Adding a second drug to tamoxifen, the breast cancer drug used successfully for more than 20 years, helps it retain its full strength.
December 14, 2006 (Press Release) --
Adding a second drug to tamoxifen, the breast cancer drug used successfully for more than 20 years, helps it retain its full strength, scientists at the U.S. National Cancer Institute report.
Over time, tamoxifen can lose its effectiveness. But the new molecule, called disulfide benzamide or DIBA, could provide a way to overcome that acquired resistance and restore tamoxifen's effectiveness.
DIBA "is not a new molecule," noted William Farrar, head of the Cancer Stem Cell Section of the National Cancer Institute's Center for Cancer Research at Frederick, Md., and the study's lead author. "It's been around a while."
Farrar's team gave DIBA to mice engineered to develop tamoxifen-resistant tumors and then to human breast cancer cells in the laboratory. Tumor growth slowed in both cases.
Those findings are published in the December issue of Cancer Cell.
Tamoxifen is the standard of care for women who have what's known as "estrogen-receptor positive breast cancer." When estrogen binds to the estrogen receptor, a series of events that promote rapid cell division ensues. If that cell happens to be a breast cancer cell, the cascade of events can lead to tumor growth.
Tamoxifen acts to block the effects of estrogen on breast tissue. It is routinely used in advanced breast cancer or as additional therapy after primary treatment for early-stage breast cancer.
In Farrar's study, when DIBA was added to the mix, tamoxifen easily inhibited the growth of breast cancer cells.
DIBA "switches off everything, all the molecular machinery of estrogen receptors, which results in breast cancer cell death," Farrar said. And, in the human breast cancer cell lines, "we got a 90 percent reduction in tumors," he added. In the mice studies, DIBA reduced tumor volume almost 50 percent.
DIBA is what is known as a "lead" compound, Farrar said, which means it merely opens the door to suitable drugs. DIBA itself "is probably not appropriate for humans, because of solubility problems." Farrar's team will try to develop or find another compound more suitable for human use, fashioning it after the properties of DIBA.
As research progresses from the laboratory to human clinical trials, "our goal is to develop a molecule that can be orally administered," Farrar said.
V. Craig Jordan, vice president and scientific director of the medical science division of the Fox Chase Cancer Center in Philadelphia, views the new research as promising. Jordan, known as the "father of tamoxifen," notes that tamoxifen is life-saving but also beset with resistance problems.
source: http://health.msn.com/
Over time, tamoxifen can lose its effectiveness. But the new molecule, called disulfide benzamide or DIBA, could provide a way to overcome that acquired resistance and restore tamoxifen's effectiveness.
DIBA "is not a new molecule," noted William Farrar, head of the Cancer Stem Cell Section of the National Cancer Institute's Center for Cancer Research at Frederick, Md., and the study's lead author. "It's been around a while."
Farrar's team gave DIBA to mice engineered to develop tamoxifen-resistant tumors and then to human breast cancer cells in the laboratory. Tumor growth slowed in both cases.
Those findings are published in the December issue of Cancer Cell.
Tamoxifen is the standard of care for women who have what's known as "estrogen-receptor positive breast cancer." When estrogen binds to the estrogen receptor, a series of events that promote rapid cell division ensues. If that cell happens to be a breast cancer cell, the cascade of events can lead to tumor growth.
Tamoxifen acts to block the effects of estrogen on breast tissue. It is routinely used in advanced breast cancer or as additional therapy after primary treatment for early-stage breast cancer.
In Farrar's study, when DIBA was added to the mix, tamoxifen easily inhibited the growth of breast cancer cells.
DIBA "switches off everything, all the molecular machinery of estrogen receptors, which results in breast cancer cell death," Farrar said. And, in the human breast cancer cell lines, "we got a 90 percent reduction in tumors," he added. In the mice studies, DIBA reduced tumor volume almost 50 percent.
DIBA is what is known as a "lead" compound, Farrar said, which means it merely opens the door to suitable drugs. DIBA itself "is probably not appropriate for humans, because of solubility problems." Farrar's team will try to develop or find another compound more suitable for human use, fashioning it after the properties of DIBA.
As research progresses from the laboratory to human clinical trials, "our goal is to develop a molecule that can be orally administered," Farrar said.
V. Craig Jordan, vice president and scientific director of the medical science division of the Fox Chase Cancer Center in Philadelphia, views the new research as promising. Jordan, known as the "father of tamoxifen," notes that tamoxifen is life-saving but also beset with resistance problems.
source: http://health.msn.com/
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