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Статті в журналах з теми "Glioma Stem-like Cells"
Ventosa, Maria, Padma Kadiyala, Stephen Carney, Maria Castro, and Pedro Lowenstein. "GENE-32. SYNTHETIC LETHAL INTERACTIONS WITH IDH1R132H IN GLIOMA STEM-LIKE CELLS." Neuro-Oncology 21, Supplement_6 (November 2019): vi104. http://dx.doi.org/10.1093/neuonc/noz175.434.
Повний текст джерелаNikitin, Pavel V., Guzel R. Musina, Stanislav I. Pekov, Andrey A. Kuzin, Igor A. Popov, Artem Y. Belyaev, Gregory L. Kobyakov, Dmitry Y. Usachev, Viktor N. Nikolaev, and Valentin P. Mikhailov. "Cell-Population Dynamics in Diffuse Gliomas during Gliomagenesis and Its Impact on Patient Survival." Cancers 15, no. 1 (December 26, 2022): 145. http://dx.doi.org/10.3390/cancers15010145.
Повний текст джерелаBota, Daniela A., Daniela Alexandru, Stephen T. Keir, Darell Bigner, James Vredenburgh, and 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, no. 6 (December 2013): 1415–23. http://dx.doi.org/10.3171/2013.7.jns1323.
Повний текст джерелаKim, Jun-Kyum, Hye-Min Jeon, Hee-Young Jeon, Se-Yeong Oh, Eun-Jung Kim, Xiong Jin, Se-Hoon Kim, Sung-Hak Kim, Xun Jin, and Hyunggee Kim. "Conversion of glioma cells to glioma stem-like cells by angiocrine factors." Biochemical and Biophysical Research Communications 496, no. 4 (February 2018): 1013–18. http://dx.doi.org/10.1016/j.bbrc.2017.02.076.
Повний текст джерелаAnand, Sumyuktha V., Alexander G. Skorput, Allan T. Gulledge, Isabella B. Fox, Damian A. Bonnin, Alison L. Young, and Matthew C. Havrda. "Abstract 905: Targeting muscarinic acetylcholine receptors in glioma stem like cells." Cancer Research 82, no. 12_Supplement (June 15, 2022): 905. http://dx.doi.org/10.1158/1538-7445.am2022-905.
Повний текст джерелаJadus, Martin, Neil Hoa, Lisheng Ge, Yurii Kuznetsov, Alex McPherson, Andrew Cornforth, Nabil Ahmed, and Lawrence Lamb. "Gliomas display complex cell surface topographies that resist cytolytic lymphocytes but are reversed by using fascin siRNA (48.2)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 48.2. http://dx.doi.org/10.4049/jimmunol.186.supp.48.2.
Повний текст джерелаFENG, XING, QIN ZHOU, CHONG LIU, and MEI-LING TAO. "Drug screening study using glioma stem-like cells." Molecular Medicine Reports 6, no. 5 (August 20, 2012): 1117–20. http://dx.doi.org/10.3892/mmr.2012.1040.
Повний текст джерелаPersson, Anders I., and William A. Weiss. "The Side Story of Stem-like Glioma Cells." Cell Stem Cell 4, no. 3 (March 2009): 191–92. http://dx.doi.org/10.1016/j.stem.2009.02.004.
Повний текст джерелаLichti, Cheryl F., Norelle C. Wildburger, Alexander S. Shavkunov, Ekaterina Mostovenko, Huiling Liu, Erik P. Sulman, and Carol L. Nilsson. "The proteomic landscape of glioma stem-like cells." EuPA Open Proteomics 8 (September 2015): 85–93. http://dx.doi.org/10.1016/j.euprot.2015.06.008.
Повний текст джерелаBerglar, Inka, Stephanie Hehlgans, Andrej Wehle, Caterina Roth, Christel Herold-Mende, Franz Rödel, Donat Kögel, and Benedikt Linder. "CHRDL1 Regulates Stemness in Glioma Stem-like Cells." Cells 11, no. 23 (December 3, 2022): 3917. http://dx.doi.org/10.3390/cells11233917.
