Gotowe bibliografie tematyczne / Glioma Cell Lines

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Gotowa bibliografia na temat „Glioma Cell Lines”

Autor: Grafiati
Data publikacji: 6 września 2023

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Artykuły w czasopismach na temat "Glioma Cell Lines"

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Chen, Yi-Hsuan, Dueng-Yuan Hueng i Wen-Chiuan Tsai. "Proteolipid Protein 2 Overexpression Indicates Aggressive Tumor Behavior and Adverse Prognosis in Human Gliomas". International Journal of Molecular Sciences 19, nr 11 (26.10.2018): 3353. http://dx.doi.org/10.3390/ijms19113353.

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Proteolipid protein 2 (PLP2), a membrane protein of the endoplasmic reticulum, is related to tumor proliferation and metastasis in some human cancers, but not in gliomas. First, we performed western-blot analysis, real-time quantitative PCR and immunohistochemical stains to detect PLP2 expression in 4 glioma cell lines and human glioma tissues. In addition, we used small interfering RNA (SiPLP2) and short hairpin RNA (shPLP2) to knockdown PLP2 expression in GBM8401 and LN229 glioma cell lines. After then, the alteration of PLP2 suppressed glioma cells behavior were examined by cell proliferation, wound healing, cell invasion, and colonies formation assays. Finally, the possible mechanism of PLP2 was analyzed by detecting the expression of the proteins related to cell-cycle checkpoints, cell-proliferative signaling factors, and cell-matrix interaction. Compared with normal brain cell lysates and mRNA, all glioma cell lines displayed PLP2 protein and mRNA overexpression. Besides, higher PLP2 IHC staining significantly correlated with more advanced tumor grades and poorer prognosis in human gliomas. Both siPLP2 transfected gliomas showed a clear inhibition of glioma cell proliferation, migration, and invasion as well as down-regulating p-p38, p-ERK, MMP-2, and MMP-9 expression. In conclusion, we successfully demonstrated that PLP2 overexpression played an oncogenic role in glioma development and aggressive tumor behavior.
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Tuma, Rabiya. "Repopulating glioma cell lines". Journal of Cell Biology 164, nr 3 (26.01.2004): 334–35. http://dx.doi.org/10.1083/jcb1643rr2.

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Shi, Fei, Jie Hu, Ping Zheng, Yisong Lv, Hongyu Liu, Guiyun Zhang i Hongyu Jiang. "LncRNA PANTR1 is Associated with Poor Prognostic and Suppresses Apoptosis in Glioma". Journal of Oncology 2023 (20.02.2023): 1–14. http://dx.doi.org/10.1155/2023/8537036.

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Glioma is the most common tumor in the central nervous system. High-grade gliomas confer a poor prognosis, being a serious health and economic burden. Current literature suggests the important role of long noncoding RNA (lncRNA) in mammals, especially in tumorigenesis of various tumors. The functions of lncRNA POU3F3 adjacent noncoding transcript 1 (PANTR1) have been investigated in hepatocellular carcinoma but remain yet unclear in gliomas. We evaluated the role of PANTR1 in glioma cells using published data from The Cancer Genome Atlas (TCGA), then validated it by ex vivo experiments. To investigate the potential cellular mechanism of different levels of PANTR1 expression in glioma cells, we used siRNA-mediated knockdown in low-grade (grade II) cell lines and GBM (grade IV) cell lines (SW1088 and SHG44, respectively). On the molecular level, low expression of PANTR1 caused significantly reduced glioma cell viability and enhanced cell death. Moreover, we identified the importance of PANTR1 expression for cell migration in both cell lines, a critical foundation for invasiveness in recurrent gliomas. In conclusion, this study provides the first evidence that PANTR1 has a relevant role in human glioma by influencing cell viability and cell death.
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Bota, Daniela A., Daniela Alexandru, Stephen T. Keir, Darell Bigner, James Vredenburgh i Henry S. Friedman. "Proteasome inhibition with bortezomib induces cell death in GBM stem-like cells and temozolomide-resistant glioma cell lines, but stimulates GBM stem-like cells' VEGF production and angiogenesis". Journal of Neurosurgery 119, nr 6 (grudzień 2013): 1415–23. http://dx.doi.org/10.3171/2013.7.jns1323.

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Object Recurrent malignant gliomas have inherent resistance to traditional chemotherapy. Novel therapies target specific molecular mechanisms involved in abnormal signaling and resistance to apoptosis. The proteasome is a key regulator of multiple cellular functions, and its inhibition in malignant astrocytic lines causes cell growth arrest and apoptotic cell death. The proteasome inhibitor bortezomib was reported to have very good in vitro activity against malignant glioma cell lines, with modest activity in animal models as well as in clinical trials as a single agent. In this paper, the authors describe the multiple effects of bortezomib in both in vitro and in vivo glioma models and offer a novel explanation for its seeming lack of activity. Methods Glioma stem-like cells (GSCs) were obtained from resected glioblastomas (GBMs) at surgery and expanded in culture. Stable glioma cell lines (U21 and D54) as well as temozolomide (TMZ)-resistant glioma cells derived from U251 and D54-MG were also cultured. GSCs from 2 different tumors, as well as D54 and U251 cells, were treated with bortezomib, and the effect of the drug was measured using an XTT cell viability assay. The activity of bortezomib was then determined in D54-MG and/or U251 cells using apoptosis analysis as well as caspase-3 activity and proteasome activity measurements. Human glioma xenograft models were created in nude mice by subcutaneous injection. Bevacizumab was administered via intraperitoneal injection at a dose of 5 mg/kg daily. Bortezomib was administered by intraperitoneal injection 1 hour after bevacizumab administration in doses of at a dose of 0.35 mg/kg on days 1, 4, 8, and 11 every 21 days. Tumors were measured twice weekly. Results Bortezomib induced caspase-3 activation and apoptotic cell death in stable glioma cell lines and in glioma stem-like cells (GSCs) derived from malignant tumor specimens Furthermore, TMZ-resistant glioma cell lines retained susceptibility to the proteasome inhibition. The bortezomib activity was directly proportional with the cells' baseline proteasome activity. The proteasome inhibition stimulated both hypoxia-inducible factor (HIF)–1α and vascular endothelial growth factor (VEGF) production in malignant GSCs. As such, the VEGF produced by GSCs stimulated endothelial cell growth, an effect that could be prevented by the addition of bevacizumab (VEGF antibody) to the media. Similarly, administration of bortezomib and bevacizumab to athymic mice carrying subcutaneous malignant glioma xenografts resulted in greater tumor inhibition and greater improvement in survival than administration of either drug alone. These data indicate that simultaneous proteasome inhibition and VEGF blockade offer increased benefit as a strategy for malignant glioma therapy. Conclusions The results of this study indicate that combination therapies based on bortezomib and bevacizumab might offer an increased benefit when the two agents are used in combination. These drugs have a complementary mechanism of action and therefore can be used together to treat TMZ-resistant malignant gliomas.
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Han, Jizhong, Yu Xiong, Huajiang Deng, Jie Zhou, Lilei Peng, Wei Xiang, Yang Ming i Ligang Chen. "MiR-455-3p regulates glioma cell proliferation by targeting PAX6". Tropical Journal of Pharmaceutical Research 18, nr 4 (17.05.2021): 689–95. http://dx.doi.org/10.4314/tjpr.v18i4.2.

