BTW, in reading up on a history of multiple myeloma by Dr. Kyle and Dr. Rajkumar
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2265446/, I came across the history of thalidomide (the precursor to Revlimid) usage in multiple myeloma. It's anti-angiogenesis properties were in fact what apparently first led to its use in multiple myeloma treatment.
From Wikipedia:
https://en.wikipedia.org/wiki/Thalidomide"In 1994 Harvard Professor Robert D'Amato at Boston Children's Hospital discovered that thalidomide was a potent inhibitor of new blood vessel growth (angiogenesis), which is required for tumor growth. He then showed in a rabbit cancer model that thalidomide suppressed tumor growth in animals. He also found that a subset of anti-inflammatory drugs, such as sulindac and dexamethasone, had moderate anti-angiogenic activity. When these anti-inflammatory anti-angiogenic drugs were combined with thalidomide, they increased both thalidomide's anti-angiogenic and anti-tumor activity. Based on these discoveries, numerous cancer clinical trials for thalidomide were initiated with and without dexamethasone.
Thalidomide was initially tested in humans as a single agent for the treatment of multiple myeloma due to its anti-angiogenic activity. The early foundation for this work was laid out in a 1993 keynote lecture at the American Society of Hematology by Dr. Folkman when he hypothesized that all blood borne malignancies are angiogenesis-dependent, based upon his discovery that the levels of the angiogenic growth factor FGF were elevated in the urine of patients with leukaemia. Further studies in his lab showed efficacy with the angiogenesis inhibitor TNP-470 in mouse models of leukaemia. Additionally, in 1994 Vacca had shown a fivefold increase in angiogenesis in the bone marrow of multiple myeloma patients. When the family of a patient with late stage multiple myeloma requested any possible help from Dr. Folkman in 1997, he attempted to obtain TNP-470 as a therapy. However TNP-470 could not be obtained outside of the ongoing clinical trial and thus Dr. D'Amato suggested that thalidomide be used instead for this patient. A small study was then initiated with thalidomide for this patient and several others by Dr. Bart Barlogie with dramatic effects. Since then, many studies have shown that thalidomide, in combination with dexamethasone, has increased the survival of multiple myeloma patients.
In the 2000s, the combination of thalidomide and dexamethasone, often in combination with melphalan, became one of the most common regimens for patients with newly diagnosed multiple myeloma. Thalidomide may also cause side effects, such as polyneuropathy, fatigue, skin rash, and venous thromboembolism (VTE), or blood clots, which could lead to stroke or myocardial infarction.
In 2006 the U.S. Food and Drug Administration granted accelerated approval for thalidomide in combination with dexamethasone for the treatment of newly diagnosed multiple myeloma patients. The FDA approval came seven years after the first reports of efficacy in the medical literature."