Повний текст джерелаДисертації з теми "Glioma Stem-like Cells"
Moschioni, Chiara. "Engineered bovine herpesvirus type 4: a new tool against glioma stem-like cells?" Doctoral thesis, Università degli studi di Padova, 2015. http://hdl.handle.net/11577/3423951.
Повний текст джерелаIl Glioblastoma (GBM) è un tumore cerebrale primario di IV grado (WHO 2007). Nonostante gli ultimi progressi in chirurgia, chemioterapia e radioterapia, questo tumore al cervello è ancora incurabile e recidivante (Stupp et al, 2009). È stato ipotizzato che la sua resistenza alle terapie e le recidive potrebbero essere dovute all'esistenza di una sottopopolazione di cellule tumorali, denominata cellule staminali di glioma (Glioma Stem Cells - GSC) (Galli et al, 2004; Bao et al, 2006). L'obiettivo della terapia del GBM è quindi il targeting selettivo delle GSCs e, tra le possibilità, l'uso di vettori virali è stata ampiamente studiato (Kroeger et al, 2010). Gli Herpesvirus sono stati ampiamente studiati e modificati per il trattamento del GBM (Grandi et al, 2009). In questo studio è stata valutata la capacità di un vettore ingegnerizzato dall’ Herpesvirus Bovino di tipo 4 (BoHV-4), chiamato BoHV-4TKdsRED, di uccidere selettivamente le GSC. Il vettore esprime la Timidina Chinasi di HSV-1 e quindi può essere utilizzato con il Ganciclovir (GCV) in un protocollo di terapia genica suicida. Il suo potenziale ruolo come vettore per il trattamento del GBM è già stato dimostrato (Redaelli et al, 2012). Sono stati utilizzati tre diverse colture primarie di GSC umane (GBM2, GBM4 e GBM5) e le corrispondenti cellule coltivate in siero (FBS2, FBS4 e FBS5). Sono state infettate con BoHV- 4TKdsRED ed è stato testato anche un trattamento combinato del vettore con GCV sulle GSCs. È stato anche analizzato qualora vie di segnale di apoptosi o autofagia vengano attivate nelle GSCs infettate. Per verificare l'effetto di BoHV-4TKdsRED sono stati compiuti saggi di counting/killing, saggi di placca, Western Blot e analisi FACS. BoHV-4TKdsRED è in grado di infettare le GSCs e le cellule FBS. Può replicarsi in quasi tutte le colture esaminate e le può uccidere in vitro. Il trattamento combinato del vettore col GCV porta ad un aumento della mortalità nelle GSCs. Segni iniziali di attivazione dell'autofagia sono stati rilevati con il trattamento combinato nelle GSCs. Lo studio dell’apoptosi attraverso analisi FACS ha dato risultati non affidabili. Un altro vettore derivato da BoHV-4, BoHV-4EGFPΔTK, ha dimostrato la sua capacità di infettare le cellule self-renewing, ma senza esercitare un effetto citopatico. Secondo i nostri risultati, BoHV-4TKdsRED potrebbe essere un promettente vettore per le GSCs, ma ulteriori analisi devono essere effettuate per rafforzare questi dati.
Müller-Greven, Gaëlle Melanie. "Glioma Stem-like Cell Survival is Affected by their Macropinocytic Uptake and Targeted Trafficking of Bevacizumab." Kent State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=kent1520520113612687.
Повний текст джерелаNgwabyt, Bikeye Sandra-Nadia. "Etude par ARN interférence de l’expression du gène ASPM dans les cellules souches tumorales des gliomes de haut grade." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T030/document.
