?Target? cells, cellular phenotypes, and lineage fidelity in human leukaemia

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Abstract
A detailed analysis of lymphoid leukaemia cells with a panel of monoclonal antibodies plus other markers indicates a striking conservation of phenotype that closely mimics that of normal lymphoid precursor or progenitor cells and reflects the imposition of maturation arrest. The composite phenotypes detected show some minimal deviations or asynchronies (with respect to maturation “stages”) but are faithful with respect to cell lineage. These observations are suggested to shed light on the available “target” populations for lymphoid malignancy in humans and challenge the view that de-differentiation or qualitatively aberrant gene expression is common and important in malignancy. They are further taken to support the view that normal gene products that regulate or couple proliferation and maturation are critically involved in the successive clonal selection events underlying the evolution of leukaemia. No qualitatively unique and consistent leukaemia “markers” may exist or be required. The only exception to this rule are the nonrandom chromosome changes, which, it is suggested, involve genetic loci critical to the regulation of growth and maturation in particular normal cell types.