Purpose Newly emerged or constantly enlarged contrast-enhancing (CE) lesions were the necessary signs for the diagnosis of glioblastoma (GBM) progression. This study aimed to investigate whether the T2-weighted-Fluid-Attenuated Inversion Recovery (T2/FLAIR) abnormal transformation could predict and assess progression for GBMs, especially for tumor dissemination. Methods A consecutive cohort of 246 GBM patients with regular follow-up and sufficient radiological data was included in this study. The series of T2/FLAIR and T1CE images were retrospectively reviewed. The patients were separated into T2/FLAIR and T1CE discordant and accordant subgroups based on the initial progression images. Results A total of 170 qualified patients were finally analyzed. The incidence of discordant T2/FLAIR and T1CE images was 25.9% (44/170). The median time-span of T2/FLAIR indicated tumor progression was 119.5 days (ranging from 57 days-unreached) prior to T1CE. Nearly half of patients (20/44, 45.5%) in the discordant subgroup suffered from tumor dissemination, substantially higher than accordant patients (23/126, 20.6%, p < 0.001). The median time to progression (TTP), post-progression survival (PPS), and overall survival (OS) were not statistically different (all p > 0.05) between discordant and accordant patients. Conclusions T2/FLAIR abnormity could be the sign of GBM progression, especially for newly emerged lesions disseminating from the primary cavity. Physicians should cast more attention on the dynamic change of T2/FLAIR images, which might be of great significance for progression assessment and subsequent clinical decision-making.

/pdf/t2-flair-abnormity-could-be-the-sign-of-glioblastoma-2i0d3z2c.pdf

T2/FLAIR Abnormity Could be the Sign of Glioblastoma Dissemination

Purpose Glioblastoma (GBM) is one of the most lethal human tumors with a highly infiltrative phenotype. Our previous studies showed that GBM originates in the subventricular zone, and that tumor-derived mesenchymal stem-like cells (tMSLCs) promote the invasiveness of GBM tumorspheres (TSs). Here, we extend these studies in terms of ventricles using several types of GBM patient-derived cells. Materials and Methods The invasiveness of GBM TSs and ventricle spheres (VSs) were quantified via collagen-based 3D invasion assays. Gene expression profiles were obtained from microarray data. A mouse orthotopic xenograft model was used for in vivo experiments. Results After molecular and functional characterization of ventricle-derived mesenchymal stem-like cells (vMSLCs), we investigated the effects of these cells on the invasiveness of GBM TSs. We found that vMSLC-conditioned media (CM) significantly accelerated the invasiveness of GBM TSs and VSs, compared to the control and even tMSLC-CM. Transcriptome analyses revealed that vMSLC secreted significantly higher levels of several invasiveness-associated cytokines. Moreover, differentially expressed genes between vMSLCs and tMSLCs were enriched for migration, adhesion, and chemotaxis-related gene sets, providing a mechanistic basis for vMSLC-induced invasion of GBM TSs. In vivo experiments using a mouse orthotopic xenograft model confirmed vMSLC-induced increases in the invasiveness of GBM TSs. Conclusion Although vMSLCs are non-tumorigenic, this study adds to our understanding of how GBM cells acquire infiltrative features by vMSLCs, which are present in the region where GBM genesis originates.

Mesenchymal Stem-Like Cells Derived from the Ventricle More Effectively Enhance Invasiveness of Glioblastoma Than Those Derived from the Tumor

Driver genes of GBM may be crucial for the onset of isocitrate dehydrogenase (IDH)-wildtype (WT) glioblastoma (GBM). However, it is still unknown whether the genes are expressed in the identical cluster of cells. Here, we have examined the gene expression patterns of GBM tissues and patient-derived tumorspheres (TSs) and aimed to find a progression-related gene. We retrospectively collected primary IDH-WT GBM tissue samples (n = 58) and tumor-free cortical tissue samples (control, n = 20). TSs are isolated from the IDH-WT GBM tissue with B27 neurobasal medium. Associations among the driver genes were explored in the bulk tissue, bulk cell, and a single cell RNAsequencing techniques (scRNAseq) considering the alteration status of TP53, PTEN, EGFR, and TERT promoter as well as MGMT promoter methylation. Transcriptomic perturbation by temozolomide (TMZ) was examined in the two TSs. We comprehensively compared the gene expression of the known driver genes as well as MGMT, PTPRZ1, or IDH1. Bulk RNAseq databases of the primary GBM tissue revealed a significant association between TERT and TP53 (p < 0.001, R = 0.28) and its association increased in the recurrent tumor (p  < 0.001, R = 0.86). TSs reflected the tissue-level patterns of association between the two genes (p < 0.01, R = 0.59, n = 20). A scRNAseq data of a TS revealed the TERT and TP53 expressing cells are in a same single cell cluster. The driver-enriched cluster dominantly expressed the glioma-associated long noncoding RNAs. Most of the driver-associated genes were downregulated after TMZ except IGFBP5. GBM tissue level expression patterns of EGFR, TERT, PTEN, IDH1, PTPRZ1, and MGMT are observed in the GBM TSs. The driver gene-associated cluster of the GBM single cells were enriched with the glioma-associated long noncoding RNAs.

