Cancer begins when normal cells undergo poor developmental decisions and lead to the formation of cancer cells. Now, researchers from Northwestern University have uncovered a potential location for the beginning of this process after examining the fruit fly equivalent of an oncogene implicated in human leukemia.
The team studied the behavior of normal developing eye cells in the fruit fly, Drosophila melanogaster, and found that when they changed from their primitive state into a more specialized state, levels of the protein Yan fluctuate in an erratic manner. However, when these fluctuations are absent, the cell does not switch states.
"This mad fluctuation, or noise, happens at the time of cell transition," Richard Carthew, who participated in the research, said in a press release. "For the first time, we see there is a brief time period as the developing cell goes from point A to point B. The noise is a state of 'in between' and is important for cells to switch to a more specialized state. This limbo might be where normal cells take a cancerous path."
Additionally, the team found that a specific signal received by the receptor EGFR can turn this noise off. Carthew and his colleagues believe that the identification of the importance of this "on" and "off" switch for noise can help scientists better understand how cells end up transforming into cancer cells.
In humans, Tel-1 is the protein equivalent to the Yan protein in fruit flies and has been connected to the cancerous mutations that stimulate leukemia; the EGFR equivalent is called Her-2, an oncogene that is a big factor in human breast cancer.
"On the surface, flies and humans are very different, but we share a remarkable amount of infrastructure," Carthew said. "We can use fruit fly genetics to understand how humans work and how things go wrong in cancer and other diseases."
The findings were published in the Nov. 19 issue of eLife.
