Tumor progression and oncogene addiction in a PDGF-B-induced model of gliomagenesis.

摘要: 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 nontumorigenic low-grade tumors toward highly malignant forms. This result, showing PDGF-B signaling alone is insufficient to confer malignancy cells, entails requirement for further molecular lesions in this process. Our results indicate one these represented by down-regulation oncosuppressor Btg2. By vivo transplantation assays, demonstrate fully progressed are PDGF-B-addicted because their tumor-propagating ability lost when transgene silenced, whereas it promptly reacquired after its reactivation. We provide evidence oncogene addiction not caused need as a mitogen but, rather, fact required overcome cell-cell contact inhibition and infiltrating potential on tumor cells.