"Our work shows that radiation can change the microenvironment of breast cells, and this in turn can allow the growth of abnormal cells with a long-lived phenotype that have a much greater potential to be cancerous," Paul Yaswen, a cell biologist and breast cancer research specialist with Berkeley Lab's Life Sciences Division, said in a statement to the press.
"Many in the cancer research community, especially radiobiologists, have been slow to acknowledge and incorporate in their work the idea that cells in human tissues are not independent entities, but are highly communicative with each other and with their microenvironment," he added.
For their study, Yaswen and his research teams used human mammary epithelial cells (HMECs), the cells that line breast ducts, where most breast cancers start. When placed in a culture dish, the vast majority of HMECs display a phenotype that allows them to divide between five and 20 times until they become what is known as senescent, or unable to divide. However, there are also some variants of these cells which have a phenotype that allows them to continue dividing for many weeks in culture. Known as a vHMEC phenotype, this type of breast cell arises spontaneously and is more susceptible to malignancy because it lacks a tumor-suppressing protein dubbed p16.