Повний текст джерелаGlioblastoma (GBM) is the most frequent and aggressive form of primary brain tumors in adults; it is characterized by its resistance to current treatments (surgery, chemotherapy and radiotherapy). The prognosis is grim with a median survival of only 15 months underlining the importance to develop new therapeutic strategies. The recent development of the “tumor stem cell” (TSC) concept in hemopathies has been secondarily applied to gliomas with the identification of subpopulations of GBM cells which express neural stem cell markers and fulfill the criteria for stemness. Some evidences also suggest that this subpopulation could play a primary role in resistance to radio- and chemotherapy.ASPM (Abnormal Spindle Like Microcephaly Associated) is a protein regulating the proliferation of neuroblasts, highly expressed in the embryonic stage but weakly expressed in the adult brain. Preliminary reports suggesting that it could be involved in the development of gliomas (Horvath et al., 2007, Hagemann et al., 2008) prompted us to analyze further the role of this protein, focusing on its potential as a relevant candidate therapeutic target. In a series of 175 gliomas samples of various grades, we found that ASPM mRNA expression was strongly correlated with increasing tumor grade. We also found that ASPM expression increased at recurrence when compared to the initial lesion. Subsequently, we could demonstrate in vitro and in vivo that ASPM expression also increased over serial passages in gliomaspheres and in a mouse glioma xenograft model. In a therapeutic perspective, the effect of lentivirus-mediated shRNA post-transcriptional silencing of ASPM was evaluated in two different gliomasphere models and a dramatic proliferation arrest and cell death was observed. Taken together, these data suggest that ASPM is involved in the malignant progression of gliomas, possibly through expansion of a cancer stem cell compartment, and could be an attractive therapeutic target in glioblastoma multiforme.Another potential candidate tumor stem cell target in glioma is the sonic hedgehog pathway (hedgehog-Gli) which is required for GBM growth and stem cell expansion. In a collaborative study, it was found that NANOG, a transcription factor critically involved with self-renewal of undifferentiated embryonic stem cells, modulates gliomasphere clonogenicity, CD133+ stem cell behavior and proliferation. NANOG was regulated by hedgehog-Gli signalling and was essential for GBM tumourigenicity in orthotopic xenografts suggesting that it could also be a useful potential therapeutic target.Conclusions: Accumulating evidences suggest that tumor stem cells play an important role in the oncogenesis of gliomas and in their resistance to treatment. Our data support this concept and suggest that specific stemness markers may become useful targets to improve treatment of this devastating disease
Ebert, Birgit [Verfasser], Dieter Chichung [Akademischer Betreuer] Lie, and Wolfgang [Akademischer Betreuer] Wurst. "The effect of mitochondrial dysfunction on astrocytes and radial glia like stem cells in the adult hippocampus / Birgit Ebert. Gutachter: Wolfgang Wurst ; Dieter Chichung Lie. Betreuer: Dieter Chichung Lie." München : Universitätsbibliothek der TU München, 2013. http://d-nb.info/1036262189/34.
Повний текст джерелаSilva, Joana Balça Pinheiro da Costa e. "Molecular Mechanisms of Glioblastoma Resistance: glioma stem-like and non-stem-like cells specific targets." Doctoral thesis, 2018. http://hdl.handle.net/10316/79716.
