Studies of rare blood syndrome yield novel route to cancer

t a small deletion of DNA in a region between two known genes could produce a tyrosine kinase that is essentially "turned on" in the absence of a normal activation signal. It appeared that in patients with HES, the absence of a small amount of DNA created a fusion between two genes, FIP1L1 and PDGFR alpha, which switches on PDGFR alpha, a tyrosine kinase.

The researchers later confirmed that Gleevec did specifically block the activity of the wayward kinase. They did this by analyzing the genes of a patient who developed resistance to Gleevec due to an additional mutation in the PDGR alpha gene-- as well as by analyzing the action of the drug in cell cultures.

"A key finding from this paper is this novel mechanism for generating a gain-of-function fusion gene," said Gilliland. "This FIP1L1-PDGFR alpha fusion is a constitutively activated tyrosine kinase, and it has all the hallmarks of a cancer-causing tyrosine kinase."

Until now, said Gilliland, genetic deletions were associated with inactivation of tumor suppressor genes, an event that can also trigger cancers. Discovery of this new mechanism may prompt researchers to take a fresh look at whether it initiates other forms of cancer.

"These activated tyrosine kinases can act as gas pedals for the tumors, as in acute myelogenous leukemia, breast cancers and gastrointestinal stromal cell tumors," said Gilliland. "Now that we have one example where small deletions can activate these kinases, we may find many more such examples of solid tumors with activated kinases.

"Such a finding would be especially important therapeutically because kinases are excellent drug targets. It's possible to make very specific lock-and-key inhibitors like Gleevec that selectively block kinase activity," said Gilliland.

Although the broad range of standard analytical techniques now used to detect cancer-causing abnormalities will not uncover such deletions, sa

Contact: Jim Keeley
Howard Hughes Medical Institute

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