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Discoveries thrust cancer-initiating stem cells into a larger role in cancer biology and treatment

eagues discovered that as few as 10 cells producing high amounts of CD44 were capable of creating tumors in an animal model. In contrast, other tumor cells were 10 to 50 times less tumorigenic. The fact that they were tumorigenic at all, the researchers say, indicates that CD44 alone is unlikely to be the sole indicator of stem cell-ness among the tumor cell population. However, according to Chu, the discovery that high CD44 producing cells have cancer stem cell properties provides an entry point into further research into cancer-causing stem cells.

BRCA1 regulates human mammary stem cell self-renewal and differentiation: Abstract 5700

Mutations in the well-known breast cancer susceptibility gene BRCA1 have a role in the propagation of aggressive stem cell-driven cancer. The findings, according to researchers at the University of Michigan, offer further evidence that breast cancer treatment strategies require a stronger focus on the stem cells that drive the disease.

"Our lab previously identified the presence of mammary stem cells and, since BRCA1 is such a strong predictor of breast cancer, we were interested in the involvement of the gene in stem cells," said Suling Liu, Ph.D., a researcher at the University of Michigans Comprehensive Cancer Center. "If mammary stem cells are, indeed, the driving force of breast cancer, then we need to know more about their function if we hope to create more effective therapies."

To investigate the role of the gene in stem cells, the team engineered a lentivirus to carry small interfering RNA segments that, in effect, silence the BRCA1 gene. They then observed how a population of mammary stem cells functioned without the ability to produce BRCA1. When BRCA1 was inhibited, the number of stem cells was increased by 75 percent. These new cells, in turn, produced three times the normal amount of a stem cell marker protein ALDH1.

In an animal model of the disease, the knockdow
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Contact: Staci Vernick Goldberg
goldberg@aacr.org
267-646-0616
American Association for Cancer Research
18-Apr-2007


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