Biomedical subjects

T Lang

Publications and source records attributed to T Lang.

273 records · Page 16Linked to original sources

PubMedDate not supplied

Exchange of material between the extracellular medium and macrophage phagosomes containing different species of bacteria including mycobacteria.

Pathogenic mycobacteria survive and multiply once they have infected macrophages. The aim of the present work was to determine whether the persistence of pathogenic bacteria such as M. avium inside the host cell phagosomes had any effect on the exchanges that normally occur between the extracellular medium and the macrophage vacuolar compartment. Our results indicate that fusions between phagosomes and lysosomes or/and incoming pinosomes appear to be slowed down by the presence of mycobacteria and even partially inhibited when phagosomes contain viable pathogenic mycobacteria.

Animals↗

PubMedDate not supplied

Effects of cytostatic agents on the expression of epidermal growth factor receptor in ovarian cancer cells.

The effects of cytostatic agents on proliferation and epidermal growth factor receptor (EGF-R) expression were examined in the ovarian carcinoma cell line OVCAR-3. These cells were found to express about 84,000 high-affinity EGF binding sites per cell. Treatment of OVCAR-3 cells with cisplatin, etoposide or epirubicin for two hours resulted in a marked augmentation of EGF-R expression and growth inhibition, on the other hand, incubation with substances blocking RNA or protein synthesis, actinomycin-D and cycloheximide, resulted in a reduction of both EGF-R expression and growth rate. An up-regulation of EGF-R has thus been shown only for DNA-affecting agents, but not for those inhibiting transcription or translation. This response may be explained as a frustrated escape mechanism of the cancer cell to cytotoxic agents.

Antineoplastic Agents↗

PubMedDate not supplied

Interaction of retinoic acid and interferon-alpha in breast cancer cell lines.

Retinoids and Interferons have been demonstrated to synergistically amplify the inhibition of proliferation in cultured breast cancer cells. Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. To improve the understanding of mechanism mediating synergism we extended our studies to the type I interferon-alpha. Synergistic inhibition of proliferation could be detected also by IFN-alpha and RA in BT-20 and SKBR-3 breast cancer cell lines but not in MCF-7 cells. Neither IFN-alpha nor any retinoid tested alone were able to increase RAR-gamma message, only the combination of both had this ability. In MCF-7 breast cancer cell lines the combination of any retinoid with IFN-alpha increased CRABP II expression level compared with the retinoids alone. In contrast with SKBR-3 and BT-20 cells a combination of ATRA with IFN-alpha markedly reduced ATRA mediated CRABP II induction. These results suggest that two factors may be responsible for synergistic action of RA and IFN-alpha: the inhibition of the CRABP II expression and an IFN-alpha/RA mediated upregulation of RAR-gamma.

Antineoplastic Combined Chemotherapy Protocols↗