Objective To probe into the pre-operative design and the operative approach dealing with anastomotic vein and superior sagittal sinus in patients with large meningiomas in the sagittal sinus and falx cerebri. Methods Thirty-five patients with large meningiomas in the sagittal sinus and falx cerebri, admitted to our hospital from January 2001 to December 2010, were chosen; their clinical data were analyzed retrospectively. The resection of the tumors by microsurgery (total or subtotal resection) was performed and intraoperative effective management of the sagittal sinus and falx cerebri was done. Results Resection was performed in these 35 patients, including Simpson grade Ⅰ in 21(60.0％), grade Ⅱ in 12 (34.2％), and grade Ⅲ in 2 (5.7％). Skull defect was noted in 5 patients. Unilateral　paralysis of limbs (muscle strength grade Ⅰ-Ⅳ) in 5; paralysis of both lower extremities (muscle strength grade Ⅰ-Ⅱ) in 1; good results were achieved after 1-6 months of hyperbaric oxygen, acupuncture and physiotherapy. During the follow-up period for 6 to 24 months, the tumor recurred in 2 with Simpson Ⅲstage resection (5.7％). Conclusion Designing a detailed pre-operative design according to the MRI,MRA, DSA and CTA, application of microsurgical techniques, avoidance of damage to the cerebral cortex and veins of central suleus and protection of the sagittal sinus are important factors that increase the success rate of surgical resection, reduce complications, prevent the tumor recurrence and improve the survival outcome in patients with parasagittal meningiomas.

Pituitary adenomas (PAs) are well known as a common intracranial benign tumor, and a portion of PAs are refractory to current therapeutic methods. ErbB receptors family signaling pathway regulates the expression of PAs activation associated gene. Inhibition of epidermal growth factor receptor (EGFR) can inhibit proliferation of PAs. Leucine-rich repeats and immunoglobulin-like domains protein 1 ( LRIG1), a negative mediated gene of ErbB receptors family, plays a role in many tumors. However, there are seldom researches about the functional role of LRIG1 in PAs. The aim of this study is to explore the potential effect of LRIG1 and its regulating mechanism in PAs. First, we investigated the role of LRIG1 in cell migration, invasion of PAs with transfected LRIG1 or control. Then, we explored its impact on cell proliferation and apoptosis of PAs in vivo. To study the regulating mechanism of LRIG1, we examined the expression of molecular factor of PI3K/AKT and Ras/Raf/ERK pathway using Western blotting in vitro and RT-PCR in vitro and in vivo. It was found that LRIG1 over-expression inhibited cell migration, invasion and proliferation, and promoted apoptosis of PAs in vivo and in vitro. Furthermore, LRIG1 suppressed the expression of signaling of PI3K/AKT and Ras/Raf/ERK pathways in PAs. LRIG1, as a negative mediated gene of tumor, can inhibit biological function of PAs via inhibiting PI3K/AKT and Ras/Raf/ERK pathways, and it might be a new target for gene therapy of PAs.
Animals ; Apoptosis ; genetics ; Brain Neoplasms ; genetics ; pathology ; Cell Line, Tumor ; Cell Movement ; genetics ; Cell Proliferation ; genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; MAP Kinase Signaling System ; genetics ; Membrane Glycoproteins ; biosynthesis ; genetics ; Mice ; Oncogene Protein v-akt ; biosynthesis ; Phosphatidylinositol 3-Kinases ; genetics ; Pituitary Neoplasms ; genetics ; pathology ; Xenograft Model Antitumor Assays ; raf Kinases ; biosynthesis ; genetics