Another distinction between the two inhibitors was the type of vessel development that was blocked. Blocking VEGF prevented dangerous vessels from developing such as the ones that feed tumors. But it stopped beneficial vessels from growing also, such as the ones that help injured tissues heal. Blocking M-CSF, however, only impeded poor vessel growth. In the meantime, the scaffold of mice treated with anti-VEGF remained intact. M-CSF levels soar in sufferers with osteosarcoma , breast tumor and prostate cancer, making these cancers potentially the most attentive to M-CSF-blocking drugs Whether other types of cancer rely more on M-CSF than on VEGF for their blood supply remains unknown..In sufferers without disease progression, imaging was repeated almost every other routine. Tumor measurements based on the Response Evaluation Criteria in Solid Tumors , version 1, were made within 1 week prior to the next planned cycle.21 After discontinuation of treatment, disease was assessed every three months for 2 years, followed by assessment every six months for three years until disease progression was documented. Three validated, sensitive instruments were used to measure health-related standard of living. Pain was measured with the use of the Brief Pain Inventory . Neurotoxicity was measured with the use of the neurotoxicity subscale brief form .22 Baseline assessments had been completed before randomization, before cycles 2 and 5, and 6 and 9 weeks after cycle 1.