Robert D'Amato discovered that thalidomide is an angiogenesis inhibitor. In doing so, he not only provided an explanation for the drug's notorious ability to cause birth defects, but also suggested a therapeutic use for thalidomide in inhibiting abnormal angiogenesis in disease. Thalidomide has recently been shown to be useful in the treatment of multiple myeloma and may also be useful in the treatment of other malignancies.

His lab has subsequently identified a new derivative of thalidomide, S-3APG, with dual activity against B-cell neoplasias. S-3APG was able to directly inhibit the proliferation of myeloma and Burkitt's lymphoma cell lines in the laboratory. In animal studies, it has has been demonstrated to be a powerful anti-myeloma and anti-B-cell-lymphoma agent with reduced toxicity to normal bone marrow cells.

Safer, more potent thalidomide analogs are now in clinical trials for the treatment of cancer.

Dr. D'Amato's current research focuses on the genetic control of angiogenesis and the development of new therapeutic agents, especially for the treatment of eye disease.

His laboratory is exploring the role of genetics in determining an individual's angiogenic responsiveness. He has found that different strains of inbred mice have an approximately 10-fold range of response to growth factor stimulated angiogenesis in the corneal micropocket assay. These results suggest the presence of genetic factors that control individual angiogenic potential. He has used recombinant inbred strains and genetic mapping techniques to identify the chromosomal location of the ocular angiogenesis modifying loci. The laboratory is currently screening candidate genes and performing positional cloning techniques to isolate the responsible genes. By identifying the genetic determinates of angiogenic responsiveness within inbred mouse strains, he hopes to further understand the factors that regulate ocular angiogenesis in humans.