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Purpose: To investigate the role of miR-455-3p in gliomas. Method: Quantitative real-time polymerase chain reaction was used to measure miR-455-3p and paired box 6 (PAX6) levels in glioma cell lines. Western blot analysis was used to determine the expression of cell cycle regulators. In addition to over-expression, silencing of miR-455-3p or PAX6 was performed to study the functions of miR-455-3p in gliomas. Results: The levels of miR-455-3p were significantly up-regulated in glioma cell lines (p < 0.05), while miR-455-3p over-expression increased glioma cell proliferation and interfered with the progress of the cell cycle (p < 0.01). Furthermore, endogenous miR-455-3p silencing prevented glioma cell proliferation by regulating cell cycle progression (p < 0.05).The results also showed that PAX6 controlled the cell cycle while PAX6 silencing selectively regulated p21 expression (p < 0.01). Furthermore, miR-455-3p and PAX6 influenced p53 expression. Re-introduction of PAX6 expressing vector into glioma cells rescued the pro-tumoral effect of miR-455-3p overexpression. Conclusion: These findings demonstrate the role of miR-455-3p as a tumour oncogene in gliomas via regulation of the cell cycle, indicating that miR-455-3p might act as a new treatment strategy for glioma cell tumours and a predictor of survival in glioma patients.
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Matsumoto, Tsuyoshi, Eiichi Tani, Keizo Kaba, Hideki Shindo i Katsuya Miyaji. "Expression of P-glycoprotein in human glioma cell lines and surgical glioma specimens". Journal of Neurosurgery 74, nr 3 (marzec 1991): 460–66. http://dx.doi.org/10.3171/jns.1991.74.3.0460.

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✓ The expression of P-glycoprotein, a product of multidrug resistance gene 1, was studied by Western blotting and immunohistochemistry in five human glioma cell lines. One glioma cell line was resistant to vincristine, Adriamycin (doxorubicin), and etoposide, and the other four glioma cell lines were sensitive to each drug. The multidrug-resistant cell line showed a high expression of P-glycoprotein in Western blot analysis and a positive immunostaining for P-glycoprotein mainly along the cell membrane, whereas all multidrug-sensitive glioma cell lines demonstrated no expression of P-glycoprotein in Western blotting and no immunostaining for P-glycoprotein, thus showing a good correlation between the expression level of P-glycoprotein and the extent of multidrug resistance. In 18 human surgical glioma specimens, there was no evidence of complete absence of immunostaining for P-glycoprotein. With a definition of more than 20% of P-glycoprotein-positive cells as positive, from 10% to 20% as intermediate, and less than 10% as negative, immunostaining for P-glycoprotein was positive in one specimen and intermediate in six of 15 specimens taken from virgin gliomas, and positive in two specimens and intermediate in one of three recurrent gliomas treated previously with irradiation, ACNU (1-(4-amino-2-methyl-pyrimidine-5-yl)-methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride), cisplatin, vincristine, and/or procarbazine.
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Nakano, Atsuhisa, Eiichi Tani, Kaoru Miyazaki, Yoshihiro Yamamoto i Jun-ichi Furuyama. "Matrix metalloproteinases and tissue inhibitors of metalloproteinases in human gliomas". Journal of Neurosurgery 83, nr 2 (sierpień 1995): 298–307. http://dx.doi.org/10.3171/jns.1995.83.2.0298.

