No abstract available.
Glioblastoma*

Background & Objective: Radiotherapy and temozolomide are the standard therapy for newly diagnosed glioblastoma multiforme (GBM). However, it is unclear whether adding another agent to the commonly used radiotherapy-temozolomide (RT + TMZ) benefits newly diagnosed GBM patients. The present network meta-analysis aimed to assess the efficacy of combining other agents with RT + TMZ for GBM treatment. Methods: A comprehensive literature search was conducted on PubMed, EMBASE.com, Web of Science, and the Cochrane Central Register of Controlled Trials from inception to September 23, 2014, to include all randomized controlled trials of RT + TMZ-based therapy in GBM patients. Pairwise and network meta-analyses were performed to compare the therapeutic regimens. Results: Seventeen studies involving 4,148 patients were identified. The results of pairwise meta-analysis indicated no significant differences among most comparison groups, except for bevacizumab + RT + TMZ versus RT + TMZ for progression-free survival (hazard ratio [HR] = 0.71, 95% confidence interval [CI]: 0.59–0.86; P = 0.000) and RT + TMZ versus RT alone for overall survival (HR = 0.71, 95% CI: 0.58–0.88; P = 0.001). The results of network meta-analysis also showed no significant differences in most comparisons; however, adverse events were more common among patients receiving additional therapeutic agents other than RT + TMZ. The ranking probability analysis indicated that bevacizumab + RT + TMZ and nimustine + cisplatin + RT + TMZ were associated with the best progression-free and overall survival, but they also caused the most adverse events in GBM patients. RT + bevacizumab + irinotecan had the highest probability of being the best regimen for minimizing adverse events. Conclusions: The addition of other targeted agents, particularly bevacizumab and nimustine, to RT + TMZ could be slightly effective for the treatment of newly diagnosed GBM patients; however, adverse events remained common.
Glioblastoma

No abstract available.
Glioblastoma* ; HIV* ; Toxoplasmosis, Cerebral*

No abstract available.
Glioblastoma* ; Keratosis, Seborrheic

To assess the degree of malignancy in cerebral gliomas at the time of diagnosis, we compared the metabolic ratio using 18F-fluorodeoxyglucose(FDG)-Positron Emission Tomography(PET) with histologic grading and proliferative index(Ki-67) of cerebral gliomas. Materials for this study were histologically-examined 21 gliomas and they were divided into glioblastomas as group 1, anaplastic gliomas as group 2, and low-grade gliomas as group 3. The visual analysis of FDG-PET images showed hypermetabolic lesions in 14(87.5%) out of 16 high-grade gliomas (glioblastomas and anaplastic gliomas), and hypometabolic lesions in 4(80%) out of 5 low-grade gliomas. Tumor to cerebellum ratio(T/Cbll) in FDG-PET was used as metabolic ratio and the values of T/Cbll in each group were 1.30+/-0.10, 0.73+/-0.07, 0.70+/-0.07, respectively. In comparision of T/Cbll between group 1 with remaining two groups, differences were statistically significant(p=0.0002, p=0.0002, respectively), however, there was no statistical difference between group 2 and group 3. The values of Ki-67 were 24.16+/-5.66 in group 1, 8.10+/-2.70 in group 2, 5.46+/-1.23 in group 3, and differences were statistically significant between group 1 and group 2, 3(p=0.015, p=0.015, respectively), but there was no statistical difference between group 2 and group 3. The correlation between T/Cbll and Ki-67 was good and statistically significant(p=0.0047). In conclusion, the visual and semiquantitative analysis of FDG-PET would be helpful in determining the degree of malignancy in cerebral gliomas.
Cerebellum ; Diagnosis ; Glioblastoma ; Glioma*

No abstract available.
Cell Line* ; Glioblastoma* ; Humans*

It is well known that the cell type and histopathological grading of gliomas correlate well with clinicalcourse and prognosis. Therefore, it is tempting to set certain criteria that could predict the histopathologiccharacteristics of the gliomas before the surgical intervention. With a total of 56 cases of gliomas which wereverified histopathologically in Seoul National University Hospital between July 1978 and May 1983, a statisticalanalysis of the computed tomographic findings was done with the particular emphasis on the correlation withhistopatholoigcal features. The results are as follows; 1. The calcification is observed in 27 cases (48.2%) intotal: in 20 cases (62.5%) among low grade group, in 6 cases (46.1%) among high grade group and in 1 case (9.1%)among glioblastoma multiformed group respectively. 2. The mass effect, especially surrounding low densitycorrelates well with the grade of malignancy. 3. The contrast enhancement is observed in 43 cases (76.8%). Thepattern of enhancement provides clues for the assessment of cell type and grade with fair degree of reliability.Among low grade group, 10 cases (31.3%) show no enhancement and 10 cases show solid enhancement. Among high gradegroup, 6 cases (46.8%) show solid enhancement and nodular or ring enhancement are not observed. Among glioblastomamlultiform group, 8 cases (72.7%) show characteristic thick irregular ring enhancement. 4. Plain CT densities arenot useful in differentiating each group in statistically significant level. 5. Neither the margin of the mass northe degree of contrast enhancement contributes for the differentiation of each group. 6. Summarizing the abovementioned findings it is concluded that CT is very helpful in differentiating the gliomas with regard tohistopathological cell type and the grade of malignancy as well.
Glioblastoma ; Glioma ; Prognosis ; Seoul

