A nomogram based on radiomics and clinical information to predict prognosis in percutaneous balloon compression for the treatment of trigeminal neuralgia.

OBJECTIVE: To develop a clinical-radiomics nomogram based on clinical information and radiomics features to predict the prognosis of percutaneous balloon compression (PBC) for the treatment of trigeminal neuralgia (TN). METHODS: The retrospective study involved clinical data from 149 TN patients undergoing PBC at Zhongnan Hospital, Wuhan University from January 2018 to January 2022. The free open-source software 3D Slicer was used to extract all radiomic features from the intraoperative X-ray balloon region. The relationship between clinical information and TN prognosis was analyzed by univariate logistic analysis and multivariate logistic analysis. Using R software, the optimal radiomics features were selected using the least absolute shrinkage and selection operator (Lasso) algorithm. A prediction model was constructed based on the clinical information and radiomic features, and a nomogram was visualized. The performance of the clinical radiomics nomogram in predicting the prognosis of PBC in TN treatment was evaluated using the area under the receiver operating characteristic curve (AUC) and decision curve analysis (DCA). RESULTS: A total of 149 patients were eventually included. The clinical factors influencing the prognosis of TN in univariate analysis were compression severity score and TN type. The lasso algorithm Max-Relevance and Min-Redundancy(mRMR) was used to select two predictors from 13 morphology-related radiomics features, including elongation and surface-volume ratio. A total of 4 predictors were used to construct a prediction model and nomogram. The AUC was 0.886(95% confidence interval (CI), 0.75 to 0.96), indicating that the model's good predictive ability. DCA demonstrated the nomogram's high clinical applicability. CONCLUSION: Clinical-radiomics nomogram constructed by combining clinical information and morphology-related radiomics features have good potential in predicting the prognosis of TN for PBC treatment. However, this needs to be further studied and validated in several independent external patient populations.

A nomogram based on clinical multivariate factors predicts delayed cure after microvascular decompression for hemifacial spasm.

BACKGROUND: The course of disease after microvascular decompression (MVD) in patients with hemifacial spasm (HFS) is variable. The purpose of this study was to develop and validate a nomogram to predict the probability of delayed cure after microvascular decompression in patients with hemifacial spasms based on clinical multivariate factors. METHODS: A retrospective data collection was performed on 290 patients with HFS undergoing MVD at our center from January 2017 to January 2022. The patients were randomly assigned to the training cohort (n = 232) and validation cohort (n = 58) at a ratio of 8:2. Retrospective analysis was performed of information on clinical, radiological, and intraoperative findings and clinical outcomes. Univariate and multivariate analyses were performed in the training cohort, and a nomogram was constructed using a stepwise logistic regression approach. The receiver operating characteristic (ROC) was calculated to evaluate the reliability of the nomogram model. Decision curve analysis (DCA) was used to assess the clinical application value of the nomogram model. RESULTS: In the training cohorts, 73 patients (73/232) had a delayed cure. In the validation cohorts, 18 patients (18/58) had a delayed cure. We developed a novel nomogram model to predict the risk of delayed cure after MVD in HFS patients based on the presence of vertebral artery compression, venous compression, absence of LSR, degree of facial nerve indentation, degree of neurovascular compression, and internal auditory canal vascular looThe area under the curve (AUC) of the nomogram model was 0.9483 in the training cohort and 0.9382 in the validation cohort. The calibration curve showed good correspondence between the predicted and actual probabilities in the training and validation groups. The decision curve showed that the nomogram model had good performance in clinical applications. CONCLUSIONS: We developed and validated a preoperative and intraoperative multivariate factors nomogram to predict the possibility of delayed cure after MVD in HFS patients, which may help clinicians in the comprehensive management of HFS.

Mechanistic insight into glioma through spatially multidimensional proteomics.

