"Thalidomide and Other Angiogenesis Agents", Robert Amato, DO


Dr. Robert Amato, DO is Associate Professor of Medicine at Baylor college of Medicine, Houston, TX. He received his Doctor of Osteopathic Medicine from Texas College of Osteopathic Medicine where he also did postgraduate training followed by a four year fellowship in medical oncology at the U. of Texas MDAnderson Cancer Center. He does extensive research, and has 76 journal papers plus 89 published abstracts.


Renal cell carcinoma is highly vascular and resistant to most chemotherapy agents. Immunotherapy has been the main treatment course. The vascularity has led to a focus on anti-angiogenesis. As tumors grow, they need an expanding blood supply, and are able to control the body function of angiogenesis to grow new blood supply. Healthy adults do not need the angiogenesis process as our vasculature is already established.

Thalidomide is being investigated as an anti-angiogenesis agent. Its mechanism is not understood, however it acts in at least three ways: immune system modulation, cytokine inhibition, and anti-angiogensis.

Clinical studies use dosages up to 1600 mg/day, typically starting with 200mg/day and escalating 100 to 200 mg/day each week. For trial inclusion patients typically have metastatic disease and previous immunotherapy which has failed. Dr. Amato doesn't take patients with brain mets into Thalidomide trials as there was no activity on brain mets in the original trials. However patients who were treated for brain mets and now "clean" are accepted.

Thalidomide has various toxic responses: slow heart rate, neuropathy (irreversible typically), skin rash, lung blood clots, deep venous thrombosis, drowsiness, dizziness.

In combination with IL-2 in Phase 1 studies, thalidomide showed responses at 12 weeks.

He has another trial combining thalidomide with capcitebine (chemo agent).

This Kidney Cancer FAQ Page By PJ Boyle. Copyright 2001 PJ Boyle
Last Updated August 5, 2001