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✓ The gene expression of five matrix metalloproteinases (MMPs) and two tissue inhibitors of metalloproteinases (TIMPs) was studied in human gliomas in vivo and in vitro to evaluate their roles in glioma invasion. Simultaneous expression of one to four MMP genes and two TIMP genes was found in 17 surgical glioma specimens, and one MMP (gelatinase A) gene and two TIMP genes were simultaneously expressed in tissue of three brains. The concomitant overexpression of gelatinase A, gelatinase B, and occasional matrilysin genes was associated with the malignancy of gliomas and accompanied by overexpression of the TIMP-1 gene. In five human glioma cell lines, gelatinase A, TIMP-1, and TIMP-2 genes were constitutively expressed in all cell lines: the matrilysin gene in three cell lines; the stromelysin gene in two cell lines; and the interstitial collagenase gene in one cell line. There was a clear difference in the expression of gelatinase B and stromelysin genes between surgical glioma specimens and glioma cell lines: the gelatinase B gene was not expressed constitutively in vitro but was overexpressed in vivo, whereas the stromelysin gene was not expressed in vivo but was expressed in some cell lines. To find the cause of that difference in vivo and in vitro, the transcriptional regulations of MMP and TIMP genes by tumor promoter, growth factors, or cytokines were studied in vitro. Interstitial collagenase, gelatinase B, stromelysin, and TIMP-1 genes were upregulated in many cell lines by phorbol-12-myristate-13-acetate (PMA) and in some cell lines by epidermal growth factor, tumor necrosis factor-α, or interleukin-1β. Transforming growth factor-β1 (TGFβ1) upregulated gelatinase A and matrilysin genes in some cell lines, and there were no clear responses from any MMP and TIMP genes to interleukin-6. Thus, the transcriptional modulation of MMP genes by these growth factors and cytokines seemed insufficient to explain the difference in gelatinase B and stromelysin gene expressionsin vivo and in vitro and was suggestive of the genetic alteration of glioma cells in vitro, the heterogeneous cell population in glioma tissues, or both. Furthermore, the in vitro invasion of glioma cells through Matrigel in response to PMA, TGFβ1, or TIMP-1 was assessed by chemoinvasion assay. In most cell lines, invasion was significantly stimulated by PMA or TGFβ1 but suppressed by TIMP-1. These in vivo and in vitro studies are strongly suggestive of the important roles of some MMPs, especially gelatinase A, gelatinase B, and matrilysin, in the glioma invasion.
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Zhou, You-xin, San-song Chen, Ting-feng Wu, Da-dong Ding, Xiong-hui Chen, Jin-ming Chen, Zuo-peng Su i in. "A Novel Gene RNF138 Expressed in Human Gliomas and Its Function in the Glioma Cell Line U251". Analytical Cellular Pathology 35, nr 3 (2012): 167–78. http://dx.doi.org/10.1155/2012/519037.

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Background: The gliomas represent the most common primary malignant brain tumors; however, little is known about the molecular pathogenesis of these tumors. Recent research reveals that the oncogenesis and development of gliomas have a close relation to the overexpression of several oncogenes and the inactivation of tumor suppressor genes. Whether the RING finger protein, RNF138, a newly discovered protein, plays a role in glioma oncogenesis is unknown. The present study investigates the expression levels of RNF138 mRNA in glioma samples and noncancerous brain samples and its function in the human glioma cell line U251.Methods: RT-PCR was used to ascertain the expression of RNF138 mRNA in the glioma cell lines U251, SHG44, U87, A172, and U373. The RNF138 mRNA expression levels of 35 pathological confirmed glioma samples (Grade I – 4 cases, Grade II – 13 cases, Grade III – 11 cases, and Grade IV – 7 cases) and five noncancerous brain tissue samples were analyzed by real-time quantitative PCR. By RNA interference (RNAi) with the lentivirus vector system, the expression of RNF138 was inhibited in the human astrocytomas-glioblastoma multiforme cell line U251. The effects of RNF138-knockdown on cell proliferation were assessed by Cellomics, and cell cycle and cell apoptosis were assessed by FACS.Results: The RNF138 mRNA is expressed in the five glioma cell lines, and its expression level is significantly higher in glioma tissue than in noncancerous brain tissue. By down-regulation of RNF138 expression, U251 cell proliferation was inhibited and cell apoptosis increased. At the same time, S stage cells lessened and G2 stage cells increased.Conclusion: The RNF138 gene is highly expressed in glioma tissue and glioma cell lines. It plays an important role in glioma cell proliferation, apoptosis, and cell cycle.
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Alexiou, George A., Xanthi Xourgia, Evrysthenis Vartholomatos, Spyridon Tsiouris, John A. Kalef-Ezra, Andreas D. Fotopoulos i Athanasios P. Kyritsis. "Comparison of 99mTc-Tetrofosmin and 99mTc-Sestamibi Uptake in Glioma Cell Lines: The Role of P-Glycoprotein Expression". International Journal of Molecular Imaging 2014 (10.11.2014): 1–5. http://dx.doi.org/10.1155/2014/471032.

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Tc-Tetrofosmin (Tc-TF) and Tc-Sestamibi (Tc-MIBI) are SPECT tracers that have been used for brain tumor imaging. Tumor’s multidrug resistance phenotype, namely, P-glycoprotein (p-gp), and the multidrug resistance related proteins (MRPs) expression have been suggested to influence both tracers’ uptake. In the present study we set out to compare Tc-MIBI uptake in high-grade glioma cell lines and to investigate the influence of gliomas p-gp expression on both tracers’ uptake. We used four glioma cell lines (U251MG, A172, U87MG, and T98G). The expression of p-gp protein was evaluated by flow cytometry. Twenty μCi (7.4·105 Bq) of Tc-TF and Tc-MIBI were used. The radioactivity in the cellular lysate was measured with a dose calibrator. P-gp was significantly expressed only in the U251MG cell line (). In all gliomas cell lines (U251MG, U87MG, A172, and T98G) the Tc-TF uptake was significantly higher than Tc-sestamibi. The U251MG cell line, in which significant p-gp expression was documented, exhibited the strongest uptake difference. Tc-TF uptake was higher than Tc-MIBI in all studied high-grade glioma cell lines. Thus, Tc-TF may be superior to Tc-MIBI for glioma imaging in vivo.
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Jung, Tae-Young, Shin Jung, Hyang-Hwa Ryu, Young-Il Jeong, Yong-Hao Jin, Shu-Guang Jin, In-Young Kim, Sam-Suk Kang i Hyung-Seok Kim. "Role of galectin-1 in migration and invasion of human glioblastoma multiforme cell lines". Journal of Neurosurgery 109, nr 2 (sierpień 2008): 273–84. http://dx.doi.org/10.3171/jns/2008/109/8/0273.