Characterizing the tumor microenvironment at the molecular level is essential for understanding the mechanisms of tumorigenesis and evolution. However, the specificity of the blood proteome in localized region of the tumor and its linkages with other systems is difficult to investigate. Here, we propose a spatially multidimensional comparative proteomics strategy using glioma as an example. The blood proteome signature of tumor microenvironment was specifically identified by in situ collection of arterial and venous blood from the glioma region of the brain for comparison with peripheral blood. Also, by integrating with different dimensions of tissue and peripheral blood proteomics, the information on the genesis, migration, and exchange of glioma-associated proteins was revealed, which provided a powerful method for tumor mechanism research and biomarker discovery. The study recruited multidimensional clinical cohorts, allowing the proteomic results to corroborate each other, reliably revealing biological processes specific to gliomas, and identifying highly accurate biomarkers.

Predictive value of the SLC22A18 protein expression in glioblastoma patients receiving temozolomide therapy.

BACKGROUND: Our previous study showed that SLC22A18 downregulation and promoter methylation were associated with the development and progression of glioma and the elevated expression of SLC22A18 was found to increase the sensitivity of glioma U251 cells to the anticancer drug 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). In this study, we investigated the predictive value of SLC22A18 promoter methylation and protein expression in glioblastoma multiforme (GBM) patients receiving temozolomide (TMZ) therapy. PATIENTS AND METHODS: SLC22A18 promoter methylation and protein expression were examined by methylation-specific polymerase chain reaction (MSP) and Western blotting respectively, then we compared SLC22A18 promoter methylation and protein expression in tumor cell explants in regard to prediction of TMZ response and survival time of 86 GBM patients. RESULTS: SLC22A18 promoter methylation was detected in 61 of 86 (71%) samples, whereas 36 of 86 (42%) cases were scored positive for SLC22A18 protein expression. Overall SLC22A18 promoter methylation was significantly related to SLC22A18 protein expression, but a subgroup of cases did not follow this association. Multivariate Cox regression analysis indicated that SLC22A18 protein expression, but not promoter methylation, was significantly correlated with TMZ therapy. SLC22A18 protein expression predicted a significantly shorter overall survival in 51 patients receiving TMZ therapy, whereas no differences in overall survival were observed in 35 patients without TMZ therapy. CONCLUSIONS: These results show that lack of SLC22A18 protein expression is superior to promoter methylation as a predictive tumor biomarker in GBM patients receiving temozolomide therapy.

[Retracted] Anti­carcinogenic activity of anandamide on human glioma in vitro and in vivo.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the scratch-wound data shown in Fig. 3A were strikingly similar to data appearing in different form in another article by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 13: 1558­1662, 2016; DOI: 10.3892/mmr.2015.4721].

Upregulation of SATB1 is associated with the development and progression of glioma.

BACKGROUND: Special AT-rich sequence-binding protein-1 (SATB1) has been reported to be expressed in several human cancers and may have malignant potential. This study was aimed at investigating the expression and potential role of SATB1 in human glioma. METHOD: The relationship between SATB1 expression, clinicopathological parameters, Ki67 expression and MGMT promoter methylation status was evaluated, and the prognostic value of SATB1 expression in patients with gliomas was analyzed. SATB1-specific shRNA sequences were synthesized, and U251 cells were transfected with SATB1 RNAi plasmids. Expression of SATB1 mRNA and protein was investigated by RT-PCR and immunofluoresence staining and western blotting. The expression of c-Met, SLC22A18, caspase-3 and bcl-2 protein was determined by western blotting. U251 cell growth and adherence was detected by methyl thiazole tetrazolium assay. The apoptosis of U251 cells was examined with a flow cytometer. The adherence, invasion, and in vitro angiogenesis assays of U251 cells were done. The growth and angiogenesis of SATB1 low expressing U251 cells was measured in an in vivo xenograft model. RESULTS: Of 70 tumors, 44 (62.9%) were positive for SATB1 expression. SATB1 expression was significantly associated with a high histological grade and with poor survival in univariate and multivariate analyses. SATB1 expression was also positively correlated with Ki67 expression but negatively with MGMT promoter methylation in glioma tissues. SATB1 shRNA expression vectors could efficiently induce the expression of SLC22A18 protein, increase the caspase-3 protein, inhibit the expression of SATB1, c-Met and bcl-2 protein, the growth, invasion, metastasis and angiogenesis of U251 cells, and induce apoptosis in vitro. Furthermore, the tumor growth of U251 cells expressing SATB1 shRNA were inhibited in vivo, and immunohistochemical analyses of tumor sections revealed a decreased vessel density in the animals where shRNA against SATB1 were expressed. CONCLUSIONS: SATB1 may have an important role as a positive regulator of glioma development and progression, and that SATB1 might be a useful molecular marker for predicting the prognosis of glioma.