Повний текст джерелаGlioblastoma (GBM) is the most malignant primary tumor of the central nervous system. Despite all efforts, the median survival time for GBM patients remains approximately between 12 to 15 months under therapy. GBM is a diffuse astrocytoma, highly proliferative, angiogenic, and locally invasive, that develops resistance to the alkylating agents used in chemotherapy, such as temozolomide (TMZ), which is considered part of the gold standard treatment. This limited success appears to be related with several mechanisms, namely: 1) the occurrence of gene mutations, that cause permanent activation and/or inhibition of several molecular signalling pathways involved in tumor growth and proliferation, such as protein kinase C (PKC) activation, cell survival, tumor suppressor genes and apoptosis; 2) the presence of a population of cells known to be chemo and radioresistant, the glioma stem-like cells (GSCs), that are responsible for generating tumor heterogeneity and recurrence after therapy, and; 3) the inexistence of a specific therapeutic target for non-GSCs and GSCs that would permit the development of more specific therapeutic approaches for this neoplasia. Therefore, in this work we aimed to: 1) study the PKC activation contribution to the aggressiveness of GBM, emphasizing the importance of combined therapeutic protocols, including TMZ with PKC inhibitors, namely tamoxifen (TMX); 2) characterize the GSCs and study their plasticity to understand glioma stem-like cells state and its differentiation properties, in order to contribute to the prevention of tumor recurrence; and 3) evaluate the potential of specific cell surface markers as therapeutic targets to non-GSCs and GSCs, allowing the accessibility of therapeutic agents most exclusively to the tumor niche, by a liposome-mediated drug delivery approach. First, using two GBM cell lines, the U87 and U118 cells, we observed that the combination of TMX and TMZ alters the phosphorylation status of PKC, by western blot. We found that TMX is an inhibitor of the p-PKC and that this combination is more effective in the reduction of proliferation and in the increase of apoptosis than each drug alone, by flow cytometry, which presents a new therapeutic strategy in GBM treatment. We then concluded that the combination of TMX and TMZ seems to potentiate the effect of each other in GBM cell lines. In order to study the heterogeneity between GBM cells and further understand the variability in the chemotherapeutic response, we next isolated and characterized a human GBM cell line, termed GBM11, obtained by surgical biopsy from a patient bearing a recurrent GBM, and compared the effect of TMX in monotherapy and in combination with TMZ on this GBM cell line with that observed in U87 and U118 cell lines. We observed that the effect of TMX plus TMZ or with TMX alone on GBM11 cells proliferation, death or migration capability, by flow cytometry and scratch assays, was similar, suggesting that, for recurrent tumors, the best choice of second-line treatment may be TMX alone, which may also reduce putative side effects of combined treatment with TMZ. The chemo- and radioresistance of GBM are also due to GSCs which contribute to tumor growth and relapse, highlighting this cell population as a main focus for GBM therapeutic research. We considered that the understanding of GBM stem state plasticity is of utmost importance to identify the mechanisms involved in GSCs resistance to therapy, which may justify tumor recurrence and so, constitute a step forward to the identification of new approaches to treat GBM. Our results demonstrated that, in four GBM cell lines and in the respectively GSC lines, the plasticity of the GBM stem-like cell state is based on the modulation of specific markers expression associated with this state, such as SOX2 or as Connexin 46 and 43, through immunofluorescence, western blot and PCR real time assays. Moreover, by immunohistochemistry analyses, we observed that this dynamic expression is in accordance with the upregulation of these stem-like cell markers in human samples of higher glioma grades, namely GBM, compared to lower grades, suggesting a direct correlation with the poor prognosis of GBM patients. As so, due to the plasticity of the stem-like cells status, the strategy of targeting both GSCs and non-GSCs may represent a promising approach in order to overcome tumor aggressiveness, and eventually to avoid the known chemotherapeutic side effects, which could improve the survival time and quality of life of GBM patients. In this regard, we next evaluate the potential of the cell surface nucleolin (NCL), described as overexpressed in cancer cells, as a target to specifically recognize non-GSCs and GSCs, taunting a possible therapeutic target for drug delivery in two different GBM cell lines. For that, we used a previously designed F3-peptide-targeted sterically stabilized pH-sensitive liposome (SLpH), which specifically recognizes nucleolin, as a tool to target overexpressed-nucleolin cells. Overall, we showed that NCL overexpression ensures an efficient drug delivery in both cells with stem-like and non-stem-like phenotypic characteristics, by flow cytometry assays, which could validate NCL as a potential therapeutic target in GBM. Altogether, our results showed: 1) a synergistic effect of TMX and TMZ in GBM cell lines and a more efficient effect of TMX alone in recurrent GBM compared to the combined therapy; 2) the plasticity of stem-like cell state through the reversibility of stem-like cell markers expression, and the identification of putative markers associated with this reversibility, the SOX2 and Cx46 and 43, which constitutes a step closer to the understanding of stem cell behaviour; and 3) that the success of targeting both non-GSCs and GSCs, through the nucleolin target, may be the basis for developing a specific treatment for GBM.