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Object Galectin-1 is highly expressed in motile cell lines. The authors investigated whether galectin-1 actually modulates the migration and invasion of human glioblastoma multiforme (GBM) cell lines, and whether its expression with respect to invasion and prognosis is attributable to certain glioma subgroups. Methods In the human GBM cell lines U343MG-A, U87MG, and U87MG-10′, the RNA differential display was evaluated using Genefishing technology. The results were validated by reverse transcription polymerase chain reaction and Northern blot analysis to detect possible genetic changes as the determining factors for the motility of the malignant glioma. The migration and invasion abilities were investigated in human GBM cell lines and galectin-1 transfectant using an in vitro brain slice invasion model and a simple scratch technique. The morphological and cytoskeletal (such as the development of actin and vimentin) changes were examined under light and confocal microscopy. Galectin-1 expression was assessed on immunohistochemical tests and Western blot analysis. Results Endogenous galectin-1 expression in the human GBM cell lines was statistically correlated with migratory abilities and invasiveness. The U87-G-AS cells became more round than the U87MG cells and lacked lamellipodia. On immunohistochemical staining, galectin-1 expression was increased in higher-grade glioma subgroups (p = 0.027). Conclusions Diffuse gliomas demonstrated higher expression levels than pilocytic astrocytoma in the Western blot. Galectin-1 appears to modulate migration and invasion in human glioma cell lines and may play a role in tumor progression and invasiveness in human gliomas.
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Rozprawy doktorskie na temat "Glioma Cell Lines"

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Gee, Abigail Louise. "Proton beam irradiation of glioma cell lines in vitro". Thesis, University of Liverpool, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439489.

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Florian, Catarina Ligia. "Proton nuclear magnetic resonance studies of human glioma cell lines". Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309218.

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Ferreira, Matthew Thomas. "Analysis of how the production and activity of PGD2 affects glioma cell lines". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-10042015-120110/.

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The World Health Organization classifies glioblastoma (GBM) as a type IV astrocytoma, making it one of the most fatal tumors that exists. Despite the advances in chemotherapy, surgery, and radiation treatments that improve a patients length of survival, the overall trajectory of the disease remains unchanged. It has been shown that GBM cells produce significant levels of prostaglandins, including prostaglandin D2 (PGD2). PGD2 possesses pro- and anti-tumorigenic properties. Hence, a more complete understanding of PGD2 activity in GBM could yield more effective treatments against GBM. Through techniques like RT-PCR, immunohistochemistry, and HPLC tandem mass spectrometry, we were able to confirm the presence of the PGD2 synthesis in GBM cell lines. We treated GBM cell lines with various concentrations of exogenous PGD2 over 72 hours and observed its effects on cell count, apoptosis, mitosis and viability. Our results suggest that PGD2 possesses contradictory functions in GBM depending on concentration (mM PGD2 vs. nM PGD2) and receptor activation.
A Organização Mundial de Saúde classifica glioblastoma (GBM) como um astrocitoma tipo IV, fazendo uns dos tumores mais fatais que existe. A pesar dos avanços em quimioterapia, cirurgia e radioterapia que melhoram a longevidade de sobrevivência, a trajetória geral da doença permanece imutável. Tem sido demonstrado que células de GBM produzem níveis significativos de prostaglandinas, incluindo prostaglandina D2 (PGD2). PGD2 possui propriedades pro- e anti-tumorigenicos. Então, um entendimento mais completo da atividade de PGD2 em GBM pode gerar tratamentos mais efetivos. Através de técnicas como RT-PCR, imunohistoquimicas e HPLC espectrometria de massa em tandem, conseguimos confirmar a presença da síntese de PGD2 em linhagens de GBM. Tratamos linhagens de GBM com concentrações variáveis de PGD2 exógeno durante 72 horas e observamos seus efeitos na contagem de células, apoptose, mitose e viabilidade. Nossos resultados sugerem que PGD2 possui funções opostas em GBM dependendo em concentração (mM PGD2 vs. nM PGD2) e ativação de receptores.
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Giegerich, Anna [Verfasser], Eric Thomas [Gutachter] Hahnen i Thorsten [Gutachter] Simon. "Identification of CD133-positive cell populations within glioma cell lines / Anna Giegerich ; Gutachter: Eric Thomas Hahnen, Thorsten Simon". Köln : Deutsche Zentralbibliothek für Medizin, 2021. http://d-nb.info/1236928091/34.

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Moore, Casey Benjamin. "Cell cycle affects accumulation of β-D-5-o-Carboranyl-2'-Deoxyuridine(D-CDU) in human glioma cell line". Thesis, Georgia Institute of Technology, 2002. http://hdl.handle.net/1853/16348.

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CILIBRASI, CHIARA. "CHROMOSOMAL INSTABILITY IN GLIOMA STEM CELL LINES FROM GLIOBLASTOMA MULTIFORME: IMPLICATIONS FOR NEW THERAPEUTIC STRATEGIES". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/158150.

