Identification ofaCommonEcotropic Viral Integration Site, Evi-), intheDNA ofAKXD MurineMyeloid Tumors

AKXD-23recombinant inbred micedevelop myeloid tumorsata highfrequency, unlike otherAKXD recombinant inbred strains whichdevelop B-cell lymphomas, T-cell lymphomas, orboth. AKXD-23myeloid tumorsaremonoclonal, andtheir DNA contains somatically acquired proviruses, suggesting thattheyare retrovirally induced. Weidentified acommonsite ofecotropic proviral integration that ispresent intheDNA ofallAKXD-23myeloid tumorsthat wereanalyzed andintheDNAofallmyeloid tumorsthat occurinAKXD strains othefr thanAKXD-23. We designated this locus Evi-l (ecotropic viral integration site 1).Rearrange- mentsintheEvi-l locus werealso detected intheDNAofanumberofmyeloid tumorsandmyeloid cell lines isolated fromstrains other thanAKXD.Incontrast, fewEvi-l rearrangements weredetected intheDNA ofT- orB-cell tumors. Evi-) maythusidentify anewproto-oncogene locus thatisinvolved inmyeloid disease. Micefrom21of23AKXD recombinant inbred mouse strains derived fromAKR/J, astrain with ahigh incidence of lymphoma, andDBA/2J, astrain withalowincidence of lymphoma, develop hematopoietic neoplasms atahighfre- quency(27; D.J.Gilbert, unpublished data). However, the average ageofonsetandthecell typeofhematopoietic neoplasms varies fromstrain tostrain, suggesting thatin these strains anumberofgenesthat affect susceptibility to lymphoma anddisease typehavebeensegregated during inbreeding. MicefromsixoftheAKXD strains diedpredom- inantly ofT-cell lymphomas, micefromsixstrains died predominantly ofB-cell lymphomas, andmicefromone strain diedpredominantly ofmyeloid tumors. Micefrom eight strains wereequally susceptible tolymphomas ofT-or