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[PMID]: 29524717
[Au] Autor:Wang T; Gao T; Niu X; Xing X; Yang Y; Liu Y; Mao Q
[Ad] Address:Department of Neurosurgery, West China Hospital, Sichuan University, Guoxue Alley 37, Chengdu, 610041, China; Department of Neurosurgery, Xi'an Central Hospital, Xi'an, China.
[Ti] Title:Clinical Characteristics and Prognostic Analysis of Glioma with HIV Patients.
[So] Source:World Neurosurg;, 2018 Mar 07.
[Is] ISSN:1878-8769
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: The aim of this study was to perform an survival analysis of HIV patients with glioma and to assess the relationship between various prognostic factors and overall survival. METHODS: We reported in detail the management and prognosis of two patients in our hospital and performed a quantitative and comprehensive systematic literature review of patients with HIV-associated glioma. We combined our treatment experience with retrospectively obtained treatment information and studied the resultant survival time to statistically analyze and discuss whether age, surgery, gender, WHO grade, radiotherapy, chemotherapy and RT combined CTh could predict patients' survival. RESULT: We included 34 cases in our study, including two of our cases. The median survival was 9 months. On survival analysis, among the aforementioned parameters, WHO grade(LGG/HGG), surgery(SR/SB) and radiotherapy showed significant association with overall survival by univariate analysis. Multivariable analysis showed WHO grade and surgery were a significant predictor of OS. CONCLUSION: Most patients had astrocytoma or high-grade glioma. The median survival of all of glioma in HIV patients was shorter than that of GBM patients. Surgery and WHO grade were independent prognostic factors for overall survival.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 40526 MEDLINE  
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[PMID]: 29524715
[Au] Autor:Ramakrishna R; Hsu WC; Mao J; Sedrakyan A
[Ad] Address:- Department Of Neurological Surgery, Weill Cornell Medical College, New York Presbyterian Hospital, New York, New York USA.
[Ti] Title:Surgeon Annual and Cumulative Volumes Predict Early Postoperative Outcomes After Brain Tumor Resection.
[So] Source:World Neurosurg;, 2018 Mar 07.
[Is] ISSN:1878-8769
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Surgeon volume has been previously shown to impact patient outcomes. However, data related to neuro-oncologic surgery is limited and does not include neurologic morbidities as an outcomes measure. In this study, we aimed to determine if 5-year surgeon cumulative and annual volumes predict early postoperative outcomes in patients following brain tumor surgery. METHODS: A population-based cohort of patients (n=10, 258) undergoing brain tumor resection between 2005 and 2014 were included for study utilizing the New York Statewide Planning and Research Cooperation System. Surgeons were categorized by their cumulative and annual surgical volume. RESULTS: Patients treated by high cumulative/high annual (HC/HA) volume surgeons had shorter length of stay (median 5 days vs 8 days vs 8 days vs 6 days respectively, p<0.01), lower charges (median 70,025 vs $77,043 vs $93,715 vs $77,018 respectively, p<0.01) and less non-routine discharge (41% vs 48% vs 50.9% vs 43.9% respectively, p<0.01) compared with patients treated by surgeons from the LC/LA, LC/HA, HC/LA groups. Similarly, HC/HA volume surgeons also had lower rate of hydrocephalus (9.9% vs 10.4% vs 13.7% respectively, p=0.02), medical complications (6.9% vs 11.2% vs 11.5% respectively, p<0.01), neurologic complications (44.1% vs 46.8% vs 48.1% respectively, p=0.03), 30-day reoperation (5.1% vs 6.9% vs 7.1% respectively, p<0.01) and 30-day death (3.3% vs 5.4% vs 5.2%, p<0.01) compared with LC/LA and LC/HA volume surgeons. CONCLUSION: There is some evidence for improved postoperative outcomes when surgery is performed by high cumulative and high annual volume surgeons. This suggests that subspecialization in surgical neurooncology should be considered.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 40526 MEDLINE  
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[PMID]: 29511178
[Au] Autor:Kirkin AF; Dzhandzhugazyan KN; Guldberg P; Fang JJ; Andersen RS; Dahl C; Mortensen J; Lundby T; Wagner A; Law I; Broholm H; Madsen L; Lundell-Ek C; Gjerstorff MF; Ditzel HJ; Jensen MR; Fischer W
[Ad] Address:Danish Cancer Society Research Center, 2100, Copenhagen, Denmark. aki@cytovac.dk.
