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A v-H-ras-dependent hemopoietic tumor model involving progression from a clonal stage of transformation competence to autocrine interleukin 3 production
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 153506
Author(s) Nair, A P; Diamantis, I D; Conscience, J F; Kindler, V; Hofer, P; Moroni, C
Author(s) at UniBasel Moroni, Christoph
Year 1989
Title A v-H-ras-dependent hemopoietic tumor model involving progression from a clonal stage of transformation competence to autocrine interleukin 3 production
Journal Molecular and cellular biology
Volume 9
Number 3
Pages / Article-Number 1183-90
Keywords Animals; Cell Line; Transformed; Cell Transformation; Neoplastic; *Genes; ras; Genetic Complementation Test; Interleukin-3/*biosynthesis/genetics; Mast-Cell Sarcoma/*genetics/immunology; Mice; Inbred DBA; Phenotype
Abstract Autocrine interleukin 3 (IL-3)-secreting tumors were generated from an IL-3-dependent mouse mast cell line (PB-3c) after introduction of the v-H-ras oncogene. Tumor progression was characterized by four distinct phenotypes. The first corresponded to immortalized mast cells unresponsive to the oncogenic effect of v-H-ras. The second was expressed in a clonable subpopulation of PB-3c cells and was marked by the competence to form v-H-ras-dependent tumors (immortalized transformation competence). The third was a direct effect of v-H-ras expression on all PB-3c cells and was characterized in vitro by a reduced IL-3 requirement. Upon injection of v-H-ras-expressing, transformation-competent cells into mice, the final, fully malignant phenotype developed with a long latency period and was marked in vitro by independence of exogenous IL-3 and by autocrine IL-3 stimulation. Northern (RNA) blot analysis and an RNase A-T1 protection assay showed that IL-3 production was strictly associated with the tumor phenotype. Two of six tumors showed an alteration at the 5' region of the IL-3 gene. We conclude that v-H-ras required complementation by IL-3 gene rearrangement or an alternate event to generate autocrine mastocytomas.
Publisher American Society for Microbiology
ISSN/ISBN 1098-5549
edoc-URL http://edoc.unibas.ch/dok/A5257908
Full Text on edoc No
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/2498644
ISI-Number WOS:A1989T444300034
Document type (ISI) Journal Article
 
   

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