Human /3-¡nterferon(IFN) induced an antiviral state in two fetal brain and six glioma cell lines. The growth-inhibitory effect of IFN was most pronounced on three glioblastoma lines and least on fetal brain and oligodendroglioma cells; IFN growth inhibition of one schwannoma and one anaplastic cell line was intermediate between the two other groups. Thus, the growth-inhibitory effect of IFN generally correlated with the degree of anaplasia of the tissue from which the cells were derived. IFN (1000 units/ml) had to be present for 24 to 48 hr to have a significant inhibitory effect on growth of glioblastoma (12-18) cells. However, growth inhi bition of 12-18 cells exposed to IFN for 3 days persisted for 3 weeks. Both sialic acid-A/-acetylgalactosamine ganglioside and a mixture of normal human brain gangliosides (50 U.M)inhibited growth of fetal brain (CHII) but not glioblastoma 12-18 cells. However, preincubation of cells with either sialic acid-A/-acetylgalactosamine or a mixture of gangliosides did not augment the growth-inhibitory effects of IFN on either CHII or 12-18. These results indicate that gangliosides and IFN may be operating through different mechanisms to cause growth inhibition.

High-dose chemotherapy (HDC) with autologous stem cell transplant (ASCT) has improved response rates and survival for patients with multiple myeloma (MM). We report a single-institution experience using two conditioning regimens, busulfan, cyclophosphamide, and etoposide (BCV) or high-dose melphalan (HDM). Between July 1992 and August 2003, 110 patients with MM (median age=56.1) underwent HDC with ASCT using either BCV (n=62) or HDM (n=48) in sequential cohorts as the preparative regimen. Overall response rates, progression-free survival, and median overall survival were similar. BCV and HDM confer similar long-term outcomes with similar toxicity profiles as conditioning regimens prior to autologous stem cell transplant in patients with MM.

Sialyltransferase-1 activity was studied in cultured 12–18 human glioma cells. The apparent Km and Vmax with variable LacCer concentrations were 32μM and 197 pmoles/mg protein/hr and with variable CMP-NeuAc concentrations were 172μM and 877 pmoles/mg protein/hr., respectively. The pH optimum towards exogenous LacCer was 6.0 and towards endogenous acceptors was 6.2. The optimum protein:detergent ratio was 1:1. Humanβ interferon (1000 units/ml medium) increased sialyltransferase-1 activity only slightly on a protein basis but increased it 47% on a per cell basis. These results demonstrate that one of the biochemical effects ofβ-interferon on 12–18 human glioma cells is to stimulate ganglioside synthesis.

Natural killer cells (NK) demonstrate cytotoxicity against a wide range of cultured cells without prior sensitization, and the sensitivity of many target cells to NK attack is altered by exposure to interferon. The structures on the target cells conferring sensitivity or resistance to NK are not known, but glycolipids are suggested to be related to NK susceptibility. To determine possible relationships between target cell glycolipids and NK cytolysis, the effects of human beta-interferon (IFN) on the neutral glycolipid composition and sensitivity to NK cytolysis of cultured cells from four human gliomas and two fetal brains were analyzed. Compared to MOLT-4 and Raji cells all six neural cell lines were quite resistant to NK, and IFN slightly increased this resistance. IFN also caused increases in the amounts of non-hydroxy fatty acid cerebroside, ceramide trihexoside, asialo-GM1, asialo-GM2 and globoside. Increased molar proportions of ceramide tri- and tetra-saccharides occurred in the two glioma lines which had the greatest increases in NK resistance following IFN exposure. It is concluded that neutral glycolipids may play a role in the mechanisms responsible for resistance of some glioma cells to NK cytolysis.