New research shows that a biomarker occurring on the surface of tumors may promote the proliferation and resilience of cancerous tissue, providing a new clue as to how some cancers become resistant to drugs during treatment.

The findings, published in the journal  Nature Cell Biology, suggest that the molecule CD61 strengthens tumors by enhancing the stem cell-like properties of cancerous tissue. “There are a number of drugs that patients respond to during their initial cancer treatment, but relapse occurs when cancer cells become drug-resistant,” Dr. David Cheresh, a researcher at the University of California, San Diego, School of Medicine and lead author of the study, said. “We looked at the cells before and after they became resistant and asked, ‘What has changed in the cells?'”

To investigate, the researchers analyzed how samples of cancerous tissue interacted with commonly used drugs like erlotinib and lapatinib, known collectively as tyrosine kinase inhibitors. They found that, as the samples developed resistance, they expressed more and more stem cell-like properties associated with the CD61 pathway.

Conversely, when they administered treatment designed to exploit the same pathway, they found that the samples became re-sensitized to drugs and gradually lost their stem cell qualities. “The good news is that we’ve uncovered a previously undefined pathway that the tumor cells use to transform into cancer stem cells and that enable tumors to become resistant to commonly used cancer drugs,” Cheresh explained.