14 DAY TRIAL // New research sheds some light on the causes of hemangioma, one of the most common childhood tumors, which seems to be caused by unchecked growth of endothelial cells. The tumor manifests itself even from the first few days of an infant's life, usually as a tiny red dot on the face and forehead and then quickly expands and multiplies. Though they are benign, meaning they can't cause permanent damage or multiply out of control, the tumors could lead to disfigurement and may require surgery to correct.
Scientists at the Harvard Medical School and the Harvard School of Dental Medicine, working in collaboration with Children's Hospital Boston, and the de Duve Institute, a part of the Catholique University of Louvain in Brussels, studied the blood vessel growth that is characteristic to hemangioma, and they uncovered that the spread of the vessels originated from the same cell that caused the endothelial cells to multiply.
The team concluded that, in order for an endothelial cell to mutate, it needs the influence of a hormone called vascular endothelial growth factor (VEGF), which is usually inhibited by a specific, complementary protein that is located on the edges of these cells. But somehow, in all nine distinct samples the researchers analyzed, two mutating genes seemed to somehow inhibit VEGF's receptor, so the endothelial cells were permitted to grow unchecked, without triggering any kind of immune response.
"What the data suggests is that any therapy that is directed against vascular endothelial growth factor – anti-VEGF therapy – is the rational therapy to use in these tumors," explained Bjorn R. Olsen, leader of the study, professor of cell biology at Harvard Medical School. The scientist is also a professor of developmental biology and the dean for research at Harvard School of Dental Medicine. "After finding out why these tumors grow, we are now starting to direct our research at understanding why they regress," he added.
The behavior these tumors exhibit has puzzled doctors for some time. They slow their growth as the child grows up and, when the patient reaches puberty, they regress and disappear entirely. To find the answer as to why this happens, Olsen and his team turned their attention to anti VGEF therapies, which are currently employed in treatments against macular degeneration and some forms of cancer. If they discover the way in which the tumors work, they could be able to prevent them from occurring in the first place, by developing vaccines containing VGEF inhibitors.