Growth factor receptor signaling critical to intestinal tumor development, studies show

, growth and progression of the polyps appeared to be independent of Egfr, and so a small percentage of tumors might not need Egfr to grow, Roberts said. Microscopic examination of intestinal tissue in the youngest mice also revealed no differences in the number of lesions believed to be precursors of larger intestinal polyps and cancer. Most just failed to progress.

Humans who inherit a bad copy of the Apc-Min gene can develop hundreds of tumors throughout their intestinal tracts, he said. That illness, however, represents only about 1 percent of human colon cancer cases.

Mice with the waved 2 mutation have wavy hair and curly whiskers but are otherwise healthy and lead essentially normal lives, Roberts said. Rodents with entirely dysfunctional Egfr die within two weeks of birth, which shows the gene is essential for life.

Related work conducted in Coffeys laboratory at Vanderbilt involved placing human tumors in mice and then treating the mice with Egfr tyrosine kinase inhibitors -- compounds that block the action of an Egfr signaling enzyme.

They saw a drastic reduction in tumor growth, depending on the dose they gave the mice, Roberts said. That showed the approach definitely holds promise for using these drugs to treat human cancers.

How well our results in mice wind up correlating with human treatment remains to be seen, but at this point were excited about the possibilities.

Several clinical trials of drugs that block Egfr already have begun, Roberts said. Results from two previous mouse studies of compounds targeting the molecule have been contradictory, probably because drugs used were not precise enough in their action.


Contact: David Williamson
University of North Carolina at Chapel Hill

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