O Glioblastoma (GBM) é o tumor primário mais maligno do sistema nervoso central. Apesar de todos os esforços, o tempo médio de sobrevivência para doentes com GBM permanece aproximadamente entre os 12 a 15 meses sob terapia. O GBM é um astrocitoma difuso, altamente proliferativo, angiogénico e localmente invasivo, que desenvolve resistência aos agentes alquilantes utilizados na quimioterapia, como a temozolomida (TMZ), que é considerada parte do tratamento padrão. Este sucesso limitado parece estar relacionado com vários mecanismos, tais como: 1) a ocorrência de mutações genéticas que causam ativação permanente e / ou inibição de várias vias de sinalização molecular envolvidas no crescimento e proliferação de tumores, como a ativação da proteína cínase C (PKC), na sobrevivência celular, na inibição de genes supressores de tumores e apoptose; 2) a presença de uma população de células conhecidas como quimio- e radiorresistentes, as células de glioma do tipo estaminal (GSCs), que são responsáveis pela heterogeneidade tumoral e recorrência após a terapia e; 3) a inexistência de um alvo terapêutico para não-GSCs e GSCs que permita o desenvolvimento de abordagens terapêuticas mais específicas para esta neoplasia. Assim, neste trabalho, objetivámos: 1) estudar a contribuição da ativação da PKC para a agressividade do GBM, enfatizando a importância de protocolos terapêuticos combinados, incluindo a TMZ com inibidores de PKC, nomeadamente o tamoxifeno (TMX); 2) caraterizar as GSCs e estudar a plasticidade das propriedades destas células estaminais do GBM, no sentido de compreender o estado estaminal do glioma e, consequentemente, entender as propriedades de diferenciação, contribuindo para a recorrência do tumor; e 3) avaliar o potencial de marcadores de superfície celular específicos, como alvos terapêuticos para as não-GSCs e GSCs, a fim de permitir a acessibilidade de agentes terapêuticos mais exclusivamente ao nicho do tumor, por meio de uma abordagem de administração de fármacos mediada por lipossomas. Inicialmente, usando duas linhas celulares de GBM, a U87 e a U118, observámos que a combinação de TMX e TMZ altera o estado de fosforilação da PKC, por western blot. Descobrimos que o TMX é um inibidor da p-PKC e que esta combinação é mais eficaz na redução da proliferação e no aumento da apoptose do que cada fármaco em monoterapia, através de ensaios de citometria de fluxo, o que pode representar uma nova estratégia terapêutica no tratamento do GBM. Concluímos, então, que a combinação de TMX e TMZ potencializa o efeito entre si nas linhas celulares de GBM. No sentido de estudar a heterogeneidade entre células de GBM e compreender melhor a variabilidade da resposta à quimioterapia, isolámos e caracterizámos uma linha celular de GBM humana, denominada GBM11, obtida através de uma biópsia cirúrgica de um doente com glioblastoma recorrente, e comparámos o efeito do TMX em monoterapia e em combinação com a TMZ, nesta linha celular, com o observado nas linhas celulares U87 e U118. Na verdade, observámos que o efeito do TMX e TMZ ou do TMX sozinho nas células de GBM11 sobre a proliferação celular, morte ou capacidade de migração, através de ensaios de citometria de fluxo e migração, era semelhante, o que pode sugerir que, para os tumores recorrentes, como o caso do GBM11 previamente tratado com TMZ, a melhor escolha do tratamento de segunda linha pode ser apenas TMX, a fim de reduzir os efeitos secundários putativos do tratamento combinado com TMZ. A quimio- e a radiorresistência do GBM devem-se, também, à existência de GSCs, que contribuem para o crescimento tumoral e recorrência destacando-se, assim, esta população celular como o foco principal da investigação terapêutica no GBM. Consideramos que a compreensão da plasticidade do estado estaminal no GBM é de extrema importância para identificar os mecanismos e fatores envolvidos na resistência das GSCs à terapia, o que pode justificar a recorrência