Figure 2.
Figure 2. Establishment of a mouse myeloma model with skeletal dissemination of tumor and osteolysis. Two different mouse models were tested for myeloma osteolytic dissemination. Groups of BALB/c mice were challenged with 5 × 105 MPC-11 cells, and SCID mice were challenged with 5 × 105 CAGHep cells via tail vein. Based on constitutive expression of firefly luciferase in both cell lines, mice were monitored by noninvasive imaging to monitor tumor growth within the tibia, femur, and spine. Cohorts of mice from each group were euthanized at the indicated time points, and bones were subjected to histology (A-B; original magnification ×100, hematoxylin and eosin stain) and micro-CT (C). Representative data indicate aggressive tumor growth and skeletal damage in the BALB/c-MPC-11 model by 2 weeks. However, the growth of myeloma cells in the SCID-CAGHep model was significantly delayed, allowing a window of >6 weeks before aggressive bone destruction was noted.

Establishment of a mouse myeloma model with skeletal dissemination of tumor and osteolysis. Two different mouse models were tested for myeloma osteolytic dissemination. Groups of BALB/c mice were challenged with 5 × 105 MPC-11 cells, and SCID mice were challenged with 5 × 105 CAGHep cells via tail vein. Based on constitutive expression of firefly luciferase in both cell lines, mice were monitored by noninvasive imaging to monitor tumor growth within the tibia, femur, and spine. Cohorts of mice from each group were euthanized at the indicated time points, and bones were subjected to histology (A-B; original magnification ×100, hematoxylin and eosin stain) and micro-CT (C). Representative data indicate aggressive tumor growth and skeletal damage in the BALB/c-MPC-11 model by 2 weeks. However, the growth of myeloma cells in the SCID-CAGHep model was significantly delayed, allowing a window of >6 weeks before aggressive bone destruction was noted.

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