Comparison of Sex Differences in Outcomes of Patients With Aneurysmal Subarachnoid Hemorrhage: A Single-Center Retrospective Study.

Background: Sex differences in the outcomes of patients with aneurysmal subarachnoid hemorrhage (aSAH) remain controversial. The aim of this study was to evaluate sex differences in the outcomes of patients with aSAH. Method: This study retrospectively analyzed the clinical data of consecutive patients with aSAH, admitted to the Department of Neurosurgery, Wuhan University Zhongnan Hospital, from May 1, 2020 to December 31, 2020. The modified Rankin Scale (mRS) score was used to evaluate the prognosis of patients at discharge. Outcome indicators included cerebral ischemia, hydrocephalus, and mRS ≥ 2 at discharge. Results: The majority (65%) of the 287 patients with aSAH included in the study were females. Patients were divided into female (n = 184) and male (n = 99) groups; the female patients were significantly older than the male patients (61.3 ± 8.5 years vs. 60.0 ± 8.5 years, p = 0.032). The incidence of comorbidities (hypertension, diabetes, and heart disease) was higher in the female group than in the male group, but the difference was not statistically significant. Although more female patients than male patients underwent endovascular treatment, there was no statistical difference in the treatment approach between the two groups. Comparison of post-operative complications and mRS scores at discharge revealed that the rate of cerebral ischemia and mRS ≥ 2 at discharge were significantly higher among female patients than among male patients. Moreover, this difference persisted after propensity adjustment for age and treatment approach. Analysis of risk factors for poor prognosis at discharge in both pre- and post-adjustment patients revealed cerebral ischemia and high mFisher score (mFisher = 3/4) to be independent risk factors. Conclusion: Female patients with aSAH have a worse prognosis than male patients, and this difference may be because women are more susceptible to cerebral ischemia.

Promoter methylation and downregulation of SLC22A18 are associated with the development and progression of human glioma.

BACKGROUND: Downregulation of the putative tumor suppressor gene SLC22A18 has been reported in a number of human cancers. The aim of this study was to investigate the relationship between SLC22A18 downregulation, promoter methylation and the development and progression of human glioma. METHOD: SLC22A18 expression and promoter methylation was examined in human gliomas and the adjacent normal tissues. U251 glioma cells stably overexpressing SLC22A18 were generated to investigate the effect of SLC22A18 on cell growth and adherence in vitro using the methyl thiazole tetrazolium assay. Apoptosis was quantified using flow cytometry and the growth of SLC22A18 overexpressing U251 cells was measured in an in vivo xenograft model. RESULTS: SLC22A18 protein expression is significantly decreased in human gliomas compared to the adjacent normal brain tissues. SLC22A18 protein expression is significantly lower in gliomas which recurred within six months after surgery than gliomas which did not recur within six months. SLC22A18 promoter methylation was detected in 50% of the gliomas, but not in the adjacent normal tissues of any patient. SLC22A18 expression was significantly decreased in gliomas with SLC22A18 promoter methylation, compared to gliomas without methylation. The SLC22A18 promoter is methylated in U251 cells and treatment with the demethylating agent 5-aza-2-deoxycytidine increased SLC22A18 expression and reduced cell proliferation. Stable overexpression of SLC22A18 inhibited growth and adherence, induced apoptosis in vitro and reduced in vivo tumor growth of U251 cells. CONCLUSION: SLC22A18 downregulation via promoter methylation is associated with the development and progression of glioma, suggesting that SLC22A18 is an important tumor suppressor in glioma.

Brain abscess associated with ventricular septal defect and Eisenmenger syndrome: A case report.

