Some lung cancers develop resistance to treatment, but researchers have recently learned more about a potential mechanism that fuels the cancer growth. These findings may lead to the development of a drug that can interrupt that pathway, according to a study published recently in Genes & Cancer.
The most common form of lung cancer, called non-small-cell lung cancer, has been treated with some success with targeted therapies that work by blocking, or inhibiting, the signaling of enzymes that are responsible for activating proteins, called tyrosine kinases. However, the treatment eventually fails when a tumor develops resistance to the tyrosine kinase inhibitor therapy and progresses.
Researchers were interested in exploring if the resistance to the treatment could be explained by the activation of a protein linked with controlling cell growth (proliferation) and death (apoptosis) called Yes-associated protein (YAP), which has been found to promote the spread of cancer, leading to poor survival outcomes.
They found that if they shut off the YAP protein, the cells that were once resisting the drug became sensitive to it once again. These results suggest that YAP contributes to treatment resistance in non-small-cell lung cancer and may therefore be targeted for the development of a new drug that blocks its effects.