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Il glioblastoma multiforme rappresenta la forma più frequente e maligna fra i tumori cerebrali primari. Nonostante un approccio terapeutico multimodale, che include resezione chirurgica, radio e chemioterapia, la prognosi è generalmente infausta. La maggior parte dei pazienti muore dopo soli 12-15 mesi dalla diagnosi e la percentuale di recidiva è pari all’80%. Crescenti evidenze suggeriscono che una delle principali cause della comparsa di recidive e del fallimento delle attuali strategie terapeutiche è la presenza, all’interno del tumore, di una sottopopolazione di cellule tumorali con caratteristiche staminali, chiamate glioma stem cells (GSCs). Le GSCs sono caratterizzate da un aumentato self-renewal, come dimostrato dall’espressione di tipici marcatori di staminalità, quali CD133 e Nestina, da un’elevata invasività, dalla capacità di differenziare in diversi lineages neurali e da una spiccata chemo e radio resistenza. Una tipica caratteristica delle GSCs è anche l’elevata instabilità cromosomica (CIN). Infatti, tali cellule, presentano numerose alterazioni numeriche e strutturali, delezioni, amplificazioni e perdite di eterozigosità. Diverse alterazioni sono state indicate come responsabili dell’instabilità cromosomica, tra cui difetti in geni codificanti per proteine coinvolte nel macchinario mitotico, come le Aurora chinasi, rendendole un possibile e promettente target terapeutico. La mia tesi si propone, perciò, di indagare due aspetti principali di quest’area di ricerca, con l’obiettivo di individuare nuove possibili strategie terapeutiche GSC-targeted, necessarie per una completa eradicazione del GBM. Nella prima parte del mio progetto ho indagato l’effetto di Danusertib, un inibitore delle Aurora chinasi, su 5 linee di cellule staminali tumorali isolate da glioblastoma, precedentemente caratterizzate nel nostro laboratorio da un punto di vista citogenomico ed epigenomico. I risultati ottenuti hanno mostrato una risposta eterogenea delle diverse linee cellulari all’inibitore: alcune di esse sono risultate maggiormente sensibili, mostrando evidenti alterazioni della morfologia, un considerevole aumento della ploidia e la presenza di un fenotipo senescente associato ad una riduzione del potenziale clonogenico e della proliferazione cellulare. Tuttavia un risultato particolarmente interessante è che anche le linee cellulari più resistenti dopo diversi rounds di esposizione all’inibitore diventano maggiormente sensibili, suggerendo la presenza di una sorta di soglia della plodia superata la quale le cellule vengono indotte alla senescenza. Nella seconda parte della mia tesi ho presentato alcuni dati preliminari ottenuti nel laboratorio del Dr. Hochegger (Genome Damage and Stability Center, University of Sussex, Brighton, UK), dove ho trascorso sei mesi durante il dottorato. Durante questo periodo ho preso parte ad un progetto mirato a sviluppare alcune linee di GSCs in cui i marcatori di staminalità CD133 e Nestina sono taggati con proteine fluorescenti attraverso la tecnica CrispR/Cas9. L’obiettivo è quello di utilizzare tali linee cellulari modificate geneticamente per studiare attraverso tecniche di live imaging la modalità di divisione cellulare messa in atto dalle GSCs, attraverso la quale esse sarebbero in grado, non solo di mantenere in pool di cellule staminali tumorali, ma anche di generare cellule più differenziate che costituiscono la maggior parte della massa tumorale. La comprensione di tale modalità di divisione cellulare potrebbe favorire l’individuazione di nuove strategie terapeutiche, attraverso l’individuazione di nuovi target coinvolti nel controllo della divisione asimmetrica delle GSCs nel tessuto cerebrale.
Glioblastoma is the most common primary malignant brain tumour in the adult population. Despite multimodality treatment with surgery, radiotherapy and chemotherapy, outcomes are very poor, with less than 15% of patients alive after two years. Increasing evidence suggests that Glioma stem cells (GSCs) are likely to play an important role in the biology of this disease and are involved in treatment resistance and tumour recurrence following standard therapy. GSCs are characterized by enhanced self-renewal, highlighted by the expression of stem cell markers, such as CD133 and Nestin, elevated invasive behaviour, chemo and radiotherapy resistance, and the ability to generate multi-lineage progenities. A typical feature of GSCs is also the elevated chromosomal instability (CIN): they are characterized by various numerical and structural aberrations, deletions, amplification and loss of heterozygosity. A variety of alterations have been proposed as being responsible for CIN, including defects in genes involved in the regulation of the mitotic machinery, such as the Aurora Kinases, making them a promising therapeutic target for GSCs depletion. My thesis address two main aspects of this research area, aiming at the identification of new GSCs-targeted therapeutic strategies for GBM complete eradication. In the first part of my project I investigated the effect of Danusertib, a pan-Aurora kinases inhibitor on 5 GSC lines isolated from glioblastoma patients, previously characterized in our laboratory from a cytogenomic and epigenomic point of view. Results showed that response to Danusertib exposure was heterogeneous among GSC lines. Some of them were more sensitive to subtle changes in Aurora kinases activity, which result in huge morphological alterations, a rapid increase in polyploidy and subsequently in senescence, with a consistent reduction in clonogenic survival and proliferation. Interestingly I also observed that the more resistant cell lines showed an increase in ploidy and senescence after repeated rounds of Danusertib exposure, suggesting that there could be the presence of an intolerable ploidy threshold that leads cells to senescence. In the second part of my thesis I presented some preliminary results I achieved in Dr Hochegger’s lab (Genome Damage and Stability Center, University of Sussex, Brighton, UK), where I took part in a project aimed on setting up CrispR/Cas9 mediated GFP or RFP-tagged CD133 (PROM1 gene) and Nestin (NES gene) glioma stem cell lines in order to look, with live cell imaging techniques, for signs for asymmetric cell division, by which a single GSC would be able to both maintain a pool of self-renewing stem cells and produce differential progeny, using live cell imaging. The biological significance of asymmetric or symmetric division modes is not yet fully understood, but improved understanding of this phenomenon may lead to the development of preventative treatments or improved therapeutic options for brain tumour patients through the identification of novel targets that are involved in the control of asymmetric cell division in human brain tissue.
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Stutzman, Alan. "The effect of Neuregen nutrient medium on the growth of rat glioma cell lines F98 and 9L /". Available to subscribers only, 2007. http://proquest.umi.com/pqdweb?did=1456287431&sid=9&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Thesis (M.S.)--Southern Illinois University Carbondale, 2007.
"Department of Molecular Biology, Microbiology and Biochemistry." Includes bibliographical references (leaves 109-126). Also available online.
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Tassone, Evelyne. "Extracellular matrix-degrading enzymes and control of fibroblast growth factor-2 (FGF-2) signaling in pediatric glioma cell lines". Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3422194.

