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C M Steel

Publications and source records attributed to C M Steel.

202 records · Page 12Linked to original sources

Allele loss on chromosome 11p is associated with poor survival in ovarian cancer.

RFLP (restriction fragment length polymorphism) analysis in 46 ovarian tumour and paired blood samples shows that 33 per cent (5/15) of informative carcinomas had loss of heterozygosity (LOH) at 11p15.4 (Calcitonin locus) and 18% (4/22) had LOH at 11p15.5 (Ha-ras). No LOH was detected in five borderline and four benign ovarian tumours. Analysis of survival in the carcinoma group (37 patients) showed a significantly poorer survival in patients whose tumours showed LOH at either or both of these 11p loci (chi 2 = 7.771, p = 0.005). This suggests the presence of a tumour suppressor gene (tsg) on the short arm of chromosome 11 whose loss is associated with particularly aggressive disease.

Alleles↗

Human lymphoid cell lines and glucocorticoids: I. Characterization and cytolethal responses of lymphoblastoid, leukaemia and lymphoma lines.

Using various genotypic and phenotypic markers 20 human lymphoid cell lines have been classified as lymphoblastoid, leukaemia or lymphoma subtypes. Each cell line type exhibited characteristic morphological and behavioural properties in suspension culture. Whilst most lymphoblastoid and lymphoma cell lines manifested B-cell phenotypes and contained Epstein Barr virus (EBV) genome, leukaemia lines demonstrated T-cell markers and lacked EBV genome. Individual cell lines demonstrated unique isoenzyme profiles for the seven polymorphic enzymes studied without subtype specificity. None of the cell lines studied was entirely homogeneous although lymphoblastoid lines contained only a minor subpopulation of other cell line types. The mixed population of cells indicate the need for caution in the use of these cell lines as in vitro models of lymphoid cancer and suggests further refinement of classification methods is required. Incubation of different cell line types with prednisolone for 48-168 h revealed most were highly resistant to cytolethal and cytostatic effects of glucocorticoids in vitro. Suprapharmacological doses of steroid (10(-3) M) were required in most instances before significant cytolethal responses occurred. Only one lymphoblastoid, one lymphoma and two leukaemia lines responded to pharmacological doses (10(-5)-10(-6) M) of prednisolone.

B-Lymphocytes↗

Human lymphoid cell lines and glucocorticoids: II. Whole cell and cytoplasmic binding properties of lymphoblastoid, leukaemia and lymphoma lines.

The glucocorticoid binding properties of 18 human lymphoid cell lines (HLCL) have been investigated. The specificity of steroid binding was confirmed with various glucocorticoid agonists and antagonists. A gradation in whole cell and cytoplasmic glucocorticoid binding capacity was observed in the different cell line types: lymphoblastoid greater than lymphoma greater than leukaemia. The cytoplasmic receptors of leukaemia and lymphoblastoid lines appeared to contain both proteinaceous and phospholipid components. Cytoplasmic steroid-receptor complexes exhibited a wide range of sedimentation coefficients (8.5-11.3S) in low ionic strength buffer but there was no correlation with cell line type or glucocorticoid sensitivity. Activation of these complexes by heat (37 degrees C) or exposure to high ionic strength buffer (0.3 M NaCl) induced nuclear binding of steroid but only complexes in high ionic strength buffer manifested changes in sedimentation coefficient. No correlation was observed between the level or nature of glucocorticoid binding and the cytolethal or cytostatic responsiveness of HLCL to glucocorticoid treatment in vitro. The resistance to cytolethal effects cannot be ascribed to a failure of cells to take up and bind steroid or to significant differences in the molecular species of cytoplasmic receptors present. The molecular mechanisms by which glucocorticoids achieve cytolethal responses in human lymphoid cells has still to be resolved.

Cell Line↗