differentiate into mature mast cells. The exact mechanisms of migration and differentiation of mast cells are largely unknown, stem cell factor, which is produced by endothelial cells, fibroblasts or epithelial cells and is known to promote the differentiation of mast cells likely plays a role in this process [1]. Mast cell angiogenic factors such as TNF, bFGF, VEGF, and IL-8 act in part by stimulating endothelial cells to secrete proteases to degrade the existing basement membrane, followed by the proliferation and migration of endothelial cells towards the angiogenic stimulus. Other proteases (chymase, tryptase, MMP-9) released by mast cells assist in the degradation of the extracellular matrix to facilitate the migration of the endothelial cells. Degradation of the extracellular matrix results in release of pro-angiogenic factors (VEGF, bFGF, TGF-beta) and anti-angiogenic factors (factor 4, thrombospondin 1, angiostatin, endostatin). The balance of pro- and anti-angiogenic factors determines the extent of angiogenesis
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