[Ti] Title:Adoptive cancer immunotherapy using DNA-demethylated T helper cells as antigen-presenting cells.
[So] Source:Nat Commun;9(1):785, 2018 Mar 06.
[Is] ISSN:2041-1723
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:In cancer cells, cancer/testis (CT) antigens become epigenetically derepressed through DNA demethylation and constitute attractive targets for cancer immunotherapy. Here we report that activated CD4 T helper cells treated with a DNA-demethylating agent express a broad repertoire of endogenous CT antigens and can be used as antigen-presenting cells to generate autologous cytotoxic T lymphocytes (CTLs) and natural killer cells. In vitro, activated CTLs induce HLA-restricted lysis of tumor cells of different histological types, as well as cells expressing single CT antigens. In a phase 1 trial of 25 patients with recurrent glioblastoma multiforme, cytotoxic lymphocytes homed to the tumor, with tumor regression ongoing in three patients for 14, 22, and 27 months, respectively. No treatment-related adverse effects were observed. This proof-of-principle study shows that tumor-reactive effector cells can be generated ex vivo by exposure to antigens induced by DNA demethylation, providing a novel, minimally invasive therapeutic strategy for treating cancer.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41467-018-03217-9

  4 / 40526 MEDLINE  
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[PMID]: 29510196
[Au] Autor:Qiu XY; Hu DX; Chen WQ; Chen RQ; Qian SR; Li CY; Li YJ; Xiong XX; Liu D; Pan F; Yu SB; Chen XQ
[Ad] Address:Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Institute of Brain Research, Key Laboratory of Neurological Diseases, Ministry of Education, Hubei Provincial Key Laboratory of Neurological Diseases, Huazhong University of Science and Technology, Wuhan 430030, China.
[Ti] Title:PD-L1 confers glioblastoma multiforme malignancy via Ras binding and Ras/Erk/EMT activation.
[So] Source:Biochim Biophys Acta;1864(5 Pt A):1754-1769, 2018 Mar 03.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Glioblastoma multiforme (GBM) is the most aggressive primary brain tumor due to the lack of effective therapeutic drugs. Cancer therapy targeting programmed cell death protein 1 (PD-1) or programmed death ligand-1 (PD-L1) is of revolutionary. However, the role of intrinsic PD-L1, which determines immune-therapy outcomes, remains largely unclear. Here we demonstrated an oncogenic role of PD-L1 via binding and activating Ras in GBM cells. RNA-sequencing transcriptome data revealed that PD-L1 significantly altered gene expression enriched in cell growth/migration/invasion pathways in human GBM cells. PD-L1 overexpression and knockout or knockdown demonstrated that PD-L1 promoted GBM cell proliferation and migration in vitro and in vivo. Mechanistically, PD-L1 prominently activated epithelial mesenchymal transition (EMT) process in a MEK/Erk- but not PI3K/Akt-dependent manner. Further, we identified intracellular interactions of PD-L1 and H-Ras, which led to Ras/Erk/EMT activation. Finally, we demonstrated that PD-L1 overexpression promoted while knockdown abolished GBM development and invasion in orthotopic GBM models of rodents. Taken together, we found that intracellular PD-L1 confers GBM cell malignancy and aggressiveness via binding Ras and activating the downstream Erk-EMT signaling. Thus, these results shed important insights in improving efficacy of immune therapy for GBM as well as other malignant tumors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 40526 MEDLINE  
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[PMID]: 29486328
[Au] Autor:Mendes M; Miranda A; Cova T; Gonçalves L; Almeida AJ; Sousa JJ; do Vale MLC; Marques EF; Pais A; Vitorino C
[Ad] Address:Faculty of Pharmacy, University of Coimbra, Pólo das Ciências da Saúde, Azinhaga de Santa Comba, 3000-548 Coimbra, Portugal; Centre for Neurosciences and Cell Biology (CNC), University of Coimbra, Rua Larga, Faculty of Medicine, Pólo I, 1st floor, 3004-504 Coimbra, Portugal.
