The hypothesis holds that tumors are propelled forward by a small group of stem cells or "mother" cells that are resistant to existing therapies, explained Dr. Jenny Chang, lead author of this study and professor of medicine at Baylor College of Medicine in Houston.
In fact, studies have suggested that chemotherapy can actually increase the number of these stem cells, Chang said.
Investigating further, Chang said she and her colleagues "isolated these cells and found that the [molecular] pathway that regulated cancer stem cells was the 'Notch' pathway."
So called gamma-secretase inhibitor drugs, which activate the Notch pathway, succeeded in rendering cancer stem cells vulnerable to chemotherapy in an animal model.
And in one human patient, the drug managed to shrink a tumor in a woman who had failed all attempts at chemotherapy.
"She is now about to go for surgery," Chang reported. "Previously, a patient like this is inoperable."
A final study found that treating estrogen receptor-positive breast cancer tumors with a combination of an experimental drug called fidarestat and Femara (the aromatase inhibitor letrozole) either delayed or eliminated tumors that had developed a resistance to hormone therapy.
Researchers at the University of Texas Health Science Center, San Antonio, found that fidarestat affects cellular metabolism of glucose, which provides energy for cells, sustaining tumor growth.
There's more on breast cancer at the U.S. National Cancer Institute.
SOURCES: Dec. 11, 2009 teleconference with C. Kent Osborne, M.D., director, Dan L. Duncan Cancer Center and the Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston; Jenny Chang, M.D., professor of medicine, Baylor College of Medicine, Houston; Angelo Di Leo, M.D., Ph.D., director, department of oncology, Hospital of Prato, Italy; William Gradishar, M.D., professor of medicine, Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago; study abstracts