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- W1931031804 abstract "Platelet-derived growth factor B (PDGF-B) overexpression induces gliomas of different grades from murine embryonic neural progenitors. For the first time, we formally demonstrated that PDGF-B-induced neoplasms undergo progression from nontumorigenic low-grade tumors toward highly malignant forms. This result, showing that PDGF-B signaling alone is insufficient to confer malignancy to cells, entails the requirement for further molecular lesions in this process. Our results indicate that one of these lesions is represented by the down-regulation of the oncosuppressor Btg2. By in vivo transplantation assays, we further demonstrate that fully progressed tumors are PDGF-B-addicted because their tumor-propagating ability is lost when the PDGF-B transgene is silenced, whereas it is promptly reacquired after its reactivation. We provide evidence that this oncogene addiction is not caused by the need for PDGF-B as a mitogen but, rather, to the fact that PDGF-B is required to overcome cell-cell contact inhibition and to confer in vivo infiltrating potential on tumor cells." @default.
- W1931031804 created "2016-06-24" @default.
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- W1931031804 date "2008-12-01" @default.
- W1931031804 modified "2023-10-16" @default.
- W1931031804 title "Tumor Progression and Oncogene Addiction in a PDGF-B-Induced Model of Gliomagenesis" @default.
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- W1931031804 doi "https://doi.org/10.1593/neo.08814" @default.
- W1931031804 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2586688" @default.
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