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"The BCR-ABL oncogene is central in the pathogenesis of CML," Dr. Robert C. Rees of Nottingham Trent University and associates report the November 15th issue of Blood. Using tandem nanospray mass spectometry, Dr. Rees' group demonstrated cell surface HLA-associated expression of a BCR-ABL oncogene peptide. A cytotoxic T-lymphocyte response to the peptide was able to kill autologous CML cells.
The BCR-ABL-peptide-specific T cells were detectable by tetramer staining in the peripheral circulation of CML patients, but not in an AML patient or in two control subjects.
Stimulation with the peptide increased the positive-staining cells from 0.3% to 2.5%, suggesting the "potential to expand leukemia-reactive T cells in vitro and that tetramer staining may be helpful in monitoring their expansion."
Dr. Rees's team notes that although "both BCR-ABL antigen presentation and cytotoxic T-lymphocyte response are intact in CML, these mechanisms cannot operate optimally in vivo, otherwise the disease would never come to clinical attention."
They suggest that low T-cell receptor avidity or T-cell tolerance in patients with a massive leukemic burden may be responsible for the inadequate response. Other potential reasons include absent or anergic CD4+ cells or weak antigen expression.
The investigators estimate that it will 2 to 5 years before a potential vaccine is available for clinical use.
Blood 2001;98:2887-2893
Source: Reuters
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