In particular, models have been generated where human MM cells grow in human fetal bone transplants in immunodeficient SCID mice. More recently three-dimensional bone-like scaffolds were coated with mouse or human bone marrow stromal cells and implanted under the skin of SCID mice. Subsequently, injection of purified primary myeloma cells into these scaffolds gave rise to tumor formation that could be followed by measuring myeloma protein concentration. Although these models allow experiments of human MM cells in vivo in mice, the models are demanding and not completely physiological. Mouse models where MM cells can be transferred Tulathromycin B between syngeneic mice are also available. However, mouse MM models do not necessarily accurately reflect human disease. MM-like disease arises spontaneously in aged C57BL/KaLwRij mice. The 5T2MM and the 5T33MM cell lines were established from such mice, and have been extensively used for studying homing mechanisms of MM cells to bone marrow, interaction of MM cells with the bone marrow environment, and evaluation of new therapies. Both models are characterized by MM cell infiltration restricted to bone marrow and spleen. The 5T2MM model, but not 5T33MM, is associated with an extensive osteolysis, seen on plain radiographs of femur and tibia. Finally, three different transgenic mice models have recently been developed based on double-transgenic Myc/Bcl-XL mice, the activation of MYC under the control of a light chain gene, or cloning of a spliced form of mouse XBP-1 downstream of the immunoglobulin VH promoter and enhancer elements. Although they recapitulate several characteristics of MM, these models are time-consuming and costly, perhaps explaining their limited use thus far. In Cinoxacin summary, the available MM models presented above can be technically challenging and require large investments. Thus, there is a need for an MM model where MM cells can be grown in vitro and when i.v. injected in a common laboratory inbred mouse strain, such as BALB/c, faithfully duplicate the major characteristics of MM disease seen in patients. Plasmacytomas can be experimentally induced in certain strains of mice by i.p. injection of mineral oil, adjuvants and alkanes. Such mineral oil-induced plasmacytomas can be serially transplanted s.c. or i.p. and have been extensively used in tumor immunological studies. However, these plasmacytomas typically grow locally at the site of injection, and only infrequently metastasize to the bone marrow. Due to their local growth, it has been questioned if MOPC tumors represent good models for human MM that primarily affects bone marrow. We have previously described an in vivo-selected variant of MOPC315, MOPC315.4, which efficiently forms local tumors after s.c. injection. We here show that repeated i.v. injections of MOPC315.4 cells, followed by isolation of tumor cells from femurs between passages, enriches for a stable variant that can be grown in vitro, has tropism for bone marrow after i.v. injection, and causes osteolytic lesions. Spatiotemporal development of disease may be monitored by serial and noninvasive measurement of the bioluminescent signal of luciferase-labeled cells. Luciferase-labeled cells allow spatiotemporal resolution of bone disease development by repeated in vivo imaging. Injected mice develop osteolytic lesions, a hallmark of human MM. This novel mouse MM model could be useful for studies of bone marrow tropism, efficacy of drugs, mechanism of osteolysis, and immunotherapy.