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The main purpose of my research project was to investigate the role of two extracellular matrix-degrading enzymes, heparanase (HPSE) and membrane-type 1 matrix metalloproteinase (MT1-MMP), in pediatric gliomas. I spent the first two years of my PhD program in Dott. Maurizio Onisto’s laboratory (University of Padua). Then I continued my work at New York University School of Medicine, under the supervision of Prof. Paolo Mignatti, whose experimental work focuses on the molecular mechanisms of proteolysis-independent signaling by MT1-MMP and its physiological inhibitor, tissue inhibitor of metalloproteinase-2 (TIMP-2). Gliomas, the most common primary brain tumors, comprise a heterogeneous group of neoplasms that originate from glial cells. Despite recent advances in the management of these tumors, children affected by gliomas, particularly the more aggressive forms, have a poor prognosis. Gliomas can diffusely penetrate throughout the brain, even though they remain localized in this organ. One of the most important events during glioma cell invasion is extracellular matrix (ECM) degradation, a complex mechanism that involves both glycosidic and proteolytic enzymes. HPSE is an endo-β-D-glucuronidase secreted in the ECM, where it cleaves the heparan sulfate side chains of both soluble and membrane-bound proteoglycans. MT1-MMP, a cell membrane-bound proteinase with an extracellular catalytic domain and a short cytoplasmic tail, has been implicated in the proteolytic degradation of extracellular and transmembrane proteins. High levels of HPSE and MT1-MMP are present in a variety of aggressive malignancies, a finding that highlights their important role in cancer invasion and metastasis. In this study we characterized pediatric glioma cell lines derived from different types of gliomas: two glioblastoma multiforme, one anaplastic astrocytoma, one diffuse astrocytoma and one pilocytic astrocytoma. In addition, we used a human breast adenocarcinoma cell line to examine the role of MT1-MMP, because these cells do not express this proteinase and thus represent an ideal model for the regulation of its expression. The data reported here show that MT1-MMP controls activation of intracellular signaling by fibroblast growth factor-2 (FGF-2) and FGF-2 binding to the breast adenocarcinoma cells. We found no clear correlation between HPSE, MT1-MMP or FGF-2 expression and the aggressiveness of the pediatric astrocytoma cells. Gene silencing of HPSE in a pediatric glioblastoma cell line does not affect vascular endothelial growth factor (VEGF) expression or cell proliferation, but upregulates matrix metalloproteinase-2 (MMP-2) and MT1-MMP expression. Moreover, ERK1/2 activation by FGF-2 does not correlate with MT1-MMP expression and is modified by an MMP inhibitor in these pediatric glioma cells. Finally, TIMP-2 controls ERK1/2 activation in all glioma cells. Taken together, the results show that MT1-MMP does not have the same effects in breast carcinoma and pediatric glioma cells, indicating a different and more complex control mechanism of intracellular signaling. This initial characterization of these unique pediatric astrocytoma cell lines provides new insights into the knowledge of this poorly studied group of tumors.
L’obiettivo principale del mio progetto di ricerca è stato analizzare il ruolo di due enzimi che degradano la matrice extracellulare, l’“heparanase” (HPSE) e la “membrane-type 1 matrix metalloproteinase” (MT1-MMP), nei gliomi pediatrici. Ho trascorso i primi due anni di Dottorato nel laboratorio del Dott. Maurizio Onisto (Università di Padova). Ho poi continuato il mio lavoro presso la New York University School of Medicine, sotto la supervisione del Prof. Paolo Mignatti, il cui lavoro sperimentale è focalizzato sull’approfondimento dei meccanismi molecolari alla base dell’attivazione del segnale intracellulare da parte di MT1-MMP e del suo inibitore fisiologico, il “tissue inhibitor of metalloproteinases-2” (TIMP-2). I gliomi, i più comuni tumori cerebrali primari, comprendono un gruppo eterogeneo di neoplasie che originano dalle cellule gliali. Nonostante i recenti progressi raggiunti nel trattamento e nel controllo di tali tumori, la prognosi dei bambini affetti da glioma, ed in particolare dalle sue forme più aggressive, rimane tuttora infausta. Pur essendo confinati nell’organo nel quale originano, i gliomi possono invadere tutte le aree del cervello. Uno degli eventi più importanti che caratterizzano l’invasività dei gliomi è costituito dalla degradazione della matrice extracellulare, un complesso meccanismo che coinvolge enzimi sia glicosidici sia proteolitici. HPSE è una endo-β-D-glucuronidasi secreta nella matrice extracellulare, nella quale taglia le catene di eparan solfato dei proteoglicani solubili e legati alla membrana. MT1-MMP, una proteasi legata alla membrana e composta da un dominio catalitico extracellulare e da una piccola coda citoplasmatica, è coinvolta nella degradazione proteolitica di proteine extracellulari e di membrana. Elevati livelli di HPSE e MT1-MMP sono stati riscontrati in numerosi tipi di tumore e tale evidenza sottolinea il ruolo chiave che essi svolgono nell’invasività tumorale e nella formazione di metastasi. In questo studio sono state caratterizzate cinque linee cellulari di glioma pediatrico derivanti da diversi tipi di glioma: due glioblastomi multiformi, un astrocitoma anaplastico, un astrocitoma diffuso ed un astrocitoma pilocitico. Con lo scopo iniziale di esaminare il ruolo di MT1-MMP nell’attivazione del segnale indotto dall’FGF-2, è stata inoltre utilizzata una linea cellulare di carcinoma mammario, la quale non esprime MT1-MMP e perciò rappresenta un modello ideale per studiare la regolazione della sua espressione. I dati riportati mostrano che, nelle cellule di carcinoma mammario, MT1-MMP regola l’attivazione del segnale intracellulare da parte del “fibroblast growth factor-2” (FGF-2) e controlla il legame di questo fattore di crescita alla superficie delle cellule. Nelle cellule di astrocitoma pediatrico non è stata identificata alcuna chiara correlazione tra espressione di HPSE, MT1-MMP o FGF-2 ed aggressività tumorale. I risultati inoltre dimostrano che il silenziamento genico di HPSE in una linea cellulare di glioblastoma pediatrico non influenza l’espressione del “vascular endothelial growth factor” (VEGF) o la proliferazione cellulare, ma determina la sovraespressione della “matrix metalloproteinase-2” (MMP-2) e di MT1-MMP. Inoltre, nelle cellule di glioma, l’attivazione di ERK1/2 da parte di FGF-2 non correla con l’espressione di MT1-MMP e risulta modificata dal trattamento con un inibitore di MMP. Infine, in tutte le cellule di glioma, anche TIMP-2 regola l’attivazione del segnale intracellulare. In conclusione, i risultati ottenuti mostrano che MT1-MMP non ha gli effetti nelle cellule di carcinoma mammario e di glioma pediatrico, indicando l’esistenza di un differente e più complesso meccanismo di controllo del segnale intracellulare. La caratterizzazione delle linee cellulari di astrocitoma pediatrico presentata in questa tesi offre una più completa conoscenza di questo gruppo di tumori ancora poco studiati.
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BARONCHELLI, SIMONA. "Cytogenetic, genimic, epigenomic and drug sensitivity landscapes to unravel the complexity of glioma stem cell lines: a multi-level approach". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/27138.

