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The role of hypoxia and SRC tyrosine kinase in glioblastoma invasiveness and radioresistance
Filippo Torrisi, Nunzio Vicario, Federica Spitale, Francesco Cammarata, Luigi Minafra, Lucia Salvatorelli, Giorgio Russo, Giacomo Cuttone, Samuel Valable, Rosario Gulino, Gaetano Magro, Rosalba Parenti

The role of hypoxia and SRC tyrosine kinase in glioblastoma invasiveness and radioresistance

Science & Mathematics Published 2020 Verification Pending

Overview & Synopsis

Advances in functional imaging are supporting neurosurgery and radiotherapy for glioblastoma, which still remains the most aggressive brain tumor with poor prognosis. The typical infiltration pattern of glioblastoma, which impedes a complete surgical resection, is coupled with a high rate of invasiveness and radioresistance, thus further limiting efficient therapy, leading to inevitable and fatal recurrences. Hypoxia is of crucial importance in gliomagenesis and, besides reducing radiotherapy efficacy, also induces cellular and molecular mediators that foster proliferation and invasion. In this review, we aimed at analyzing the biological mechanism of glioblastoma invasiveness and radioresistance in hypoxic niches of glioblastoma. We also discussed the link between hypoxia and radiation-induced radioresistance with activation of SRC proto-oncogene non-receptor tyrosine kinase, prospecting potential strategies to overcome the current limitation in glioblastoma treatment.

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Document Information

Document Title The role of hypoxia and SRC tyrosine kinase in glioblastoma invasiveness and radioresistance
Author / Organization Filippo Torrisi, Nunzio Vicario, Federica Spitale, Francesco Cammarata, Luigi Minafra, Lucia Salvatorelli, Giorgio Russo, Giacomo Cuttone, Samuel Valable, Rosario Gulino, Gaetano Magro, Rosalba Parenti
Subject & Discipline Multidisciplinary Academic Open Research
Categories Science & Mathematics
Publication Year 2020
License / Rights Open Access / Creative Commons
Resource Verification Listed PDF (Verification Pending)
Original Host Website HAL Open Science (hal.science)
File Format application/pdf (Portable Document Format)
Language EN
Catalog ID DOC-174911
Original Source Link Visit Source Page on hal.science »