Brian J. Druker and colleagues, investigators from the Howard Hughes Medical Institute, have developed a new technique that could help in identifying previously// unknown genetic mutations that can trigger cancerous growth. The researchers by using a new technique, where in they analyse the proteins instead of the genes, which are present inside acute myeloid leukemia (AML) cells, have significantly reduced the time it takes to target the molecular abnormalities that might be vulnerable to specific drug treatments.
"This approach gives us a way to figure out what's driving the growth of a cancer in an individual patient and ultimately match that patient with the right drug," said Druker, who is based at the Oregon Health & Science University in Portland. Druker's team collaborated on the research, which was published in the July 17, 2006, issue of the journal Cancer Cell, with scientists in the lab of D. Gary Gilliland, an HHMI investigator at Brigham and Women's Hospital, as well as researchers at the Portland VA Medical Center, Cell Signalling Technology, the University of Chicago, and Yale University.
Traditionally, cancer-gene hunters have scanned the genome looking for mutations that trigger out-of-control cell growth. Druker tried this approach, but found it wanting. "We were doing some high-throughput DNA sequencing, and we weren't really finding much," he said.
Instead, the team added tools from the burgeoning field of proteomics, the study of proteins. "We decided this more functional assay would get us to the disease-causing genes more rapidly," said Druker, who has been studying a group of cell-signalling proteins called tyrosine kinases for 20 years.
Tyrosine kinases play a key role in many cancers. In healthy cells, they help form a chain of signals that prompt normal cell growth and division. Sometimes, though, a tyrosine kinase gets stuck in an "on" position, driving out-of-control cell division and, ult
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