Secondary transplant recipients in which graft failure or late-onset hematologic malignant disease develops have provirally marked clones from the primary animal.

Bone marrow and spleen cells from primary mice (1°) withTEL-ABL–induced SBS or CML-like disease (CML) were transplanted into lethally irradiated secondary recipients (2°). Genomic DNA from spleens of 2 secondary recipient mice that died with early graft failure (egf) and pancytopenia between 14 and 18 days after transplantation (lanes 1 and 2 and lanes 3 and 4) and from a recipient with late graft failure (lgf) that had pancytopenia and hypocellular bone marrow at 99 days after transplantation (lanes 5 and 6) contained provirally marked cells that shared some clones with myeloid cells from the primary mouse. Spleen DNA from several secondary recipient mice in which macrophage tumors developed (mφ) after long latent periods also shared proviral clones with myeloid cells from the donor (lanes 9, 10, and 11 and lanes 12 and 13), as did thymus DNA from a secondary recipient in which T-ALL developed (lanes 14 and 15). However, some macrophage tumors and cases of T-ALL that arose in secondary recipients were derived from proviral clones that were not represented at significant levels in the myeloid cells of the donor (lanes 16, 17, and 18).