INTRODUCTION AND IMPORTANCE: Brain abscess is a potentially fatal neurological infection, despite the development of new antimicrobial agents and modern neurosurgical techniques. CASE PRESENTATION: We present an uncommon case where a large brain abscess was treated successfully in a patient with Eisenmenger syndrome. He was underwent neurosurgical treatment and eventually recovered. CLINNICAL DISCUSSION: The etiology of a brain abscess in patients with congenital cyanotic heart disease has multiple aspects. In this patient population was high risk for developing perioperative complications.The preoperative evaluation, intraoperative management and postoperative care are important steps in the treatment of cardiac patients undergoing noncardiac surgery, and essential for patient's safe and fast recovery. CONCLUSIONS: We highlight the importance of the diagnosis and management of Eisenmenger syndrome to help us further understand this rare and fatal disease.

Immunohistochemistry analysis of Pygo2 expression in central nervous system tumors.

Pygo2 as a Wnt signaling pathway component has been detected in multiple cancer types. In this study, we identified Pygo2 expression features by immunohistochemistry in 73 central nervous system tumor specimens, in comparison with 14 normal brain tissues and surrounding non-tumorous tissues of tumor. Our study indicated that 59% of the patient tumor specimens exhibited positive Pygo2-staining and increases intensity with the grade of malignancy, especially for WHO grade III and IV gliomas, was observed high level expression, compared with normal brain tissues. Five out of nine WHO grade III anaplastic astrocytomas and seven out of nine WHO grade IV glioblastomas showed Pygo2-positive staining. The analysis of Pygo2 gene expression by quantitative real-time PCR of additional ten fresh patient samples yielded similar results. Further studies performed with stable cell lines in vitro demonstrated that Pygo2 render cells higher proliferation rate, migration and anchorage-independent colony-forming ability in soft agar. Taken together, our studies suggest an important role of Pygo2 in brain tumor progression.

The use of endoscopic-assisted burr-hole craniostomy for septated chronic subdural haematoma: A retrospective cohort comparison study.

OBJECTIVE: To complete a retrospective comparison of endoscope-assisted burr-hole craniostomy (EBHC) and ordinary burr-hole craniostomy (OBHC) in the treatment of septated chronic subdural hematoma (SCSH). METHODS: A retrospective case note review comparing EBHC and OBHC of SCSH was therefore performed. Data of patients with a SCSH for EBHC or OBHC during the period from January 2011 to December 2016 were retrospectively collected and analysed. Of 73 patients, 42 underwent EBHC and 31 patients were treated by OBHC. The primary outcome measure was recurrence rate and secondary outcome measures were clinical outcome at first postoperative day, discharge and 6 months, the length of hospital stay for neurosurgery, the operative time, and the placement time of drainage tube. RESULT: The rate of recurrence was significantly lower in the EBHC (0/42 0%) than in the OBHC (8/31, 25.8%) group (p = .0030). The rate of morbidity was significantly lower in the EBHC (2/42, 4.8%) than in the OBHC (11/31, 35.5%) group (p = .0121). At 30 days, mortality did not differ between groups. Significantly more patients treated with EBHC were alive at 6 months than were those with OBHC. No patient died as a consequence of the operative procedure in the both groups. A discharge GCS of 15 was recorded in more participants with EBHC than in those with OBHC. Gross neurological deficit was significantly less frequent in those with EBHC than in those with OBHC at first postoperative day and discharge, but did not differ at 6 month follow-up. The mean placement time of drainage tube was significantly less in those with EBHC (27.2 h) than in those with OBHC (52.0 h, p = .0055). The mean length of hospital stay for neurosurgery was 4 days in the EBHC group, while it was 5 days in the OBHC group (p = .0015). The mean hematoma reduction rate was significantly higher in those with EBHC than in those with OBHC at first postoperative day (85.3% vs 72.5%, p = .0037) and discharge (90.3% vs 85.1%, p = .0127). CONCLUSION: Comparing two minimally invasive procedure protocols for treatment of SCSH, EBHC is a safe and effective surgical technique. It significantly surpasses the results obtained in OBHC in lowering recurrence rate, morbidity rate, placement time of drainage tube, and length of hospital stay for neurosurgery. We recommend EBHC technique to be widely used in the treatment of SCSH, even common chronic subdural hematoma (CSH), subacute and acute subdural hematomas, acute epidural hematomas and empyemas to avoid large craniotomies, particularly in elderly patients, so that patients can receive the best treatment on the basis of minimal trauma.