do tumor e, portanto, constituir um progresso na identificação de novas abordagens terapêuticas. Os nossos resultados demonstraram, em quatro linhas celulares de GBM e nas respetivas linhas de GSCs, a plasticidade do estado estaminal com base na modulação da expressão de marcadores específicos associados, tais como o SOX2 e outros marcadores como a Conexina 46 e 43, através de ensaios de imunofluorescência, western blot e PCR em tempo real. Além disso, através de ensaios de imunohistoquímica, verificámos que essa expressão dinâmica está de acordo com a regulação positiva destes marcadores celulares em graus superiores de amostras humanas de glioma, nomeadamente no GBM, comparativamente a graus inferiores, sugerindo uma correlação direta com o mau prognóstico de doentes com GBM. Assim, devido à plasticidade do estado estaminal, a estratégia de atingir designadamente ambas as GSCs e não-GSCs pode representar uma abordagem importante no sentido de diminuir a agressividade do tumor e, eventualmente, evitar os efeitos colaterais quimioterapêuticos conhecidos, o que pode melhorar o tempo e a qualidade de vida de doentes com GBM. Neste sentido, avaliámos o potencial da nucleolina (NCL) de superfície celular, descrita como estando sobre-expressa nas células tumorais, como um alvo terapêutico para o reconhecimento específico de ambas as não-GSCs e GSCs, contribuindo para a entrega direcionada de fármacos encapsulados em nanopartículas, em duas linhas celulares de GBM. Para isso, utilizámos um lipossoma previamente desenhado, sensível ao pH e estericamente estabilizado, contendo na sua constituição um péptido F3, capaz de reconhecer especificamente a nucleolina constituindo, assim, uma ferramenta- alvo para as células com sobre-expressão de nucleolina. Em suma, demostrámos que a sobre-expressão de nucleolina per se pode identificar ambas as não-GSCs e GSCs, através de ensaios de citometria de fluxo, mediando a entrega direcionada intracelular, o que pode validar a NCL como um potencial alvo terapêutico no GBM. Em conclusão, o presente estudo demonstrou: 1) um efeito sinergístico do TMX e TMZ em linhas celulares de GBM e um efeito mais eficiente do TMX em monoterapia numa situação de GBM recorrente em comparação com a terapia combinada; 2) a plasticidade do estado estaminal através da reversibilidade da expressão dos marcadores de células do tipo estaminal e a identificação de dois marcadores putativos associados a essa reversibilidade, o SOX2 e a Cx46 e 43, constituindo um passo mais próximo na compreensão do comportamento das células estaminais; e 3) que o sucesso em atingir especificamente células não-GSCs e GSCs, através da sobre-expressão de nucleolina, poderá ser a base de desenvolvimento de um tratamento específico para o GBM.
Conselho Nacional de Desenvolvimento Tecnológico (CNPq), Brasil; Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), Brasil; Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ); Pró-Saúde - Associação Beneficente de Assistência Social e Hospitalar, Brasil; FEDER/COMPETE/ FCT PTDC/EBB-EBI/120634/2010 e PDTC/QUI-BIQ/120652/2010
Visvanathan, Abhirami. "Deciphering the Role of METTL3-Dependent m6A-epitranscriptome in Glioma Stem-like Cells." Thesis, 2017. http://etd.iisc.ac.in/handle/2005/4166.
Повний текст джерелаMala, Uchurappa. "An integrative analysis of Cell Adhesion Molecules (CAMs) in Glioma: The Essential role of PTGFRN and ASTN1 in Glioma and Glioma Stem-like Cells." Thesis, 2020. https://etd.iisc.ac.in/handle/2005/4658.
Повний текст джерелаBhargava, Shruti. "Panoramic View of RNA Binding Proteins (RBPs) in Glioblastoma : IMP3, an RBP, is Essential for Glioma Stem-like Cell Maintenance." Thesis, 2016. https://etd.iisc.ac.in/handle/2005/4377.
Повний текст джерелаRübsam, Anne. "Molekulare Mechanismen des radiosensibilisierenden Effektes von Chloroquin beim Glioblastoma multiforme." Doctoral thesis, 2013. http://hdl.handle.net/11858/00-1735-0000-0001-BBE9-8.