/pdf/co-expression-of-cancer-driver-genes-idh-wildtype-k7fdkqwe7y.pdf

Co-expression of cancer driver genes: IDH-wildtype glioblastoma-derived tumorspheres

Gap junctional intercellular communication (GJIC) composed of connexin proteins is considered vital to cancer onset and progression since 50 years ago based on Lowenstein and Kano's works, however altered expression of connexins is still a lesser known "hallmark" of cancer. Although many studies support the hypothesis that connexins are tumor suppressors, recent evidence indicates that, in some tumor types including glioma, they may play contradictory role in some specific stages of tumor progression. We thus conduct a meta-analysis to evaluate the prognostic role of Cx43 in glioma for the unanswered questions that whether Cx43 is a beneficial or insalubrity factor for glioma. Eight studies with 1,706 patients were included for meta-analysis. The results showed that Cx43 expression was a clearly negative factor with tumor grades (I 2 = 34%, P < 0.001) and beneficial for OS (n = 3, HR 2.62, 95%CI 1.47-4.68; P = 0.001). Subgroup analysis also found that Cx43 had different expression in Asian young patients vs. other groups. In conclusion, this article summarize the prognostic value of Cx43 and offer a clinical evidence for the notion that Cx43 is generally a tumor suppressor and beneficial for the patients' survival time.

Prognostic and Clinic Pathological Value of Cx43 Expression in Glioma: A Meta-Analysis.

\n \n \n Following resection of glioblastoma (GBM), microscopic remnants of the GBM tumor remaining in nearby tissue cause tumor recurrence more often than for other tumors, even after gross-total resection (GTR). Although surgical oncologists traditionally resect some of the surrounding normal tissue, whether further removal of nearby tissue may improve survival in GBM patients is unknown. In this single-center retrospective study, the authors assessed whether lobectomy confers a survival benefit over GTR without lobectomy when treating GBMs in the noneloquent area.\n \n \n \n The authors selected 40 patients who had undergone GTR of a histopathologically diagnosed isocitrate dehydrogenase (IDH)-wild type GBM in the right frontal or temporal lobe and divided the patients into 2 groups according to whether GTR of the tumor involved lobectomy, defined as a supratotal resection (SupTR group, n = 20) or did not (GTR group, n = 20). Progression-free survival (PFS), overall survival (OS), and Karnofsky Performance Status (KPS) scores were compared between groups (p ≤ 0.05 for statistically significant differences).\n \n \n \n The median postoperative PFS times for each group were as follows: GTR group, 11.5 months (95% CI 8.8–14.2) and SupTR group, 30.7 months (95% CI 4.3–57.1; p = 0.007). The median postoperative OS times for each group were as follows: GTR group, 18.7 months (95% CI 14.3–23.1) and SupTR group, 44.1 months (95% CI 25.1–63.1; p = 0.040). The mean postoperative KPS scores (GTR, 76.5; SupTR, 77.5; p = 0.904) were not significantly different. In multivariate analysis, survival for the SupTR group was significantly longer than that for the GTR group in terms of both PFS (HR 0.230; 95% CI 0.090–0.583; p = 0.002) and OS (HR 0.247; 95% CI 0.086–0.704; p = 0.009).\n \n \n \n In cases of completely resectable, noneloquent area GBMs, SupTR provides superior PFS and OS without negatively impacting patient performance.\n

http://academic.oup.com/neuro-oncology/article-pdf/21/Supplement_3/iii77/30129212/noz126.279.pdf

P14.44 Survival benefit of lobectomy over gross-total resection without lobectomy in cases of glioblastoma in the noneloquent area: a retrospective study

Exth-28. 5-aminolevulinic acid-based photodynamic therapy of glioblastoma tumorsphere and acquired resistance by tumor mesenchymal stem-like cells

PCM (Phase Change Memory) that takes center stage has characteristics of non-volatile memory, but as it has a limited number of write times, we wear-leveling technique is required. WL-Reviver (Wear Leveling – Reviver) system is a wear-leveling technic tailored to the PCM, but if internal and external errors occur, it gets failed. This paper proposes a recovery model based on WL-Reviver system for internal and external error situations. Compared to previous work, our newly suggested model improves the system reliability.

A Recovery Model for Improving Reliability of PCM WL-Reviver System

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P14.44 Survival benefit of lobectomy over gross-total resection without lobectomy in cases of glioblastoma in the noneloquent area: a retrospective study

Exth-28. 5-aminolevulinic acid-based photodynamic therapy of glioblastoma tumorsphere and acquired resistance by tumor mesenchymal stem-like cells

A Recovery Model for Improving Reliability of PCM WL-Reviver System