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Biomedical subjects

F Wiener

Publications and source records attributed to F Wiener.

At least 109 records · Page 6Linked to original sources
PubMed1977

Histochemical studies on the EBV-determined nuclear antigen (EBNA).

The EBV-determined nuclear antigen (EBNA) was studied with regard to several histochemical properties. Proteolytic enzymes destroyed EBNA staining. RNAse DNAse and hyaluronidase had no effect on the number of EBNA positive cells. Intensive treatment with DNAse weakened the chromosomal fluorescence of EBNA, whereas the staining of interphase nuclei was relatively enzyme resistant. When EBV-associated soluble complement-fixing antigen of Raji cells (CFA-R) was added to methanolacetic acid-fixed chicken red blood cells, brilliant and specific EBNA staining was obtained by anti-complement fluorescence (ACIF) with anti-EBNA positive sera. DNAse treatment abolished the ability of the nuclei to bind the antigen (CFA-R), whereas DNAse treatment following CFA-R antigen binding had no effect on the ACIF staining. EBNA was relatively heat stable. Somewhat weakened, but still fully positive EBNA reaction was obtained after 56 degrees C heating for 30 minutes in BSS. Periodate destroyed the EBNA reaction. Formaldehyde also abolished the staining, whereas methanol, acetone, methanol-acetone and methanol-hexyleneglycol-water preserved the staining relatively well.

Antigens, Viral↗
PubMed1976

Tumor-host cell hybrids in radiochimeras reconstituted with bone marrow and thymus grafts.

CBA/H and CBA/HT676 radiation chimeras were prepared by lethal irradiation and subsequent reconstitution with bone marrow of the host karyotype and thymocytes of the opposite karyotype. After T- and B-cell chimerism had been established, the animals were inoculated with SEWA or TA3Ha ascites tumor--donor cell hybrids were isolated following the explantation of TA3Ha tumor in selective HAT medium and by selecting for adherent cells from SEWA. The T6T6 chromosomal marker served to distinguish between the type of cell involved in the fusion. In all hybrids the donor component was a nonthymus-derived cell.

Animals↗
PubMed1976

The expression of differentiated functions in somatic cell hybrids: retention and activation of C3 production.

Rat and mouse fibroblasts which do not secrete the third component of complement (or secrete it at a very low rate), were respectively hybridized with mouse and rat hepatoma cells which actively produce C3. These interspecific hybrids actively secrete both mouse and rat C3. The production of C3 coded by the hepatoma cell genome is thus retained, but in addition, the secretion of C3 coded by the fibroblast genome is activated. On the other hand, intraspecific hybrids have been isolated from normal diploid C3 producing cells and non-producing cells. These cell hybrids also retain the capacity to secret C3. Retention of C3 production thus does not appear to be peculiar to hybrides derived from hepatoma cells.

Cell Fusion↗
PubMed1976

Tumorgenicity of L cell derivatives and hybrid cells derived from them.

Hybridization studies on high and low malignant L cell derivatives support our previous conclusions, in showing that crosses between highly tumorigenic and poorly tumorigenic lines to a marked suppression of the malignant phenotype. Malignant behaviour is not, however, suppressed when cells from one highly tumorigenic line are crossed with those of another tumorigenic line. The present results show further that these rules apply even when all the cells crossed are closely related derivatives of one cell line.

Animals↗
PubMed1975

Genetic determinants of morphological differentiation in a lymphoma-sarcoma hybrid.

Hybrid cells, YACIR/MSWBS were produced by fusion of the cells of a methylcholanthrene induced murine sarcoma MSWBS and a virus induced murine lymphoma YACIR. The hybrid cells were maintained in vitro and syngenic mice challenged at various periods after fusion. Karyological analysis has been performed on the cell line, and on the tumours which arose in vivo. The tumours were also examined histologically. Over the 2 yr following fusion there was a progressive loss of chromosomes but biarmed MSWBS derived chromosomes were selectively retained. Tumours could be divided into those whith a chromosome complement similar to that of the early line in vitro, those in which chromosome loss had occurred and those in which karyology showed a mixture of the two foregoing types. Histology showed a minority of sarcoma-like tumours reminiscent of MSWBS and the majority of these showed little chromsome loss. Most tumours showed an intermediate morphology and the great majority of these had lost moderate numbers of chromosomes. There was a very small number of lymphomatoid tumours in which chromosome loss was marked.

