A new Epstein-Barr virus nuclear antigen (EBNA) negative cell line SKW 4 has been established in vitro from a patient with diffuse histiocytic lymphoma. The SKW 4 seems to be an authentic human tumour cell line as evidenced by its EBV negativity, monoclonality and aneuploidy tested during early in vitro passage. The cell line expresses surface mu and kappa-chains, HLA-DR antigen, C3 and Fc receptors and B-cell lineage antigens. The karyotypic analyses demonstrated many numerical and structural aberrations. No Burkitt lymphoma associated translocations (t8;14, t2;8, t;22) were detected, but most of the markers found are those commonly associated with various types of human cancer. The SKW 4 thus represents the most common type of 'histiocytic lymphoma', that with a B-lymphoid cell phenotype, but is unique among HL derived lymphoma lines in its strong expression of a Helix pomatia A agglutinin binding surface glycoprotein of an apparent molecular weight of 75 000 daltons.

Antibodies, Monoclonal↗

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The effect of phytohemagglutinin on growth and DNA synthesis of some protozoa.

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Cell Division↗

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Dry weight and DNA content in sisters of Bursaria truncatella during the interdivision interval.

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Cell Division↗

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Inversion of chromosome 14 marks human T-cell chronic lymphocytic leukaemia.

Rare cases of chronic lymphocytic leukaemia (CLL) in man stem from the malignant proliferation of T cells. The disease is usually more aggressive clinically than B-cell-derived CLL. Various haematological tumours are associated with specific chromosome aberrations (for example, refs 1, 2). Only limited numbers of T-cell CLL patients have so far been studied cytogenetically and, whereas chromosome 12 seems particularly to be involved in B-cell CLL, several markers have been found in T-cell tumours. Recently, by stimulating malignant clones with different mitogens, novel chromosome abnormalities have been detected in T-cell CLL. Using the same approach for additional cases of T-cell CLL, we now report that the most consistent chromosome change is an inversion of the long arm of chromosome 14, inv(14)(q11 q32), in four of five patients. Another remarkable chromosome aberration is trisomy for the long arm of chromosome 8, found in three of five patients.

Chromosome Aberrations↗

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Triglyceride and cholesterol metabolism in primary hypertriglyceridemia.

To determine mechanisms of elevated plasma triglycerides (TG) in patients with primary hypertriglyceridemias, simultaneous studies were carried out on kinetics of very low density lipoprotein-triglycerides (VLDL-TG) and synthesis of cholesterol and bile acids. Sixteen hypertriglyceridemic patients with familial combined hyperlipidemia (FCHL) and 12 patients with poorly classified, primary hypertriglyceridemia were studied, and their results were compared to a series of normal and obese subjects previously studied in our laboratory. The mean value for transport (synthesis) of VLDL-TG in patients with FCHL was about twice normal. Although the upper normal synthesis rates overlapped with transport rates of some patients with FCHL, it appeared that the major cause of hypertriglyceridemia in FCHL was an elevated production of VLDL-TG. However, the height of the plasma TG in FCHL patients also was influenced by individual clearance capacities for VLDL-TG, and fractional clearance rates in several seemed particularly low. Synthesis rates for cholesterol and/or bile acids were high in several patients with FCHL, suggesting simultaneous overproduction of VLDL-TG and sterols; however, increased synthesis of both was not observed in all the patients. Most patients with poorly classified hypertriglyceridemia had over-production of VLDL-TG, but an apparent reduction in clearance was common. In these patients, increased synthesis of cholesterol and bile acids was infrequent. Our results indicate that abnormally high production of VLDL-TG seemed to be the major factor in causing primary hypertriglyceridemia, but that clearance capacity can play an important role in determining the the severity of the TG elevation.

Adult↗