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creased proliferation, growth, and survival by means other than Ras V12 are not sufficient to cause the metastatic progression of scrib –/ – cells. Thus, the metastasis-promoting effect of scrib inactivation is highly dependent on its specific cooperation with the Ras V12 allele. Moreover, aside from its known effects on proliferation, growth, and survival, Ras V12 may function through an as yet undefined cellular mechanism to elicit metastatic progression in scrib –/ – cells. It has proven difficult to systematically study the genetic basis of metastasis with the currently available techniques. The Drosophila system described here circumvents the complication of acquired background mutations

Year: 2009
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