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Biomedical subjects

V Rotter

Publications and source records attributed to V Rotter.

136 records · Page 8Linked to original sources
PubMed1973

Studies on characterization of the lymphoid target cell for activity of a thymus humoral factor.

The immune response to SRBC was measured in the spleens of adult thymectomized, total body irradiated mice injected with various combinations of thymus and bone marrow cells together with thymic humoral factor (THF). It was found that the number of plaque-forming cells was significantly increased when THF was given in vivo immediately after thymus cell administration or when thymus cells were incubated in THF before injection. On the other hand, bone marrow cells equally treated did not manifest any T cell activity, since THF-treated bone marrow cells were not able to substitute thymus cells in the system used. The results accumulated in the present experiments indicate, therefore, that the target cells for THF activity are thymus cells which acquire a higher T helper cell capacity after THF treatment.

Animals↗
PubMedDate not supplied

The expression of transformation-related protein p53 and p53-containing mRNA in murine RAW117 large cell lymphoma cells of differing metastatic potential.

The relationship between the expression of a transformation-related cellular-encoded phosphoprotein, p53, and the potential to form distant metastases was investigated in Abelson murine leukemia virus-transformed murine large cell lymphoma sublines of differing metastatic behaviors. Low metastasis RAW117-P and high metastasis RAW117-H10 cells were labeled with 35S-methionine, and several anti-p53 monoclonal antibodies were used to immunoprecipitate p53 from the cell lysates. Using these procedures, similar amounts of p53 were detected in the RAW117-P and -H10 cells. In addition, the expression of 2.0 Kb mRNA containing p53-specific sequences was equivalent in RAW117-P and -H10 cells. The results indicate that p53 expression, although apparently required for neoplastic transformation, is not quantitatively related to metastatic behavior in RAW117 large cell lymphoma cells.

Abelson murine leukemia virus↗
PubMedDate not supplied

Expression of abl and other oncogenes is independent of metastatic potential in Abelson virus-transformed malignant murine large cell lymphoma.

The role of oncogene expression in tumor metastasis was examined using the Abelson leukemia virus-transformed murine large cell lymphoma RAW117. Cell sublines of low and high metastatic potential expressed equally abl oncogene-coded mRNA and its phosphoprotein product p160, and the capacity of p160 to become autophosphorylated with gamma-[32P]ATP was the same among low and high metastatic cells. The expression of other oncogene-coded mRNAs (fos, myc, myb), if present, was also similar in low and high metastatic RAW117 cells. Although oncogene expression is thought to be important in initiating, and in some cases maintaining, the transformed phenotype, its expression in RAW117 lymphoma cells appears to be unrelated to metastatic phenotype.

Abelson murine leukemia virus↗
PubMedDate not supplied

Cooperation between gene encoding p53 tumour antigen and ras in cellular transformation.

The protein p53 is highly expressed in a large variety of transformed cell types originating from diverse species. These include cells transformed by Simian virus 40 (SV40), adenovirus and Abelson virus, as well as a variety of chemically transformed cells. Substantial amounts of p53 are also present in certain non-transformed cells, for example, some embryonic tissues. The protein may be localized in different cellular compartments in normal and transformed cells. The strong correlation between tumorigenicity and high levels of p53 suggests an important role of p53 in tumorigenesis. We report here experiments in which we have co-transfected the murine cellular gene encoding for p53 with a ras gene into primary rat embryo fibroblasts. Our results indicate that the p53-encoding gene can play a causal role in the conversion of normal fibroblasts into tumorigenic cells.

Animals↗
PubMedDate not supplied

Human p53 gene localized to short arm of chromosome 17.

The p53 gene codes for a nuclear protein that has an important role in normal cellular replication. The concentration of p53 protein is frequently elevated in transformed cells. Transfection studies show that the p53 gene, in collaboration with the activated ras oncogene, can transform cells. Chromosomal localization may provide a better understanding of the relationship of p53 to other human cellular genes and of its possible role in malignancies associated with specific chromosomal rearrangements. A recent study mapped the human p53 gene to the long arm of chromosome 17 (17q21-q22) using in situ chromosomal hybridization. Here, by Southern filter hybridization of DNAs from human-rodent hybrids, we have localized the p53 gene to the short arm of human chromosome 17.

Chromosome Mapping↗
PubMedDate not supplied

Polymorphisms of the p53 gene in women with ovarian or endometrial carcinoma.

The p53 gene is frequently mutated in various human tumors. Polymorphism is an additional genetic alteration observed in exons and introns of the p53 gene of normal tissues and tumors. Distributions of alleles of three common polymorphisms of the p53 gene; a 16 bp duplication in intron 3, codon 72 of exon 4 and a sequence in intron 6, were studied in peripheral white blood cells (WBC) of patients with ovarian or endometrial carcinomas. The analysis was performed by PCR and direct sequencing. The 100% linkage observed between the most common haplotypes of each polymorphism in healthy subjects was lower in the patients. A significant difference was observed between frequencies of genotype and haplotype combinations in patients with ovarian carcinoma and endometrial carcinoma. The incidence of heterozygosity was increased in ovarian carcinoma and decreased in endometrial carcinoma. Our results suggest that the p53 gene may be involved in susceptibility and predisposition to various cancers not only by mutations but also by preferential presentation of polymorphic alleles.

Adult↗