Повний текст джерелаЧастини книг з теми "Glioma Stem-like Cells"
Sørensen, Mia Dahl, Sigurd Fosmark, Sofie Hellwege, Dagmar Beier, Bjarne Winther Kristensen, and Christoph Patrick Beier. "Chemoresistance and Chemotherapy Targeting Stem-Like Cells in Malignant Glioma." In Advances in Experimental Medicine and Biology, 111–38. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16537-0_7.
Повний текст джерелаVisvanathan, Abhirami, and Kumaravel Somasundaram. "Glioma Stem-Like Cells in Tumor Growth and Therapy Resistance of Glioblastoma." In Advances in Biology and Treatment of Glioblastoma, 191–218. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56820-1_8.
Повний текст джерелаKarambizi, David, and Nikos Tapinos. "The Dynamic m6A Epitranscriptome in Glioma Stem Cell Plasticity and Function." In CNS Malignancies [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96792.
Повний текст джерелаТези доповідей конференцій з теми "Glioma Stem-like Cells"
Ahmed, Atique U., Brenda Auffinger, Alex Tobias, Bart Thaci, Yu Han, and Maciej S. Lesniak. "Abstract 5021: Temozolomide-induced conversion of glioma cells into glioma “stem-like” cells with enhanced invasion properties." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5021.
Повний текст джерелаWang, Lei, Ziyan Liu, Sivasai Balivada, Marla Pyle, Gilbert J. Cote, Jishu Shi, and Deryl Troyer. "Abstract LB-98: Reprogramming towards glioma stem-like cells by cytokines." In 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-lb-98.
Повний текст джерелаDeng, Changwang, Son B. Le, and David D. Tran. "Abstract 1141: A novel regulatory gene subnetwork of glioma stem-like cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1141.
Повний текст джерелаPark, Soon Young, Yuji Piao, Emmanuel Martinez-Ledesma, Jianwen Dong, Sabbir Khan, Sandeep Mittal, Ze-yan Zhang, Erik P. Sulman, Veerakumar Balasubramaniyan, and John F. de Groot. "Abstract 4678: Targeting MEK in EGFR amplified glioma stem like cells induces differentiation." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4678.
Повний текст джерелаPark, Soon Young, Yuji Piao, Emmanuel Martinez-Ledesma, Jianwen Dong, Sabbir Khan, Sandeep Mittal, Ze-yan Zhang, Erik P. Sulman, Veerakumar Balasubramaniyan, and John F. de Groot. "Abstract 4678: Targeting MEK in EGFR amplified glioma stem like cells induces differentiation." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4678.
Повний текст джерелаShingu, Takashi, Lindsay Holmes, Verlene Henry, Khatri Latha, Anupama E. Gururaj, Laura A. Gibson, Tiffany Doucette, et al. "Abstract 3483: Synergistic combination therapy with molecular targeted drugs in glioma stem-like cells." In 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.am2015-3483.
Повний текст джерелаSpehalski, Elizabeth I., Cord Peters, Philip Tofilon, and Kevin Camphausen. "Abstract 5427: Distinctions between the metabolic changes in glioblastoma cells and glioma stem-like cells following irradiation." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5427.
Повний текст джерелаRajcevic, Uros, Sabrina Fritah, Petr V. Nazarov, Mara Popovic, Rajko Kavalar, Tadej Strojnik, Neza Podergajs, et al. "Abstract 1503: HP1-gamma's expression correlates with glioma grade and survival and is a putative marker of glioma stem like cells." In 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.am2015-1503.
Повний текст джерелаCiechomska, I., B. Gielniewski, B. Kaminska, and J. Mieczkowski. "PO-082 BMP4-induced differentiation does not enhance chemosensitivity of glioma stem-like cells to temozolomide." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.125.
Повний текст джерелаShaw, Vikram, Yuji Piao, Soon Young Park, Jianwen Dong, Emmanuel Martinez-Ledesma, Caroline Carrillo, Verlene Henry, et al. "Abstract 4858: Efficacy of the protein arginine methyltransferase PRMT5 inhibitor GSK591 in glioma stem-like cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4858.
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