Hormone replacement therapies could cause specialized cancer cells to induce growth, metastasis
- Source: University of Missouri-Columbia
- Summary:
- Women who take hormone replacement therapies have a higher incidence of breast cancer, research shows. Now, researchers have linked natural and synthetic progestins to the body's production of specialized cancer cells that act like stem cells in humans. Findings could help scientists target these rare cells that proliferate in breast cancers and metastasize elsewhere, and may help clinicians identify immunotherapies to combat the spread of the disease.
FULL STORY
Hormone replacement therapies, or medications containing female hormones, may help cancer to spread.
Credit: © Ivelin Radkov / Fotolia
Hormone replacement therapies, or
medications containing female hormones that substitute those no longer
produced by the body, often are prescribed to reduce the effects of
menopausal symptoms in women. Research has indicated that women who take
hormone replacement therapies have a higher incidence of breast cancer.
Now, researchers at the University of Missouri have linked natural and
synthetic progestins to the body's production of specialized cancer
cells that act like stem cells in humans. Findings could help scientists
target these rare cells that proliferate in breast cancers and
metastasize elsewhere, and may help clinicians identify immunotherapies
to combat the spread of the disease.
"In previous studies, we have shown that both natural and synthetic
progestins accelerate the development of breast cancer and increase
their metastasis to lymph nodes," said Salman Hyder, the Zalk Endowed
Professor in Tumor Angiogenesis and professor of biomedical sciences in
the College of Veterinary Medicine and the Dalton Cardiovascular
Research Center. "Our laboratory is committed to identifying the cell
mechanisms that bring about increased breast cancer risks. Recently, our
research focused on special cells which are called 'cancer stem
cell-like cells' -- that induce aggressive tumor growth, metastasis and
cancer recurrence."
In a series of tests, the team used hormone-responsive human breast cancer cells to examine the effects of progestin on the cell markers typically found in breast cancers. Both natural and synthetic progestins significantly increased protein expression of CD44, a molecule involved in cell proliferation, cell communication and migration. Additionally, the presence of progestins caused these components to behave like cancer stem cell-like cells.
These rare cells are a small population of cells that -- acting like normal stem cells are self-renewing, create identical copies of themselves and proliferate exponentially. Further testing showed that the rare subset of cancer cells actually were enriched by progestin.
"The findings show that exposure to natural and synthetic progestins leads to the development of these cancer stem-cell like cells," Hyder said. "These cells greatly increase the likelihood of resistance to therapies and the risk for metastasis. Our findings also suggest that clinicians may be able to combat the progestin-dependent tumor growth through immunotherapy."
In a series of tests, the team used hormone-responsive human breast cancer cells to examine the effects of progestin on the cell markers typically found in breast cancers. Both natural and synthetic progestins significantly increased protein expression of CD44, a molecule involved in cell proliferation, cell communication and migration. Additionally, the presence of progestins caused these components to behave like cancer stem cell-like cells.
These rare cells are a small population of cells that -- acting like normal stem cells are self-renewing, create identical copies of themselves and proliferate exponentially. Further testing showed that the rare subset of cancer cells actually were enriched by progestin.
"The findings show that exposure to natural and synthetic progestins leads to the development of these cancer stem-cell like cells," Hyder said. "These cells greatly increase the likelihood of resistance to therapies and the risk for metastasis. Our findings also suggest that clinicians may be able to combat the progestin-dependent tumor growth through immunotherapy."
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