Evi-2 is located within a large intron of the Nf1 tumor suppressor gene, raising the possibility that proviral integration at Evi-2 predisposes mice to myeloid tumor development by disrupting Nf1 expression.
The overall odds in favor of NF1 lying within this linkage group in the families studied are over 150,000:1, with a maximum location score of 5.112 for the interval D17S58-EVI2A.
We have mapped the human homologue of a murine gene (Evi-2) that is implicated in myeloid tumors, to a location between two NF1 translocation breakpoints on chromosome 17.
Identification and characterization of transcripts from the neurofibromatosis 1 region: the sequence and genomic structure of EVI2 and mapping of other transcripts.
The probable role of Evi-2 in murine neoplastic disease and the map location of the human homolog suggest a potential role for EVI2 in NF1, but no physical rearrangements of this gene locus are apparent in 87 NF1 patients.