[Ti] Title:Modeling of ultra-small lipid nanoparticle surface charge for targeting glioblastoma.
[So] Source:Eur J Pharm Sci;117:255-269, 2018 Feb 24.
[Is] ISSN:1879-0720
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Surface modification of ultra-small nanostructured lipid carriers (usNLC) via introduction of a positive charge is hypothesized to prompt site-specific drug delivery for glioblastoma multiforme (GBM) treatment. A more effective interaction with negatively charged lipid bilayers, including the blood-brain barrier (BBB), will facilitate the nanoparticle access to the brain. For this purpose, usNLC with a particle size of 43.82 ±â€¯0.03 nm and a polydispersity index of 0.224 were developed following a Quality by Design approach. Monomeric and gemini surfactants, either with conventional headgroups or serine-based ones, were tested for the surface modification, and the respective safety and efficacy to target GBM evaluated. A comprehensive in silico-in vitro approach is also provided based on molecular dynamics simulations and cytotoxicity studies. Overall, monomeric serine-derived surfactants displayed the best performance, considering altogether particle size, zeta potential, cytotoxic profile and cell uptake. Although conventional surfactants were able to produce usNLC with suitable physicochemical properties and cell uptake, their use is discouraged due to their high cytotoxicity. This study suggests that monomeric serine-derived surfactants are promising agents for developing nanosystems aiming at brain drug delivery.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 40526 MEDLINE  
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[PMID]: 29339188
[Au] Autor:Liu DZ; Cheng Y; Cai RQ; Wang Bd WW; Cui H; Liu M; Zhang BL; Mei QB; Zhou SY
[Ad] Address:Department of Pharmaceutics, School of Pharmacy, Fourth Military Medical University, Xi'an, China.
[Ti] Title:The enhancement of siPLK1 penetration across BBB and its anti glioblastoma activity in vivo by magnet and transferrin co-modified nanoparticle.
[So] Source:Nanomedicine;14(3):991-1003, 2018 Jan 12.
[Is] ISSN:1549-9642
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In order to enhance the penetration of small interference RNA against the polo-like kinase I (siPLK1) across BBB to treat glioblastoma (GBM), transferrin (Tf) modified magnetic nanoparticle (Tf-PEG-PLL/MNP@siPLK1) was prepared. The in vitro experiments indicated that Tf-PEG-PLL/MNP@siPLK1 enhanced the cellular uptake of siPLK1, which resulted in an increase of gene silencing effect and cytotoxicity of Tf-PEG-PLL/MNP@siPLK1 on U87 cells. Besides, Tf-PEG-PLL/MNP@siPLK1 significantly inhibited the growth of U87 glioblastoma spheroids and markedly increased the BBB penetration efficiency of siPLK1 with the application of external magnetic field in in-vitro BBB model. The in vivo experiments indicated that siPLK1 selectively accumulated in the brain tissue, and markedly reduced tumor volume and prolonged the survival time of GBM-bearing mice after Tf-PEG-PLL/MNP@siPLK1 was injected to GBM-bearing mice via tail vein. The above data indicated that magnet and transferrin co-modified nanoparticle enhanced siPLK1 penetration across BBB and increased its anti GBM activity in vivo.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 40526 MEDLINE  
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[PMID]: 29524309
[Au] Autor:Yin C; Mou Q; Pan X; Zhang G; Li H; Sun Y
[Ad] Address:College of Nursing, Qingdao University, Qingdao, China.
[Ti] Title:MiR-577 suppresses epithelial-mesenchymal transition and metastasis of breast cancer by targeting Rab25.
[So] Source:Thorac Cancer;, 2018 Mar 10.
