Multiple myeloma, the second most common hematologic malignancy in the US, remains incurable. Recently, an increase in blood vessel formation (angiogenesis) in the marrow was proposed as a mechanism that promoted progression of multiple myeloma. The objective of this proposal is to compare the genomic profile of vascular cells in bone marrow in patients and healthy subjects in order to 1) identify patient candidates for antiangiogenic therapy; 2) target multiple myeloma-specific angiogenic genes; and 3) definitively determine the relationship of angiogenesis to clinical status and treatment outcome. Results can also be extrapolated to other marrow tumors to determine their response to antiangiogenic treatment.