Glioblastoma stem cells (GSCs) are cells with a self-renewal ability and capacity to initiate tumors upon serial transplantation that have been linked to tumor cell heterogeneity. Most standard treatments fail to completely eradicate GSCs, causing the recurrence of the disease. GSCs could represent one reason for the low efficacy of cancer therapy and for the short relapse time. Nonetheless, experimental data suggest that the presence of therapy-resistant GSCs could explain tumor recurrence. Therefore, to effectively target GSCs, a comprehensive understanding of their biology and the survival and developing mechanisms during treatment is mandatory. This review provides an overview of the molecular features, microenvironment, detection, and targeting strategies of GSCs, an essential information required for an efficient therapy. Despite the outstanding results in oncology, researchers are still developing novel strategies, of which one could be targeting the GSCs present in the hypoxic regions and invasive edge of the glioblastoma.
Despite all of the progress in understanding its molecular biology and pathogenesis, glioblastoma (GBM) is one of the most aggressive types of cancers, and without an efficient treatment modality at the moment, it remains largely incurable. Nowadays, one of the most frequently studied molecules with important implications in the pathogenesis of the classical subtype of GBM is the epidermal growth factor receptor (EGFR). Although many clinical trials aiming to study EGFR targeted therapies have been performed, none of them have reported promising clinical results when used in glioma patients. The resistance of GBM to these therapies was proven to be both acquired and innate, and it seems to be influenced by a cumulus of factors such as ineffective blood–brain barrier penetration, mutations, heterogeneity and compensatory signaling pathways. Recently, it was shown that EGFR possesses kinase-independent (KID) pro-survival functions in cancer cells. It seems imperative to understand how the EGFR signaling pathways function and how they interconnect with other pathways. Furthermore, it is important to identify the mechanisms of drug resistance and to develop better tailored therapeutic agents.
Schwannomas arise in the cells responsible for the mielinating the neurons distal to the Obersteiner-Redlich zone. Most of the intracranian Schwannomas are in the posterior fossa, developed from the VIIIth or Vth nerve stheath. The location on other cranian nerves is quite rare, only 6% of the orbital tumors being Schwannomas. We review the case of a 52 years old male patient, presenting for right eye exophthalmia and visual field deficit, diplopia due to VIth nerve paresis, and stubbing pain in the right eye, the MRI showing a tumor, located in the orbital apex displaced the globe forward and superiorly, and the optic nerve medially and superiorly. A modified lateral orbital approach was preferred. The choice of the orbitotomy allowed us to maintain the integrity of the lateral rim of the orbit without the need of a bony reconstruction at the end of the intervention, as it faced the anterior margin of the temporal muscle, covering it and not the skin over the zigomatic bone. The technical approach for orbital schwanomas should be tailored to reach the lesion through an esthetic incision and orbitotomy, immediately under the resected bone, with no need retracting the ocular globe or the vasculonervous elements in the orbit.
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