Finding suggests interception of this signal may thwart metastases, study says
THURSDAY, June 12 (HealthDay News) -- Primary tumors can fuel the growth of stray cancer cells elsewhere in the body, say researchers at the Massachusetts Institute of Technology.
In experiments with mice, the MIT team found that primary tumors derived from human breast cancers seem to promote the growth of distant cancers by mobilizing bone marrow cells, which then feed the growth of the secondary tumors.
The secretion of a substance called osteopontin by the primary tumor is an important part of this process, said the researchers, who noted that osteopontin is present at elevated levels in women with metastatic breast cancer.
While the researchers found that the primary tumor somehow disturbs the make-up of bone marrow, they don't know exactly how that occurs. They also know that osteopontin does not act alone in this process.
The findings, published in the June 13 issue of Cell, may lead to new cancer treatments.
"If metastases depend on stimulation by primary tumors, interception of the signal through neutralizing antibodies," may prevent the spread of cancer, researcher Robert Weinberg said in a prepared statement. "That's still speculative, but it's an interesting idea to ponder."
He noted that current treatments don't specifically target metastases, which causes the vast majority of cancer deaths.
The findings may also prove important for the pre-clinical study of cancers.
"The ability of instigating tumors to foster the growth of a human colon tumor surgical specimen underscores the power of systemic instigation," Weinberg and colleagues wrote. "Indeed, to our knowledge, methods to expedite the growth of human tumor surgical specimens in vivo have not been previously described. These results suggest that the presently described procedure can be used to study aspects of human tumor biology that would otherwise be difficult if not impossible to study."
The National Cancer Institute has more about metastatic cancer.
-- Robert Preidt
SOURCE: Cell Press, news release, June 12, 2008
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