Overexpression of TREM2 enhances glioma cell proliferation and invasion: a therapeutic target in human glioma.

Gliomas are the most common and aggressive type of primary adult brain tumors. Although TREM2 mutation is reported to be related to Nasu-Hakola disease and Alzheimer's disease, little is known about the association between TREM2 and gliomas. Here, we reported that TREM2 was significantly overexpressed in glioma tissues compared with non-tumorous brain tissues. Furthermore, TREM2 expression was closely related to pathological grade and overall survival of patients with gliomas. Down-regulation of TREM2 in two glioma cell lines, U87 and U373, resulted in a significant reduction in cell proliferation, migration and invasion and a dramatic increase in S phase arrest and apoptosis. In vivo tumorigenesis experiment also revealed that depletion of TREM2 expression inhibited U87 cell proliferation. Moreover, based on gene set enrichment analysis (GSEA) with The Cancer Genome Atlas (TCGA) dataset, we found that TREM2 was positive related to Kyoto Encyclopedia of Genes and Genomes (KEGG) apoptosis, Cromer metastasis and KEGG chemokine pathways, which was further validated by western blot in TREM2 knockdown glioma cells and indicated a possible mechanism underlying its effects on glioma. In summary, our study suggests that TREM2 may work as an oncogene and a new effective therapeutic target for glioma treatment.

TMEM140 is associated with the prognosis of glioma by promoting cell viability and invasion.

BACKGROUND: Gliomas are the most common types of primary brain tumors in the adult central nervous system. TMEM140 is identified as an amplified gene in the human gastric cancer genome. However, the function of TMEM140 in gliomas has not been thoroughly elucidated. The aim of the current study was to determine the clinical significance of TMEM140 expression in patients with gliomas and its effect on tumor cell malignant phenotypes. METHODS: Immunohistochemical analysis and real-time reverse transcription PCR were performed to detect the expression levels of TMEM140 in 70 glioma brain tissue samples. Next, the correlation between the TMEM140 expression levels and the clinical characteristics and outcomes of glioma patients was statistically analyzed. TMEM140 expression was inhibited in two glioma cell lines (i.e., U87 and U373) using a knockdown method with small interfering RNA. Cell Counting Kit-8 and Transwell assays were used to investigate TMEM140 function during cell proliferation, invasion, and migration, respectively. Using flow cytometry and Western blot analysis, we subsequently determined the cell cycle and apoptosis profile of the TMEM140-silenced cells. RESULTS: TMEM140 protein expression was significantly higher in gliomas than in normal brain tissues (p < 0.0001). TMEM140 overexpression was strongly correlated with tumor size, histologic grade, and overall survival time (P < 0.05). TMEM140 decreased cell viability in vitro and dramatically decreased tumor volume in vivo. This phenomenon might be caused by G1 phase cell cycle arrest and cell apoptosis. TMEM140 silencing could suppress the viability, migration, and invasion of glioma cells. CONCLUSIONS: Our results suggest that TMEM140 expression is a prognostic factor that might play an important role in the viability, migration, and invasion of glioma cells. This study highlights the importance of TMEM140 as a novel prognostic marker and as an attractive therapeutic target for gliomas.

Clinical Characteristics and Treatment of Trigeminal Neuralgia Following Herpes Zoster.

OBJECTIVE: The aim of this study was to illustrate the clinical characteristics and treatment of trigeminal neuralgia following herpes zoster. METHODS: From August 1, 2011 to August 1, 2013, 23 consecutive patients with trigeminal neuralgia following herpes zoster underwent microvascular decompression (MVD) at our cranial nerve disease center. All patients underwent preoperative MRI evaluation, intraoperative observation, and clinical effect evaluation. Clinical data were collected and analyzed in our center. RESULTS: V2 division was the most commonly affected branch. Unlike pretrigeminal neuralgia (PTN), trigger zone was only found in a small part of patients (21.7%). Unlike PTN, the adhesions and compressions between trigeminal nerve and offending vessels were usually not serious; trigeminal nerve usually is atrophic; superior cerebellar artery was the most common offending vessels (65.2%). Of 23 patients, 19 experienced pain relief (82.6%), 1 patient suffered from hearing loss, and another one suffered from cerebrospinal fluid leak; no severe complications were found. During follow-up period, no recurrence was found (3 lost). CONCLUSIONS: For patients who suffered from trigeminal neuralgia following herpes zoster, trigger zone was only found in a small part of patients. The trigeminal nerve usually is atrophic; microvascular decompression was equally applied to these patients if vessel compression was confirmed.

