Suchergebnisse

Yang Guo,1,* Peidong Zhang,2,3,* Hongtian Zhang,4 Peng Zhang,4 Ruxiang Xu4 1Department of Neurology, 2Department of Cardiovascular Medicine, Zhujiang Hospital, 3Second Clinical Medical College, Southern Medical University, Guangzhou, 4Department of Neurosurgery, Affiliated Bayi Brain Hospital, The Military General Hospital of Beijing PLA, The Bayi Clinical Medical Institute of Southern Medical University, Beijing, People's Republic of China *These authors contributed equally to this work Abstract: Glioblastoma is the most common form of malignant brain tumors and has a poor prognosis. Glioma stem cells (GSCs) are thought to be responsible for the aberrant proliferation and invasion. Targeting the signaling pathways that promote proliferation in GSCs is one of the strategies for glioma treatment. In this study, we found increased expression of contactin 2 (CNTN2) and amyloid β precursor protein (APP) in U87-derived GSCs (U87-GSCs). RNA interference (RNAi) for CNTN2 downregulated the expression of APP intracellular domain (AICD), which is the proteolytic product of APP. Treatment with CNTN2 RNAi inhibited the proliferation of U87-GSCs. CNTN2 RNAi decreased the expression of epidermal growth factor receptor and HES1, which are potential targets of AICD. In summary, inhibition of the CNTN2/APP signaling pathway may repress the proliferation in U87-GSCs via downregulating the expression of HES1 and epidermal growth factor receptor. CNTN2/APP/AICD signaling pathway plays an important role in U87 glial tumorigenesis. Further studies are warranted to elucidate the role of these signaling pathways in other sources of GSCs. Depending on their role in proliferation in other sources of GSCs, members of the CNTN2/APP/AICD signaling pathway may provide novel targets for the development of therapy for glioblastomas. Keywords: contactin 2, CNTN2, transient axonal glycoprotein-1, TAG1, glioma stem cells

Abstract
Background Tuberculum sellae meningiomas (TSMs) account for 5 to 10% of all intracranial meningiomas. They typically invade the optic canal and displace the optic nerve upward and laterally. The transcranial approach has been the standard surgical approach, while the transsphenoidal approach has been proposed for its minimally invasive nature; however, some reservations concerning this approach remain.
Methods From January 2000 to December 2018, a total of 97 patients who were diagnosed with TSM with invasion of the optic canal were enrolled and underwent microsurgery for tumor removal with optic canal opening. A retrospective analysis was performed on the effect of optic canal opening on postoperative visual acuity improvement. The median follow-up was 17.4 months (range: 3–86 months).
Results Among the 97 patients with TSM involving the optic canal, optic canal invasion was seen on preoperative imaging in 73 patients and during intraoperative exploration in all patients. In total, 87/97 patients (89.7%) underwent optic canal opening to remove tumors involving the optic canal, and the rate of total macroscopic resection of tumors invading the optic canal was 100%. Among the 10 patients who did not undergo optic canal opening, the rate of total resection of tumors involving the optic canal was 80% (8/10, p < 0.001). There were no deaths or serious complications. The postoperative visual acuity improvement rate was 64.4%, 23.7% maintained the preoperative level, and the visual acuity deteriorated 11.9%.
Conclusion Intraoperative optic canal opening is the key to total resection of TSMs involving the optic canal and improving postoperative visual acuity.