Modeling mutations in the G1 arrest pathway in human gliomas: overexpression of CDK4 but not loss of INK4a-ARF induces hyperploidy in cultured mouse astrocytes

Article Abstract:

Cultured mouse astrocytes have been used to model gliomagenesis in humans. The role of CDK4 amplification and loss of INK4a-ARF in relation to G1 arrest has been investigated by comparing astrocytes that overexpress CDK4 with those that do not have a functional INK4a-ARF locus. The astrocytes with CDK4 overexpressed grow more slowly and readily convert to a tetraploid state, whereas the lack of INK4a-ARF causes cells to remain in a pseudodiploid state

Ploidy

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PDGF autocrine stimulation dedifferentiates cultured astrocytes and induces oligodendrogliomas and oligoastrocytomas from neural progenitors and astrocytes in vivo

Article Abstract:

Some low-grade oligodendrogliomas may be made up of proliferating glial progenitor cells blocked in ability to differentiate based on new research. Malignant gliomas have acquired other mutations as well. Chronic autocrine PDGF signaling can promote a proliferating population of glial precursors potentially adequate to bring on gliomagenesis.

Statistical Data Included, Cytochemistry, Cell differentiation, Neuroglia, Glia, Autocrine mechanisms, Cell proliferation, Carcinogenesis, Oligodendroglia

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p190RhoGAP can act to inhibit PDGF-induced gliomas in mice: a putative tumor suppressor encoded on human chromosome 19q13.3

Article Abstract:

Research has been conducted on p190RhoGAP and Rho, the regulators of oligodendrocyte differentiation. The authors suggest that p190 regulates PDGF oncogenesis' critical components and can act as a tumor suppressor in PDGF-induced gliomas.

Sweden, Science & research, Analysis, Causes of, Gene expression, Tumor suppressor genes, Genetic research, Chemical inhibitors, Human chromosomes, Tumour suppressor genes

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