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BACKGROUND. Glioblastoma multiforme (GBM) is the most common and malignant type of glioma and it is characterized by extensive heterogeneity, both at the cellular and molecular level. The poor prognosis and the lack of an effective treatment are due to the presence of a small sub-population of cells with stem-like properties, termed glioma stem cells (GSCs). At the genomic level, heterogeneity is characterized by multiple levels of alterations, including cytogenetic, genomic and epigenomic alterations. Drug sensitivity is an additional level of GSC complexity and heterogeneity and the identification of an effective treatment for GBM depends on the depletion of the GSC pool. Valproic acid (VPA) is a histone deacetylase inhibitor and so it can be used for an epigenetic therapy for cancer. Besides, a differentiation inducing ability of VPA on cancer cells was demonstrated. Paclitaxel (PTX) is a conventional chemotherapeutic agent and in the last years it was shown to be a potential therapeutic drug for gliomas. AIMS AND PROJECT DESIGN. Six GSC lines were studied, as they represent a valuable tool for the investigation of cytogenomic and epigenomic landscapes of GBM, in order to unravel specific molecular pathways, involved in the stem-like counterpart. Drug sensitivity profiles were assessed, evaluating cell viability and cytomorphological parameters (mitotic index, ploidy and polymorphic nuclei), after VPA and PTX administration. The reliability of differentiation and epigenetic therapy through the use of VPA was further investigated by morphological and molecular epigenomic analysis, investigating the DNA methylation status. RESULTS AND DISCUSSION. Several shared cytogenetic and genomic alterations linked to GBM pathogenesis were found among the GSC lines. Specifically, polysomy of chromosome 7, loss of chromosome 10, CDKN2A and CDKN2B deletions are aberrations related to highly relevant pathways in GBM tumorigenesis. Moreover, a minimal deleted region at 1p36.31 was common among the six GSC lines, including CAMTA1 gene, a putative tumor suppressor gene, specific for cancer stem-like cells. Disregulated cytogenenomic pathways in GSCs were preferentially linked to the control of stem cell proliferation, invasion, cellular development and differentiation. The evaluation of the methylation profiles of GSC lines revealed aberrant methylation of developmental genes, which are targeted by Polycomb Repressive Complex 2 in embryonic stem cells and involved in cellular development and nervous system differentiation, evidencing a specific impairment of these processes in cancer stem-like cells. VPA is able to begin a differentiation process in GSCs, as demonstrated by the study of methylation changes caused by VPA, through the methylation of pathways which are involved in self-renewal maintenance, such as Wnt/β-catenin, and several cancer-related mechanisms. Anyway, terminal differentiation was impaired, due to an intrinsic characteristic of cancer cells endowed with stem like properties. GSCs viability was severely affected by dual drug treatment, combining VPA and PTX: VPA caused an initial differentiation, enabling PTX to induce cell death of downstream cells in tumor hierarchy. Thus, a dual approach with drugs affecting different features of malignancy could be a successful approach to GBM treatment. CONCLUSIONS. A multi-level study for the evaluation of cytogenomic and epigenomic landscapes of GSCs is an effective approach for the identification of molecular pathways, specifically de-regulated in stem-like cells, giving an outstanding contribution in the identification of key mechanisms sustaining self-renewal. GSC lines are a valuable tool to evaluate the potentiality of new therapeutical approaches, which should be able to overwhelm the stem-like related counterpart. VPA and PTX combined treatment was found to fulfill the therapeutical potential of VPA and might be a successful approach to unlock the self-renewal loop, typical of GSCs and affect their growth.
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Hammerbacher, Katharina [Verfasser], i Ralf [Akademischer Betreuer] Kinscherf. "Effects of novelly synthesized nucleolipides on different tumor cell lines (HT29, HepG2, Panc-1, RenCa) with special respect to glioma cell lines (BT4Ca, GOS3, G28, G112, U251, U87) of human or other species / Katharina Hammerbacher ; Betreuer: Ralf Kinscherf". Marburg : Philipps-Universität Marburg, 2020. http://d-nb.info/120746967X/34.

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Części książek na temat "Glioma Cell Lines"

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Ohlfest, John R., i Stacy A. Decker. "Glioma Cell Lines: Role of Cancer Stem Cells". W Tumors of the Central Nervous System, Volume 1, 205–12. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0344-5_21.

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Whittle, Ian R., W. L. Kimber, M. Li, H. S. Bell i J. W. Ironside. "Glioma Cells Transduced with Selection Transgenes May Not Form Gliomas in vivo and Can Also Inhibit Glioma Formation by Admixed Wild Glioma Cell Lines". W Advances in Stereotactic and Functional Neurosurgery 12, 139–43. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6513-3_26.

