The quantitative data provide clear evidence that the major change in all these translocation-carrying leukemias is a decrease in expression of the majority of transcripts compared with normal CD15(+) cells.
Constitutive expression of Lewis X in these cells is due to the transcriptional activation of Fuc-T VII, the rate-limiting enzyme in the sialyl Lewis X synthesis, induced by the Tax protein encoded by the human T-cell leukemia virus-1, the etiological virus for this leukemia.
The present results suggest that these elements play a critical role in the colon adenocarcinoma and leukemia cell-specific transcriptional regulation of the FUT4 gene.
The therapeutic potential of the IgM complement-fixing murine monoclonal antibody (mAb) PM-81 (anti-CD15) against acute myeloid leukemia (AML) was assessed in a SCID/hu leukemia model.Intraperitoneal (i.p.) injection of NB4 leukemia cells resulted in aggressive growth of leukemia cells in the peritoneal cavity of irradiated SCID/CB-17 mice.
Enzymatic and RNA analyses [Northern blot and reverse transcription polymerase chain reaction (RT-PCR)] were used to evaluate possible control points in the biosynthetic pathway for Le(x) and sLex. beta 1,4 Galactosyltransferase (beta 1,4GalT, an enzyme involved in the synthesis of the core oligosaccharide of the three fucosylated antigens) activity and the corresponding mRNA were found in all of the leukaemia cell lines, regardless of whether or not they expressed the fucosylated antigens.
By double immunofluorescence staining it was determined that the VIM-D5(CD15) antigen was expressed by terminal deoxynucleotidyl transferase-positive blast cells, excluding the possibility of double leukemia.