Giant Serpentine Aneurysm of the Middle Cerebral Artery.

BACKGROUND: Giant serpentine aneurysms (GSAs) are a subgroup of giant intracranial aneurysms, distinct from saccular and fusiform varieties, that are defined as partially thrombosed giant aneurysms with tortuous internal vascular channel. Clinicopathologic characteristics of middle cerebral artery GSAs have been rarely reported in the literature, with discussion of radiologic characteristics only. We clarify patient clinical and neuroradiologic features and discuss the mechanism of formation and progression. CASE DESCRIPTION: A 43-year-old woman presented with a GSA arising from the middle cerebral artery. There was a separate inflow and outflow channel of the aneurysm, with the outflow channel feeding the distal branches of the parent artery and supplying normal brain parenchyma. The GSA was treated successfully by aneurysmectomy and superficial temporal artery-middle cerebral artery bypass followed by proximal occlusion and vascular reconstruction. An aneurysm specimen was examined to correlate pathologic findings and morphologic characteristics. RESULT: Pathologic results showed that thickness of the aneurysmal wall was typically increased and varied, and no internal elastic lamina or endothelial lining could be identified. The sac contained thrombi of various ages with recanalizing vessel formation and chronic inflammation infiltration. Intimal hyperplasia and neoangiogenesis in the wall and hyaline degeneration of the media were observed. Vessels coursing in their adventitia showed mucoid changes, which are responsible for the contrast enhancement of the aneurysmal rim on computed tomography scan. CONCLUSIONS: GSAs are a specific pathologic entity with unique morphologic and pathologic characteristics that can affect intracranial blood vessels. The pathogenic mechanisms are unclear; this report suggests that GSAs may be associated with degeneration of the vascular wall.

C-Met antisense oligodeoxynucleotide inhibits growth of glioma cells.

BACKGROUND: C-Met, a receptor tyrosine kinase, and its ligand, hepatocyte growth factor, are critical in cellular proliferation, motility, and invasion and are known to be overexpressed in gliomas. The aim of our study was therefore to investigate the effect of transfected caroboxyfluorescein-5-succimidyl ester (FAM)-labeled c-Met antisense oligonucleotide (ASODN) on growth of glioma cells. METHODS: Conjugated FAM-labeled c-Met ASODN was encapsulated by LIPOFECTAMINE PLUS Reagent and then added into the human glioma cell line U251. Cultured cells were divided into 5 groups: control group, 500 nmol/L nonsense oligonucleotide (NSODN) group, 250 nmol/L ASODN group, 500 nmol/L ASODN group, and 750 nmol/L ASODN group. The intracellular distribution of c-Met ASODN was observed with fluorescence microscopy; cell growth was detected by methyl thiazole tetrazolium assay. The apoptosis of U251 cells was also examined with a flow cytometer. Semiquantitative reverse transcriptase polymerase chain reaction and Western blot examinations were carried for expression of c-Met messenger RNA (mRNA) and protein. RESULTS: The blue fluorescence was seen in the cytoplast and nuclei of cells of FAM-labeled c-Met ASODN groups with fluorescence microscopy after the cells were treated with FAM-labeled c-Met ASODN-LIPOFECTAMINE PLUS Reagent complex for 3 hours. Antisense (AS) oligonucleotide caused a statistically significant reduction of cell viability (P < .05), whereas NSODN had no such changes. The cell growth was also significantly inhibited by ASODN (P < .05). After transfection, 250, 500, and 750 nmol/L ASODN induced significant apoptotic response, about 4.67% +/- 2.86%, 8.65% +/- 3.18%, and 12.76% +/- 3.15% for 24 hours (P < .05) and 7.79% +/- 1.92%, 11.43% +/- 1.54%, and 15.78% +/- 1.86% for 48 hours (P < .01), respectively. However, 500 nmol/L NSODN did not induce any significant apoptotic response until 48 hours after transfection (P > .05). A significant loss of c-Met mRNA was presented in ASODN-treated cells, and this was not seen in treatment with NSODN. Protein level was significantly decreased 48 hours after c-Met ASODN transfected. CONCLUSIONS: Antisense oligonucleotide targeting c-Met can be identified as a most potent AS compound, which can inhibit cell growth and induce cell apoptosis. This provides evidence that c-Met plays a role in tumor progression of glioma by acting as an oncogene and suggests that c-Met ASODN may provide a novel approach to therapy for human glioma.

