What can scientists studying cancer biology learn from fruit flies?
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Quite a bit, it turns out.
At a time when large projects such as the Cancer Genome Atlas seek to define changes in DNA that drive cancer formation, the insight gained from smaller arenas, such as fruit flies, is helping make sense of the mountains of data.
Emory cell biologist Ken Moberg crafted a fruit-fly–based strategy to identify growth-regulating genes that previous researchers may have missed. His approach allowed him to begin defining the function of a gene that is often mutated in lung cancer.
“Many screens have been carried out in flies looking for single gene lesions that drive tissue overgrowth,” Moberg says. “But a fundamental lesson from years of cancer research is that many and perhaps most cancer-causing mutations also drive compensatory apoptosis, and blocking this apoptosis is absolutely required for cancer outgrowth. We reasoned that this class of ‘conditional’ growth suppressor genes had been missed in prior screens, so we designed an approach to look for them.”
Moberg identified the fruit fly gene Myopic as one of these conditional growth regulators. He used a system where mutations in Myopic drive some of the cells in the fly’s developing eye to grow out more, but only when apoptosis is disabled.
Myopic’s counterpart in humans is the gene His-domain protein tyrosine phosphatase, or HD-PTP. This gene is located on the part of the human genome that is deleted in renal cancer cells and in more than 90% of both small cell and non-small cell lung cancers. How HD-PTP, when it is intact, controls growth of cells in the human lung or kidney is unknown, but Moberg’s findings suggest that HD-PTP may function through a mechanism that is similar to Myopic’s functions in the fly.—Quinn Eastman
