Rare stem-like tumor cells play a critical role in the spread of breast cancer, but a vulnerability in the pathway that powers them offers a strategy to target these cells using existing drugs before metastatic disease occurs, report University of California San Diego School of Medicine and Moores Cancer Center researchers.
In the findings, published in the Journal of Clinical Investigation on December 11, researchers reveal that co-expression of cell surface receptor integrin αvβ3 and transcription factor Slug — a master regulator of a cell’s ability to self-renew and differentiate — identifies rare stem-like cells in patient-derived tumor samples that are associated with metastasis. This co-expression occurs in up to 20 percent of primary breast cancers; independent of subtype.
“Stem-like cells work early during the spread of cancer cells, before metastasis,” said Jay S. Desgrosellier, PhD, senior author on the paper and assistant professor in the Department of Pathology at UC San Diego School of Medicine. “These are the cells that remain and grow after treatment and are responsible for tumor progression. If we are going to make a difference in the number of people who die of breast cancer, we need to stop metastasis and we think we have a way to do it.”