Clustering of self-organizing map identifies five distinct medulloblastoma subgroups.

BACKGROUND: Medulloblastoma is one the most malignant paediatric brain tumours. Molecular subgrouping these medulloblastomas will not only help identify specific cohorts for certain treatment but also improve confidence in prognostic prediction. OBJECTIVE: Currently, there is a consensus of the existences of four distinct subtypes of medulloblastoma. We proposed a novel bioinformatics method, clustering of self-organizing map, to determine the subgroups and their molecular diversity. METHODS: Microarray expression profiles of 46 medulloblastoma samples were analysed and five clusters with distinct demographics, clinical outcome and transcriptional profiles were identified. RESULTS: The previously reported Wnt subgroup was identified as expected. Three other novel subgroups were proposed for later investigation. CONCLUSIONS: Our findings underscore the value of SOM clustering for discovering the medulloblastoma subgroups. When the suggested subdivision has been confirmed in large cohorts, this method should serve as a part of routine classification of clinical samples.

Anti-carcinogenic activity of anandamide on human glioma in vitro and in vivo.

The poor prognosis of gliomas is to a large extent attributed to the markedly proliferative and invasive nature of the disease. Endocannabinoids have emerged as novel potential anti-tumor agents. The present study aimed to investigate the anti-carcinogenic activity of anandamide (AEA), an endocannabinoid, on glioma cells. To assess the functional role of AEA in glioma, the effects of AEA on cell proliferation, migration, invasion, apoptosis and the cell cycle in vitro, and tumor growth in vivo, were investigated. AEA markedly inhibited the proliferation of U251 cells in a dose- and time-dependent manner. Flow cytometric assays revealed that the apoptosis rate of U251 cells upon treatment with AEA was increased. AEA also suppressed the adhesion, migration and invasion capabilities of the U251 cells. Furthermore, AEA inhibited tumor growth in vivo. These results highlighted the potential role of AEA in the tumorigenesis and progression of glioma, and suggested that AEA exhibits therapeutic potential in the management of human glioma.

[The expression of hepatocyte growth factor and its receptor in brain astrocytomas].

OBJECTIVE: To investigate the expression of hepatocyte growth factor (HGF) mRNA and its receptor (c-Met) mRNA in brain astrocytomas and their relationships with tumor proliferation, angiogenesis, clinical pathology and prognosis. METHODS: The expression of HGF mRNA, c-Met mRNA in the resected tumor tissues of 76 patients with brain astrocytomas, 43 males and 33 females, aged 20 - 71, were detected by in situ hybridization. Immunohistochemistry technique was used to test the expression of proliferating cell nuclear antigen (PCNA) protein and the microvessel density (MVD) was determined by immunohistochemistry with monoclonal antibody against CD34. RESULTS: The positive rates of expression of HGF, c-Met and PCNA in low pathologic grades of brain astrocytoma were 34.5%, 44.8% and 15% +/- 9% respectively, and in high pathologic grades of brain astrocytoma were 34.5%, 44.8% and 48% +/- 12% respectively (P < 0.05). MVD in low and high pathologic grades of brain astrocytoma were 17 +/- 7 and 31 +/- 13 respectively (P < 0.05). The expression of HGF, c-Met, PCNA and CD34 was not related to sex, age, position of tumor and diameter of tumor. The expression of c-Met was related to the expression of HGF, PCNA and the MVD in the tumor tissues of these patients. The pathological grade, position of tumor, HGF, c-Met, PCNA, MVD had a significant influence on the survival time. CONCLUSION: HGF/c-Met plays an important role in the formation and progression of the brain astrocytoma and can promote tumor proliferation and intratumoral microvascular formation, and is closely related to the prognosis of the patients.