Animals↗
PubMed1974

Tumor-host cell hybrids in radiochimeras.

F(1) hybrid mice syngeneic or semiallogeneic with respect to the relevant tumor were lethally irradiated and then reconstituted with hemopoietic cells from strain CBAT6T6 mice. After chimerism had been established, the animals were inoculated with solid or ascites tumors. Tumor-host cell hybrids were selected from enzyme-deficient solid tumors by explanting the tumor cell suspension into hypoxanthine-amethopterin-thymidine containing medium. The selection of hybrid cells from ascites tumors was achieved by exploiting the difference between the ascites tumor cells and hybrid cells in their ability to adhere to the surface of culture vessels. T6T6 chromosomal and H-2 antigenic markers served to distinguish between the hemopoietic cells derived from the donor graft and the cells of the host. All solid tumors tested fused with cells of the irradiated host, whereas ascites tumors fused with repopulating cells of hemopoietic origin.

Adenocarcinoma↗
PubMed1974

Human leukemia-associated anti-nuclear reactivity.

A brilliant, coarsely granular nuclear antigen was detected by anti-complement immunofluorescence in the nuclei of acute myeloid leukemia myeloblasts. Designated as LANA (leukemia-associated nuclear antigen), the reactivity differs from that of the Epstein-Barr-virus-determined nuclear antigen (EBNA) in immunological specificity and morphological appearance, although it is visualized by the same method. Serum from acute myeloid leukemia patients gave positive reactions in 73% of the cases. In acute lymphatic leukemia, chronic myeloid leukemia, chronic lymphatic leukemia, and Burkitt's lymphoma the sera were positive in 35, 14, 19, and 24%, respectively. Two of five polycythemia and two of eleven myeloma sera were also positive. Among 61 healthy controls, 58 were negative, whereas three showed a diffuse nuclear staining with a different pattern. Among 24 carcinoma patients, 18 were negative, whereas six gave a nuclear staining with a different, diffuse pattern. Sera from 20 patients who had recovered from infectious mononucleosis were all negative. In addition to the blasts of acute myeloid leukemia, a similar reactivity was seen with two Epstein-Barr virus DNA and EBNA-negative African lymphoma biopsies and in a short-lived tissue culture line derived from one of them. LANA could be a fetal or tissue-specific antigen, a virally determined antigen, or a specific form of anti-nuclear reactivity.

Antibodies, Antinuclear↗
PubMed1973

The influence of the partner cell on the production of L virus and the expression of viral surface antigen in hybrid cells.

The C-type particles produced by the A9 and A9HT sublines of mouse L cells were shown to infect C3H (N type), but not C57BL (B type), mouse embryo fibroblasts. Infection was indicated by distinct single giant cell formation in the XC monolayer used to overlay the mouse embryo fibroblasts. On the basis of these results it was concluded that the L cell virus is N tropic. A9 and A9HT cells were fused to various mouse cells derived from tumors and normal tissues. The ability to produce the Moloney-type surface antigen and to release infectious virus was introduced by the A9 component into the hybrid cell. Virus production, measured by antigen induction on JLS-V9 cells, was suppressed in those hybrids in which the partner cell had a genotype determining low infectibility with that particular virus (B-type cell). It thus appears that the major genetic locus affecting resistance to infection with leukemia viruses, the Fv-1 locus, regulates infectious virus production in somatic cell hybrids also. The same genetic locus did not seem to govern the expression of all virus-related functions, for the virus-determined membrane antigen was demonstrated in many of the N x B-type hybrids in which production of infectious virus was suppressed.

Adsorption↗