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New research suggests that C-reactive protein (CRP) drives multiple myeloma (MM) to destroy bone.
Researchers found that CRP accelerated the onset of bone destruction and made bone damage more severe in mouse models of MM.
The team also observed an association between elevated serum CRP levels and greater degree of bone damage in newly diagnosed MM patients.
The researchers therefore believe that CRP might be targeted to prevent or treat MM-associated bone disease.
Qing Yi, MD, PhD, of the Lerner Research Institute at the Cleveland Clinic in Ohio, and his colleagues conducted this research and reported the results in Science Translational Medicine.
The researchers noted that high levels of circulating CRP have been associated with poor prognosis in many cancers, including MM.
In a previous study, the team found that CRP enhanced MM cell proliferation under stressed conditions and protected MM cells from chemotherapy-induced apoptosis.
Now, the researchers have found that CRP activates MM cells to promote osteoclastogenesis and bone destruction.
In experiments with mouse models, the team found that CRP promoted MM-cell-mediated lytic bone disease. The researchers said CRP enhanced osteoclast differentiation and bone resorption activity.
In vitro experiments showed that CRP stimulates MM cells to produce osteoclast activators such as RANKL, MCP-1, and MIP-1a.
Further investigation revealed that CRP binds to CD32 on MM cells. This activates a pathway mediated by the kinase p38 MAPK and the transcription factor Twist, which increases MM cells’ production of osteolytic cytokines.
Finally, the researchers analyzed samples from newly diagnosed MM patients.
The team found that serum CRP levels “significantly and positively” correlated with the number of bone lesions patients had. And CRP was abundant in lesion biopsies from individuals with severe skeletal disease. 
New research suggests that C-reactive protein (CRP) drives multiple myeloma (MM) to destroy bone.
Researchers found that CRP accelerated the onset of bone destruction and made bone damage more severe in mouse models of MM.
The team also observed an association between elevated serum CRP levels and greater degree of bone damage in newly diagnosed MM patients.
The researchers therefore believe that CRP might be targeted to prevent or treat MM-associated bone disease.
Qing Yi, MD, PhD, of the Lerner Research Institute at the Cleveland Clinic in Ohio, and his colleagues conducted this research and reported the results in Science Translational Medicine.
The researchers noted that high levels of circulating CRP have been associated with poor prognosis in many cancers, including MM.
In a previous study, the team found that CRP enhanced MM cell proliferation under stressed conditions and protected MM cells from chemotherapy-induced apoptosis.
Now, the researchers have found that CRP activates MM cells to promote osteoclastogenesis and bone destruction.
In experiments with mouse models, the team found that CRP promoted MM-cell-mediated lytic bone disease. The researchers said CRP enhanced osteoclast differentiation and bone resorption activity.
In vitro experiments showed that CRP stimulates MM cells to produce osteoclast activators such as RANKL, MCP-1, and MIP-1a.
Further investigation revealed that CRP binds to CD32 on MM cells. This activates a pathway mediated by the kinase p38 MAPK and the transcription factor Twist, which increases MM cells’ production of osteolytic cytokines.
Finally, the researchers analyzed samples from newly diagnosed MM patients.
The team found that serum CRP levels “significantly and positively” correlated with the number of bone lesions patients had. And CRP was abundant in lesion biopsies from individuals with severe skeletal disease.
New research suggests that C-reactive protein (CRP) drives multiple myeloma (MM) to destroy bone.
Researchers found that CRP accelerated the onset of bone destruction and made bone damage more severe in mouse models of MM.
The team also observed an association between elevated serum CRP levels and greater degree of bone damage in newly diagnosed MM patients.
The researchers therefore believe that CRP might be targeted to prevent or treat MM-associated bone disease.
Qing Yi, MD, PhD, of the Lerner Research Institute at the Cleveland Clinic in Ohio, and his colleagues conducted this research and reported the results in Science Translational Medicine.
The researchers noted that high levels of circulating CRP have been associated with poor prognosis in many cancers, including MM.
In a previous study, the team found that CRP enhanced MM cell proliferation under stressed conditions and protected MM cells from chemotherapy-induced apoptosis.
Now, the researchers have found that CRP activates MM cells to promote osteoclastogenesis and bone destruction.
In experiments with mouse models, the team found that CRP promoted MM-cell-mediated lytic bone disease. The researchers said CRP enhanced osteoclast differentiation and bone resorption activity.
In vitro experiments showed that CRP stimulates MM cells to produce osteoclast activators such as RANKL, MCP-1, and MIP-1a.
Further investigation revealed that CRP binds to CD32 on MM cells. This activates a pathway mediated by the kinase p38 MAPK and the transcription factor Twist, which increases MM cells’ production of osteolytic cytokines.
Finally, the researchers analyzed samples from newly diagnosed MM patients.
The team found that serum CRP levels “significantly and positively” correlated with the number of bone lesions patients had. And CRP was abundant in lesion biopsies from individuals with severe skeletal disease.