[Is] ISSN:1759-7714
[Cp] Country of publication:Singapore
[La] Language:eng
[Ab] Abstract:BACKGROUND: MicroRNAs can act as both tumor suppressor genes and oncogenes and participate in cell proliferation, metastasis, and apoptosis. Low levels of miR-577 are found in several cancers, for example, thyroid carcinoma, glioblastoma, and hepatocellular carcinoma. The aim of this study was to investigate the effect of miR-577 on breast cancer (BC). METHODS: The relative level of miR-577 in 120 BC tissues and cells was detected by real-time PCR. MDA-MB-231 cells with upregulated miR-577 and MCF-7 cells with downregulated miR-577 were established. Transwell invasion assays were used to examine the invasiveness of cells. Epithelial-mesenchymal transition (EMT) markers were evaluated by immunofluorescence and Western blot. Targeted combinations of miR-577 and Rab25 were analyzed by luciferase assays. Xenograft models were used to examine the effect of miR-577 on BC metastasis. RESULTS: MiR-577 expression was significantly suppressed in BC tissues. Tumor size, tumor stage, and lymphatic metastasis were attributed to miR-577 expression. Moreover, miR-577 overexpression strongly inhibited the invasiveness and EMT of BC cells in vitro. MiR-577 directly regulated Rab25 in BC. Rab25 upregulation by miR-577 decreased the levels of E-cadherin and increased the levels of Vimentin. Notably, Rab25 knockdown inhibited BC invasion; however, an increase in Rab25 counteracted the invasive effect of miR-577 in BC. CONCLUSION: Results indicated that miR-577 suppressed EMT by inhibiting Rab25 expression in BC. MiR-577 and Rab25 are considered potential targets of BC treatment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1111/1759-7714.12612

  8 / 40526 MEDLINE  
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[PMID]: 29524243
[Au] Autor:Elmghirbi R; Nagaraja TN; Brown SL; Keenan KA; Panda S; Cabral G; Bagher-Ebadian H; Divine GW; Lee IY; Ewing JR
[Ad] Address:Department of Physics, Oakland University, Rochester, Michigan.
[Ti] Title:Toward a noninvasive estimate of interstitial fluid pressure by dynamic contrast-enhanced MRI in a rat model of cerebral tumor.
[So] Source:Magn Reson Med;, 2018 Mar 09.
[Is] ISSN:1522-2594
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: This study demonstrates a DCE-MRI estimate of tumor interstitial fluid pressure (TIFP) and hydraulic conductivity in a rat model of glioblastoma, with validation against an invasive wick-in-needle (WIN) technique. An elevated TIFP is considered a mark of aggressiveness, and a decreased TIFP a predictor of response to therapy. METHODS: The DCE-MRI studies were conducted in 36 athymic rats (controls and posttreatment animals) with implanted U251 cerebral tumors, and with TIFP measured using a WIN method. Using a model selection paradigm and a novel application of Patlak and Logan plots to DCE-MRI data, the MRI parameters required for estimating TIFP noninvasively were estimated. Two models, a fluid-mechanical model and a multivariate empirical model, were used for estimating TIFP, as verified against WIN-TIFP. RESULTS: Using DCE-MRI, the mean estimated hydraulic conductivity (MRI-K) in U251 tumors was (2.3 ± 3.1) × 10 (mm /mmHg-s) in control studies. Significant positive correlations were found between WIN-TIFP and MRI-TIFP in both mechanical and empirical models. For instance, in the control group of the fluid-mechanical model, MRI-TIFP was a strong predictor of WIN-TIFP (R = 0.76, p < .0001). A similar result was found in the bevacizumab-treated group of the empirical model (R = 0.93, p = .014). CONCLUSION: This research suggests that MRI dynamic studies contain enough information to noninvasively estimate TIFP in this, and possibly other, tumor models, and thus might be used to assess tumor aggressiveness and response to therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1002/mrm.27163

  9 / 40526 MEDLINE  
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[PMID]: 29524050
[Au] Autor:Jindal V
[Ad] Address:Department of Internal Medicine, Saint Vincent Hospital, 123 summer street, Worcester, MA, 01608, USA. vishaljindal87@gmail.com.
