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Primary tumors can drive the growth of distant cancers 6-15-08
Primary tumors can encourage the growth of stray cancer cells lurking
elsewhere in the body that otherwise may not have amounted to much, according to
a new study in the June 13 issue of the journal Cell, a publication of Cell
Press. As people age, most may have such indolent cancer cells given the sheer
number of cells in the body, although their rarity makes them impossible to
detect, the researchers said.
The primary tumors under study, which were derived from human breast cancers,
seem to "instigate" the growth of other cancers by mobilizing bone marrow cells,
which then feed the secondary tumors' growth, they report.
One key to the process is the secretion of a substance known as osteopontin by
the instigating tumor, a finding that may have therapeutic implications. Indeed,
the researchers noted that osteopontin is present at elevated levels in women
with metastatic breast cancer, supporting the notion that the new findings may
hold clinical significance.
" If metastases depend on stimulation by primary tumors, interception of the
signal through neutralizing antibodies" might block cancer spread, said Robert
Weinberg of the Massachusetts Institute of Technology. "That's still
speculative, but it's an interesting idea to ponder," he added, noting that
treatments today don't specifically target metastases, which are responsible for
the vast majority of cancer deaths.
The researchers noted that while the effects of the tumor microenvironment has
been much studied, much less was known about how the systemic environment in the
body contributes to tumor growth. Several earlier reports had shown that
assorted bone marrow-derived cells can be incorporated to various extents into
the supportive framework, or stroma, of tumors. However, it wasn't clear whether
tumors actively recruit stromal cells by directly perturbing other cell
reservoirs, such as the bone marrow, or whether tumors are just passive
recipients of stromal cell precursors that normally circulate throughout the
body.
In the new study, the researchers injected "instigating" human tumor cells into
mice along with indolent "responding" cancer cells also derived from humans.
Those indolent cells formed vigorously growing tumors only in the presence of
the instigating tumor cells, they reported. They found further evidence that the
instigating tumor somehow perturbs the makeup of the bone marrow, although
Weinberg said they don't really know how that happens. They also show that
osteopontin is necessary to the process, but that it does not act alone.
Finally, they showed that the same instigation process can encourage the growth
of disseminated metastatic cancer cells. Instigating breast tumors in the mice
also drove the growth of implanted fragments of human colon tumors, a finding
that they said shows the generality of the physiologic signaling.
Nonetheless, the researchers said they don't yet know how universal this
systemic instigation of tumor growth might be. Still, the findings challenge the
"prevailing view that primary tumors suppress the growth of derived metastases,"
Weinberg said. "We argue they can foster cancer's spread by activating bone
marrow that is then recruited by distant metastases."
The findings also have important implications for the preclinical study of human
cancers, Weinberg emphasized.
" The ability of instigating tumors to foster the growth of a human colon tumor
surgical specimen underscores the powers of systemic instigation," the
researchers 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.
" In the longer term, identification of additional tumor-derived factors that
perturb the host systemic environment in one way or another may allow one to
predict the effects that a given primary tumor type has on the outgrowth of
indolent cancer cells that have disseminated to distant sites."
###
Researchers include Sandra S. McAllister, Whitehead Institute for
Biomedical Research, Cambridge, MA; Ann M. Gifford, Whitehead Institute for
Biomedical Research, Cambridge, MA; Ashley L. Greiner, Whitehead Institute for
Biomedical Research, Cambridge, MA; Boston University, Boston, MA; Stephen P.
Kelleher, Whitehead Institute for Biomedical Research, Cambridge, MA, Williams
College, Williamstown, MA; Matthew P. Saelzler, Whitehead Institute for
Biomedical Research, Cambridge, MA; Massachusetts Institute of Technology,
Cambridge, MA; Tan A. Ince, Whitehead Institute for Biomedical Research,
Cambridge, MA; Brigham and Women's Hospital, Harvard Medical School, Boston, MA;
Ferenc Reinhardt, Whitehead Institute for Biomedical Research, Cambridge, MA;
Lyndsay N. Harris, Yale University Medical Center, New Haven, CT; Bonnie L.
Hylander, Roswell Park Cancer Institute, Buffalo, NY; Elizabeth A. Repasky,
Roswell Park Cancer Institute, Buffalo, NY; and Robert A. Weinberg, Whitehead
Institute for Biomedical Research, Cambridge, MA, Massachusetts Institute of
Technology, Cambridge, MA, MIT Ludwig Center for Molecular Oncology, Cambridge,
MA.
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