Although dividing the posterior communicating artery (PComA) during surgery has been criticized for increasing the risk of ischaemia, this procedure increase working space improving visibility and the ability to manipulate during treatment of basilar tip aneurysms via the pterional approach. We divided a hypoplastic PComA in 4 of our cases of basilar tip aneurysm. This was necessary because either (1) the length of the PComA and intracranial internal carotid artery (ICA) limited medial retraction of the ICA and access to the basilar bifurcation region, or (2) the PComA and its perforators ran just in front of the aneurysm, interfering with its exposure. We were able to clip the aneurysm neck in all four patients, three of whom had complications including temporary impairment of consciousness, ocular movement disorders and altered sensation in the extremities. Patients with complications showed transient hypersomnolence immediately after surgery; computed tomography showed small thalamic infarctions. However, in two of three patients the ischaemic events occurred contralateral to the side of PComA section. All patients regained consciousness within a week and were discharged with mild ocular movement palsies. In our cases except one with ischaemic complications, thalamic infarction probably resulted from thalamo-perforating artery injury when the aneurysm neck was clipped, rather than tuberothalamic artery injury due to section of the PComA. Taking previous reports and our results into consideration, we believe that division of a hypoplastic PComA is a safe procedure in particular cases when the grade of subarachnoid haemorrhage is not poor and there are no cerebrovascular risk factors, although we realize it is desirable to preserve normal blood flow.
Glioma stem cells (GSCs) have the capacity to repopulate tumors and mediate resistance to radiotherapy and chemotherapy. The Notch signaling pathway is important in proliferation, stem cell maintenance, cell differentiation, and tumorigenesis in GSCs. In this study, we compared CD133, Notch, and VEGF expressions in histological sections of primary and recurrent glioblastomas after radiotherapy and chemotherapy. In vitro study, the γ-secretase inhibitor inhibited NICD, Hes1 and pVEGFR2 expressions in GSCs. GSCs cultured under endothelial conditions undergo endothelial differentiation. Tumor samples were collected from 27 patients at the time of tumor recurrence. We used immunohistochemical techniques to compare expression of CD133, Notch-1 and VEGF. Expressions of CD133-, Notch-1-, and VEGF-positive glioma cells were higher in recurrent glioblastoma after radiotherapy and chemotherapy. To determine the clinical importance of Notch-1 expression in glioblastoma, we analyzed 15 patients who had received bevacizumab therapy followed by a second surgery at recurrence. OS was significantly longer in cases with Notch-1 negativity (8.8 months) than in those with I Notch-1 positivity (6.8 months). We noted that GSCs have the potential for endothelial differentiation with Notch activity. We believe that Notch-1 is a potential target and/or biomarker for antiangiogenic treatments.
The NOTCH pathway regulates neural stem cells and glioma initiating cells (GICs). However, blocking NOTCH activity with γ-secretase inhibitors (GSIs) fails to alter the growth of GICs, as GSIs seem to be active in only a fraction of GICs lines with constitutive NOTCH activity. Here we report loss of PTEN function as a critical event leading to resistance to NOTCH inhibition, which causes the transfer of oncogene addiction from the NOTCH pathway to the PI3K pathway. Drug cytotoxicity testing of eight GICs showed a differential growth response to GSI, and the GICs were thus stratified into two groups: sensitive and resistant. In the sensitive group, GICs with loss of PTEN function appeared less sensitive to GSI treatment. Here we show that NOTCH regulates PTEN expression and the activity of the PI3K pathway in GICs, as treatment with GSI attenuated the NOTCH pathway and increased PTEN expression. NOTCH regulates PTEN expression via Hes-1, as knockdown of Notch or Hes1 increased expression of PTEN. This novel observation suggests that both pathways must be simultaneously inhibited in order to improve therapeutic efficacy in human glioblastomas (GBMs).
✓ Nontraumatic subdural hematoma following disseminated intravascular coagulation (DIC) due to advanced cancer was encountered in four patients. It is suggested that DIC plays an important role in the formation of subdural hematoma in cancer patients.
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