Surgical skills of adhesions and transposition of trigeminal nerve for primary trigeminal neuralgia.

OBJECTIVE: The aims of this study were to investigate disposal of adhesions and transposition of the trigeminal nerve during microvascular decompression and evaluate its surgical effect. METHODS: By collecting the clinical data of typical trigeminal neuralgia patients we treated from January 2013 to May 2013, we chose 120 patients with adhesions and transposition of trigeminal nerve, analyzed their preoperative imaging features and surgical procedures, and evaluated postoperative effect after 3-month follow-up. RESULTS: Among these 120 patients, 113 cases showed positive effect in magnetic resonance imaging (three-dimensional time-of-flight); the positive rate was 94.2%. During the operation, firstly we proceed to separate the nerve and artery, secondly we released the vascular compression, finally we removed the superior cerebellar artery to the nerve's head end. Postoperative effect evaluation stated that 101 patients showed immediate remission and 13 patients showed delayed remission (3 min after operation) and the surgery was ineffective for 6 patients; the remission rate was 95%. There were no severe complications. CONCLUSIONS: Magnetic resonance imaging (three-dimensional time-of-flight) before operation could clearly display the neurovascular relationship of trigeminal neuralgia patients. It offers great help for preoperative evaluation. Separation between arachnoid, nerve, and artery; vascular decompression; and removal of the superior cerebellar artery to the head end could resolve adhesions and transposition of trigeminal nerve during microvascular decompression, which showed significant effects.

The strategy of microvascular decompression for hemifacial spasm: how to decide the endpoint of an MVD surgery.

OBJECTIVE: Microvascular decompression (MVD) has become the standard treatment for hemifacial spasm. As not all patients get complete relief, this strategy is still controversial. The study aimed to figure out how to tell the proper endpoint to the surgery. METHODS: A series of 356 consecutive patients with hemifacial spasm were enrolled in this study. All patients fell into two groups according to the period they presented. Two different criteria (simple criterion vs. complex criterion) to end an operation were applied respectively. The intra-operative finding, results and complications of these two groups were compared. The advantage of the complex criterion was analyzed. RESULTS: The group which used complex criterion got better results than the group which used simple criterion. The complex criterion which combines full-length evidence, vascular evidence and electrophysiological evidence proved to be reliable to tell the proper endpoint to the surgery. CONCLUSION: MVD operations can be ended only after the full-length evidence, vascular evidence and electrophysiological evidence are all present.

Clinical characteristics and surgical techniques of trigeminal neuralgia caused simply by venous compression.

OBJECTIVE: The objective of this study was to introduce the operation essentials for treatment of patients with vein compression so as to obtain a satisfactory decompression without sacrificing veins. METHODS: We chose 15 patients with trigeminal neuralgia caused by venous from June 15, 2010, through June 15, 2011, and performed microvascular decompression for each patient. By collecting clinical data, such as preoperative magnetic resonance imaging scans, key operative procedures, surgical outcomes, and complications, we explored the operation techniques for these patients and finally summarized our experiences and ideas. RESULTS: For all the 15 patients, 9 cases had excellent remission, 3 cases had delayed excellent remission, 1 case had good remission, and 2 cases had failed result; the total remission rate was 86.7%; 3 cases had facial numbness. CONCLUSIONS: For patients with vein compression, we combine the following 4 procedures together: (1) fully releasing the arachnoid around trigeminal nerve, (2) exploration and decompression of the whole trigeminal root from Meckel cave to pons, (3) cauterization of companioned petrosal vein tributaries by bipolar coagulation, and (4) placing Teflon between trigeminal nerve and offending petrosal vein, thus could acquire a satisfactory effect (remission rate, 86.7%).