Although melanoma only accounts for 1% of skin cancers, it is responsible for most skin cancer deaths. Glioblastoma multiforme, a high-grade astrocytoma, is the most aggressive and devastating primary brain tumor. These two diseases remain to be the biggest therapeutic challenge in both specialties of dermatology and neuro-oncology. A 53-year-old Filipino male who presented with a 2-year history of generalized dark brown and black patches on the body developed weakness and numbness of the left extremities. Biopsy and immunohistochemical staining of the skin revealed nodular melanoma with adjacent regressing melanoma. Biopsy of the intracranial mass showed glioblastoma multiforme. One month after the partial excision of the intracranial mass, the patient expired due to brain herniation. Nodular melanoma and glioblastoma multiforme may occur concomitantly in a patient. A review of the literature suggests a shared genetic predisposition. Its existence carries a poor prognosis and requires early detection to start aggressive treatment.
Melanoma ; Glioma ; Glioblastoma ; Association

Glioblastoma multiforme (GBM) represents the most malignant form of brain tumor and is relatively common, comprising nearly almost 20% of all primary malignancies of the central nervous system1. GBM is a WHO grade IV tumor with several variants, depending primarily on their genetic signature and on the predominant histological architecture. Among the variants of GBM, epithelioid glioblastoma (E-GBM) has been one of the more recently described. This tumor, documented to be highly malignant and clinically aggressive, has been separated from close variants and thus differentials, pleomorphic anaplastic xanthoastrocytoma, rhabdoid GBM, small cell and giant cell GBM, GBM with neuroectodermal differentiation, and gliosarcoma2. Autoimmune diseases have been linked within creased risk of CNS complications, from the constant effects of chronic inflammatory milieu. Systemic lupus erythematosus (SLE) has been associated with several CNS abnormalities, hence the terms CNS lupus or neuropsychiatric lupus. Likewise, SLE has been repeatedly associated with CNS malignancies in several cases and case reports. To date, there is paucity in the reported cases of malignant brain tumors, especially rare variants, in patients with SLE. While it is hypothesized that the inflammatory milieu that bathes the brain in a dynamic microenvironment that influences the incidence of rare variants of GBM, clinicians should be mindful, as treatment is challenging: it may either induce exacerbation of autoimmunity or cause undertreatment of the malignancy. This complex interplay births curiosity into the enigma of autoimmunity and oncology. In this particular report, we highlight the case of a patient with SLE who developed E-GBM. We identify the clinicopathologic features of the tumor present in the patient and explore the known aspects of the crosstalk between SLE and E-GBM.
Lupus Erythematosus, Systemic ; Glioblastoma

Gliosarcoma (GS) is a rare variant (2%) of glioblastoma (GBM) that poses clinical genomic challenges because of its poor prognosis and limited genomic information. To gain a comprehensive view of the genomic alterations in GS and to understand the molecular etiology of GS, we applied whole-exome sequencing analyses for 28 GS cases (6 blood-matched fresh-frozen tissues for the discovery set, 22 formalin-fixed paraffin-embedded tissues for the validation set) and copy-number variation microarrays for 5 blood-matched fresh-frozen tissues. TP53 mutations were more prevalent in the GS cases (20/28, 70%) compared to the GBM cases (29/90, 32%), and the GS patients with TP53 mutations showed a significantly shorter survival (multivariate Cox analysis, hazard ratio=23.9, 95% confidence interval, 2.87–199.63, P=0.003). A pathway analysis showed recurrent alterations in MAPK signaling (EGFR, RASGRF2 and TP53), phosphatidylinositol/calcium signaling (CACNA1s, PLCs and ITPRs) and focal adhesion/tight junction (PTEN and PAK3) pathways. Genomic profiling of the matched recurrent GS cases detected the occurrence of TP53 mutations in two recurrent GS cases, which suggests that TP53 mutations play a role in treatment resistance. Functionally, we found that TP53 mutations are associated with the epithelial–mesenchymal transition (EMT) process of sarcomatous components of GS. We provide the first comprehensive genome-wide genetic alternation profiling of GS, which suggests novel prognostic subgroups in GS patients based on their TP53 mutation status and provides new insight in the pathogenesis and targeted treatment of GS.
Glioblastoma ; Gliosarcoma* ; Humans ; Prevalence* ; Prognosis