The researchers discovered that this population of progenitor cells depends on the activity of a protein called cyclin D1 for self-renewal and differentiation. The team generated a mouse model with inactive cyclin D1 and the gene known to promote luminal-like breast cancer. Compared to controls, the mice lacking in cyclin D1 activity contained very few lobule progenitor cells and had an absence of luminal-like tumors.

"The effects of eliminating cyclin D1 activity were profound. Depriving the lobule progenitor cells of cyclin D1 prevented self-renewal, disrupted normal mammary differentiation, and blocked the formation of luminal-like tumors," said co-senior author Philip Hinds, PhD, deputy director of the Tufts Medical Center Cancer Center. He is also a professor in the radiation oncology department at TUSM and member of the biochemistry and genetics program faculties at Sackler.

"Now that we have seen that this approach prevents mammary tumor formation, we would like to see if inhibition of cyclin D1 slows or reverses the growth of existing tumors. We predict that targeting cyclin D1 would diminish the progenitor cells that drive luminal-like tumor growth," continued Hinds.

"If we find that inhibition of cyclin D1 activity combats existing tumors, the protein may serve as a new target for breast cancer drugs," said Kuperwasser.

Source: Tufts University, Health Sciences