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We investigated whether a genetic modification of BCR-ABL-transformed mousecells that resulted in endostatin (ES) production altered their oncogenic potential.Mouse B210 cells, which express p210bcr-abl fusion protein and induce leukemia-likedisease and extremely rarely solid tumors after intravenous (i.v.) administration,were used. The cells were transfected with a plasmid carrying genes for mouseES and resistance to blasticidine. Transduced cells were isolated in media supplementedwith blasticidine. Production of ES was determined by Western blotting. For furthertests, two clones were selected, and their pathogenicity after i.v. inoculationwas tested. Compared with the parental B210 cells, the capability of both gene-modifiedcell clones to induce lethal leukemia was reduced. However, mice that did notsuccumb to leukemia subsequently developed solid tumors. They were composed ofpoorly differentiated cells with irregular nuclei and roughly granular chromatinand were well vascularized. FISH revealed the presence of the BCR-ABL fusion geneboth in tumors and spleens. Immunohistological investigation of the tumors demonstratedthe production of ES in vivo and the cell lines derived from the tumors produceddetectable amounts of ES, this demonstrating that the formation of solid tumorswas not associated with the loss or silencing of the ES gene.

Unexpected properties of endostatin-producing mouse BCR-ABL-transformed cells