Senescence of human fibroblasts induced by oncogenic Raf

Article Abstract:

Oncogenes RAF (ital) and RAS (ital) have for some time been seen as neoplastic transformation agents. In normal cells the same genes can have effects that work against oncogenic change. The Raf/MEK/MAP kinase signaling cascade is essential to bringing on signaling from Ras proteins. Thus ability of conditionally active Raf-1 forms to bring on cell cycle arrest and senescence in human cells has been studied. Activation of Raf-1 in nonimmmortalized human lung fibroblasts (IMR-90) is a prelude to irreversible and immediate stopping of cellular proliferation and premature beginning of senescence. In most tumors cells seem to be able to go on proliferating. The ability to become sensescent seems lost.

Cells, Protein kinases, Fibroblasts, Cell aging

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Transactivation-defective c-MycS retains the ability to regulate proliferation and apoptosis

Article Abstract:

Transcriptional activation by c-Myc from certain E box elements is considered essential for a biological role, but c-MycS cannot activate transcription through these elements. Nevertheless it keeps ability to induce anchorage-independent growth and stimulate proliferation as well as bringing on apoptosis. Also, c-MycS keeps ability to repress transcription of a number of specific promoters. Moreover c-MycS can rescue the c-myc null phenotype in fibroblasts that have homozygous c-myc deletion. Findings indicate that the model that has all biological functions of c-Myc mediated by transcriptional activation of certain target genes by E box elements is not valid.

United States, Cellular signal transduction

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A new mouse model to explore the initiation, progression, and therapy of [BRAF.sup.V600E]-induced lung tumors

Article Abstract:

A mice carrying a genetically modified allele of BRaf, [BRaf.sup.CA] which expresses normal BRaf prior to Cre-mediated recombination after which [BRaf.sup.VE] is expressed at physiological levels is described. The findings suggest that [BRaf.sup.VE]-induced lung tumors were prevented by pharmacological inhibition of MEK1/2.

Science & research, Research, Usage, Lung tumors, Animal models in research, Animal research models, Lung tumours, Clinical report

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