[Ti] Title:Role of Chimeric Antigen Receptor T Cell Therapy in Glioblastoma Multiforme.
[So] Source:Mol Neurobiol;, 2018 Mar 09.
[Is] ISSN:1559-1182
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Glioblastoma multiforme (GBM) is the most common primary malignant cancer of brain, which is extremely aggressive and carries a dreadful prognosis. Current treatment protocol runs around radiotherapy, surgical resection, and temozolomide with median overall survival of around 12-15 months. Due to its heterogeneity and mutational load, immunotherapy with chimeric antigen receptor (CAR) T cell therapy can be a promising treatment option for recurrent glioblastoma. Initial phase 1 studies have shown that this therapy is safe without dose-limiting side effects and it also has a better clinical outcome. Therefore, CAR T cell therapy can be a great future tool in our armamentarium to treat advanced GBM. In this article, we have explained the structure, mechanism of action, and rationale of CAR T cell therapy in GBM; we also discussed various antigenic targets and clinical outcome of initial studies of this novel therapy.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s12035-018-0978-z

  10 / 40526 MEDLINE  
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[PMID]: 29523123
[Au] Autor:Aaberg-Jessen C; Sørensen MD; Matos ALSA; Moreira JM; Brünner N; Knudsen A; Kristensen BW
[Ad] Address:Department of Pathology, Odense University Hospital, J.B. Winsloews Vej 15, 5000, Odense, Denmark.
[Ti] Title:Co-expression of TIMP-1 and its cell surface binding partner CD63 in glioblastomas.
[So] Source:BMC Cancer;18(1):270, 2018 Mar 09.
[Is] ISSN:1471-2407
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: We have previously identified tissue inhibitor of metalloproteinases-1 (TIMP-1) as a prognostic marker in glioblastomas. TIMP-1 has been associated with chemotherapy resistance, and CD63, a known TIMP-1-binding protein, has been suggested to be responsible for this effect. The aim of this study was to assess CD63 expression in astrocytomas focusing on the prognostic potential of CD63 alone and in combination with TIMP-1. METHODS: CD63 expression was investigated immunohistochemically in a cohort of 111 astrocytomas and correlated to tumor grade and overall survival by semi-quantitative scoring. CD63 expression in tumor-associated microglia/macrophages was examined by double-immunofluorescence with ionized calcium-binding adapter molecule 1 (Iba1). The association between CD63 and TIMP-1 was investigated using previously obtained TIMP-1 data from our astrocytoma cohort. Cellular co-expression of TIMP-1 and CD63 as well as TIMP-1 and the tumor stem cell-related markers CD133 and Sox2 was investigated with immunofluorescence. TIMP-1 and CD63 protein interaction was detected by an oligonucleotide-based proximity ligation assay and verified using co-immunoprecipitation. RESULTS: The expression of CD63 was widely distributed in astrocytomas with a significantly increased level in glioblastomas. CD63 levels did not significantly correlate with patient survival at a protein level, and CD63 did not augment the prognostic significance of TIMP-1. Up to 38% of the CD63+ cells expressed Iba1; however, Iba1 did not appear to impact the prognostic value of CD63. A significant correlation was found between TIMP-1 and CD63, and the TIMP-1 and CD63 proteins were co-expressed at the cellular level and located in close molecular proximity, suggesting that TIMP-1 and CD63 could be co-players in glioblastomas. Some TIMP-1+ cells expressed CD133 and Sox2. CONCLUSION: The present study suggests that CD63 is highly expressed in glioblastomas and that TIMP-1 and CD63 interact. CD63 does not add to the prognostic value of TIMP-1. Co-expression of TIMP-1 and stem cell markers as well as the wide expression of CD63 might suggest a role for TIMP-1 and CD63 in glioblastoma stemness.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1186/s12885-018-4179-y


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