The study found that tumor-forming melanoma cells have the ability to throw a genetic switch that changes the types of proteins expressed on the cells' surface. The study is the first to present evidence for this type of pervasive "phenotypic plasticity" among melanoma cells from patients.
Patterns of surface proteins are used to identify different cell types and are commonly called cell surface markers.
"The fact that these markers are turned on and off by melanoma cells raises the possibility that melanoma cells may also turn on and off genes that regulate clinically important characteristics like drug resistance and metastatic ability," Morrison said. "The ability to transition between various states may make melanoma more difficult to treat."
The authors stress that while their results argue against a cancer stem cell model for melanoma, their findings do not invalidate the model. In fact, certain leukemias and other cancers appear to follow the model.
"It will be critical to determine which cancers follow a stem cell model and which do not, so therapies designed to target rare sub-populations of cells are not inappropriately tested in patients whose disease is driven by many diverse cancer cells," Quintana said.
The cancer stem cell model assumes that cells differing in marker expression also differ in function, and that only a very small subset of cancer cells displaying the critical marker pattern---less than 1 percent of cancer cells---can form tumors. The model proposes that most of the cancer cells that compose tumors have little or no capacity to proliferate or to contribute to disease progression.
"The cancer stem cell model says that tumor cells are organized hierarchically, and that only the cells at the top of the hierarchy form tumors. Cells at the
|Contact: Jim Erickson|
University of Michigan