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Shinoura, Nobusada, Tatsuya Kondou i Masumi Yoshioka. "Measuring the Effect of PDGF on Fibroblasts Using Glioma Cell Lines". W Biological Aspects of Brain Tumors, 235–43. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68150-2_30.

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Ding, G. R., X. W. Wang, K. C. Li, J. Miyakoshi i G. Z. Guo. "Hsps expression in three human glioma cell lines after radio-frequency field exposure". W 7th Asian-Pacific Conference on Medical and Biological Engineering, 458–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-79039-6_114.

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Wu, David J., Linda Reynolds, Dennis A. Carson i Tsutomu Nobori. "Molecular Genetic Analysis of Chromosome 9p in Methylthioadenosine Phosphorylase Deficient Glioma Cell Lines". W Advances in Experimental Medicine and Biology, 207–11. New York, NY: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-7703-4_47.

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Wikstrand, Carol J., Friedrich C. Grahmann, Rodney D. McComb i Darell D. Bigner. "Antigenic heterogeneity of human glioma tissue and cell lines (HGL) defined by monoclonal antibodies (MAs)". W Biology of Brain Tumour, 495–99. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2297-9_69.

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Smith, B. H., M. A. Greenwood, C. J. Cummins, J. Ellis, C. Gibson i P. L. Kornblith. "Non-nuclear cytotoxic actions of DNA cross-linking and/or alkylating agents in glioma-derived cell lines". W Biology of Brain Tumour, 91–96. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2297-9_13.

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Benabid, Alim L., Chantal Remy i Christiane Chauvin. "Experimental models of rat brain tumors by stereotactic injection of C6 glioma and HTC hepatoma cell lines". W Biology of Brain Tumour, 221–26. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2297-9_30.

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Colombatti, M., M. Bisconti, P. Lorenzi, G. Stevanoni, B. Dipasquale, M. Gerosa i G. Tridente. "Human Glioma Cell Lines: Tumour Associated Antigens Distribution and Sensitivity to Antibody-Toxin or Ligand-Toxin Conjugates. A Preliminary Report". W Proceedings of the 8th European Congress of Neurosurgery, Barcelona, September 6–11, 1987, 121–25. Vienna: Springer Vienna, 1988. http://dx.doi.org/10.1007/978-3-7091-8978-8_26.

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Zeltzer, Paul M., Sandra L. Schneider, Paul J. Marangos i Mark H. Zweig. "Differential expression of neuron specific enolase and creatine phosphokinase-BB by human medulloblastoma and glioma tumors and neuroectodermal cell lines". W Biology of Brain Tumour, 51–59. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2297-9_7.

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Streszczenia konferencji na temat "Glioma Cell Lines"

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Kofman, Alexander, Fadila Guessous, Charles G. diPierro, Evan Dupart, Yongde Bao, Susan Dhamala, Christopher Letson i in. "Abstract 3163: Exploration of microRNA-34a effects in human glioma cell lines". W Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3163.

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Zlatnik, Elena, Anastasia Sitkovskaya, Sergey Kolpakov, Elena Kolpakova, Svetlana Filippova i Irina Mezhevova. "EFFECT OF ROTAVIRUS STRAINS OF A NEW GROUP ON GLIOMA CELL LINES IN VITRO". W XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2131.sudak.ns2021-17/155-156.

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Khatami, S., A. Rendon, M. Yoshimitsu, J. Medin i L. Lilge. "Effect of GFP expression on the sensitivity of glioma cell lines to photodynamic therapy". W Photonics North 2005, redaktorzy Warren C. W. Chan, Kui Yu, Ulrich J. Krull, Richard I. Hornsey, Brian C. Wilson i Robert A. Weersink. SPIE, 2005. http://dx.doi.org/10.1117/12.628706.

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Rossi, Alex P., Eric C. Woolf, Kenneth S. Brooks, Marshall J. Fairres i Adrienne C. Scheck. "Abstract 3346: The ketone body β-hydroxybutyrate increases radiosensitivity in glioma cell lines in vitro". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3346.

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Quintavalle, Cristina, Michela Garofalo, Giulia Romano, Margherita Iaboni, Ciro Zanca, Monica Brenca, Gerald Nuovo, Carlo Maria Croce i Gerolama Condorelli. "Abstract LB-351: miR-221&222 regulate cell motility in glioma cell lines targeting the protein phosphates PTPμ". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-351.

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Hedegaard, Chris J., Charles N. Pegram, Darell D. Bigner i Hans S. Poulsen. "Abstract 2732: Internalization of the dual-specific immunotoxin D2C7-(scdsFv)-PE38KDEL in malignant glioma cell lines". W Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2732.

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Dikshit, Bhawana, Kunzang Chosdol i Subrata Sinha. "Abstract A38: Overexpression of FAT1 in human GBM (glioblastoma multiforme) and high-grade glioma cell lines". W Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-a38.

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Lespinats, Sylvain, Katja Pinker-Domenig, Georg Wengert, Ivo Houben, Marc Lobbes, Andreas Stadlbauer i Anke Meyer-Bäse. "Proteomic data analysis of glioma cancer stem-cell lines based on novel nonlinear dimensional data reduction techniques". W SPIE Commercial + Scientific Sensing and Imaging, redaktorzy Liyi Dai, Yufeng Zheng, Henry Chu i Anke D. Meyer-Bäse. SPIE, 2016. http://dx.doi.org/10.1117/12.2229133.

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Garcia-Claver, Ainoha, Gema Perez-Diaz, Carmen Granda, Yolanda Campos-Martin, Yolanda Ruano, Elisa Perez-Magan, Manuela Mollejo i Barbara Melendez. "Abstract 732: Characterization of gene expression changes associated with Erlotinib and Temsirolimus treatment in glioma cell lines". W Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-732.

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Buckingham, John, Reyda Gonzalez-Nieves i Mary L. Cutler. "Abstract 5140: Rsu1 and the IPP adhesion complex can regulate adhesion and migration in glioma cell lines". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5140.

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