In early test tube and mouse studies, investigators at Johns Hopkins Medicine and the Johns Hopkins Kimmel Cancer Center have found that nonmuscle myosin IIC (MYH14), a protein activated in response to mechanical stress, helps promote metastatic behavior in pancreatic cancer cells, and that the compound 4-hydroxyacetophenone (4-HAP), known to stiffen myosin IIC-containing cells, can send it into overdrive, overwhelming the ability of cells to invade nearby tissue.
The work, described online in July in the journal Cancer Research, found that 4-HAP reduced metastatic tumor formation in a mouse model of human pancreatic cancer by assessing the fraction of liver surface covered by tumor tissue. Read more . . .