Computational analysis identifies invasion-associated genes in pituitary adenomas.

Pituitary adenomas are considered to be benign tumours. However, they can infiltrate surrounding tissues, which may cause a failure of complete removal during surgical resection. Thus far, no molecular biomarkers have been identified, which are able to reliably predict the behaviour of this type of tumour. In the present study, a list of differentially expressed genes in invasive pituitary adenomas was obtained using a computational bioinformatics analysis on the DNA microarray expression profiles. The gene expression datasets of a total of 16 samples were retrieved from the National Center for Biotechnology Information Gene Expression Omnibus database. The gene set enrichment analysis was later conducted on the significantly (FDR<0.05) differentially expressed genes. A total of 194 genes were identified as differentially expressed. The pathway impact analysis revealed that cell adhesion molecules may be vital in the progression of pituitary adenoma invasion. A total of six genes, claudin 7, contactin associated protein-like 2, integrin α6, junctional adhesion molecule 3, protein tyrosine phosphatase, receptor type C and cadherin-associated protein α1 were identified as molecular biomarkers for pituitary adenoma invasion. The present study identified six novel molecular biomarkers, which may be used for diagnostic or therapeutic purposes. However, further experimental investigations are required to validate the present findings.

Correlation between SATB1 and Bcl-2 expression in human glioblastoma multiforme.

Special AT-rich sequence-binding protein-1 (SATB1) has been reported to be overexpressed in numerous human tumors. The aim of the present study was to determine the correlation and clinical significance between the expression of SATB1 and B-cell lymphoma 2 (Bcl-2) in human glioblastoma multiforme (GBM). Samples from 70 patients with GBMs were analyzed and 10 normal brain tissues were used as the control group. In situ hybridization was used to detect SATB1 mRNA expression and immunohistochemistry was used to detect Bcl-2 and proliferating cell nuclear antigen (PCNA) protein expression. Apoptosis was detected with flow cytometry. The SATB1 mRNA and Bcl-2 protein levels were found to be significantly higher in GBM tissues than in normal brain and their levels were associated with patient survival, but not associated with patient gender, age and tumor size and site. A positive correlation was observed between SATB1 mRNA and Bcl-2 protein and between SATB1 mRNA and PCNA. A negative correlation was observed between SATB1 mRNA and apoptosis and between Bcl-2 and apoptosis. A positive correlation existed between Bcl-2 and PCNA. Patients with GBM identified as SATB1 mRNA (+) and Bcl-2 (+) were associated with a poor prognosis. Therefore, assessment of SATB1 and Bcl-2 co-expression may provide important information for the diagnosis, therapy and prognosis of GBM.

Relationship between SATB1 expression and prognosis in astrocytoma.

Special AT-rich-sequence-binding protein 1 (SATB1), a new type of gene regulator, has been reported to be expressed in various human cancers and may be associated with malignancy. The aim of this study was to investigate the expression of SATB1 in astrocytoma and to determine its prognostic value for the overall survival of patients with astrocytoma. The expression of SATB1 protein and messenger RNA (mRNA) in human astrocytoma specimens was examined using immunohistochemistry and semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). The relationship between SATB1 expression and O-6-methylguanine-DNA methyltransferase (MGMT) promoter methylation status was also investigated. Spearman's correlation coefficient was used to describe the association between SATB1 expression and the clinical parameters of astrocytoma patients. SATB1 protein and mRNA were expressed at significant levels in astrocytoma specimens. SATB1 expression was positively correlated with astrocytoma pathological grade but negatively correlated with the life span of astrocytoma patients. SATB1 expression was also significantly lower in astrocytoma specimens with MGMT promoter methylation than in those without MGMT promoter methylation. Our findings suggest that SATB1 may have an important role as a positive regulator of astrocytoma development and progression and that SATB1 might be a useful molecular marker for predicting the prognosis of patients with astrocytoma and could be a novel target for treating astrocytoma.