CLONALITY IN CHRONIC MYELOPROLIFERATIVE DISORDERS DEFINED BY X-CHROMOSOME LINKED PROBES - DEMONSTRATION OF HETEROGENEITY IN LINEAGE INVOLVEMENT

The restriction fragment length polymorphisms (RFLP) of the X-chromoso me phosphoglycerate kinase (PGK) and hypoxanthine phosphoribosyltransf erase (HPRT) genes were used to study the clonal basis of the chronic myeloproliferative disorders (CMPD). Analyses were performed on granul ocyte and T-lymphocyte fractions obtained from 24 females; 13 had esse ntial thrombocythaemia (ET), eight polycythaemia vera (PV) and three m yelofibrosis with myeLoid metaplasia (MMM). All 24 of these patients h ad monoclonal patterns of X-inactivation in the granulocyte fraction. For the T-lymphocyte fraction, non-clonal patterns of X-inactivation w ere observed in 8/13 patients with ET, 7/8 with PV and 1/3 with MMM, w hile the remaining eight subjects were found to have monoclonal patter ns of X-inactivation. Our endings suggest that the majority of the CMP D in these patients originated from a relatively committed progenitor cell without the capacity to differentiate into T cells, and convincin gly demonstrated heterogeneity of lineage involvement.