Deficiency of malic enzyme: a possible marker for malignancy in lymphoid cells.
Soluble malic enzyme (MEs) has been examined in long-term human lymphoid cell lines cultured from 101 individuals. In 65 out of 66 lines derived from people without lymphoreticular malignancy the enzyme was very active. Lines established from 35 individuals with various forms of lymphoreticular malignancy were also examined, including in some cases more than 1 line derived from the same patient. In all cases where the cell line was thought to be derived from normal cells MEs was active, but in 27 out of 29 lines thought to be derived from malignant cells (from 25 patients) MEs was not detected. In the case of two patients with chronic lymphatic leukaemia 'normal' lines active for malic enzyme, and 'leukaemic' lines lacking malic enzyme, had been cultured from the same individual. Preliminary investigations of the lack of malic enzyme in somatic cell hybrids derived from lymphoma and leukaemia cell lines are compatible with an alteration at the level of the structural locus MEs on chromosome 6. However, the restoration of MEs activity in one line by fusion with mouse teratocarcinoma cells suggests that the alteration may be of a regulatory nature.
D000818:Animals; D002051:Burkitt Lymphoma / Q000201:enzymology; D002460:Cell Line; D002906:Chromosomes, Human, 6-12 and X; D004592:Electrophoresis, Starch Gel; D005260:Female; D005819:Genetic Markers; D006801:Humans; D006822:Hybrid Cells; D007938:Leukemia / Q000201:enzymology*; D008223:Lymphoma / Q000201:enzymology*; D008291:Malate Dehydrogenase / Q000172:deficiency* / Q000235:genetics; D051379:Mice; D014178:Translocation, Genetic
D005819:Genetic Markers; D008291:Malate Dehydrogenase