Academic literature on the topic 'Gliomi'
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Journal articles on the topic "Gliomi"
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Laigle-Donadey, F., and A. Duran-Peña. "Gliomi del tronco cerebrale dell’adulto." EMC - Neurologia 19, no. 2 (2019): 1–13. http://dx.doi.org/10.1016/s1634-7072(19)42022-9.
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Turazzi, S. "Principi di chirurgia dei gliomi." Rivista di Neuroradiologia 16, no. 1_suppl (2003): 181–82. http://dx.doi.org/10.1177/19714009030160s171.
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Darlix, A., V. Rigau, and H. Duffau. "Neoformazioni intracraniche: gliomi di grado II." EMC - Neurologia 20, no. 4 (2020): 1–14. http://dx.doi.org/10.1016/s1634-7072(20)44227-8.
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Roux, A., and J. Pallud. "Gravidanza e gliomi diffusi di basso grado." EMC - Neurologia 18, no. 1 (2018): 1–8. http://dx.doi.org/10.1016/s1634-7072(17)87847-8.
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Bradač, G. B., A. Riva, S. Sales, and G. Stura. "Chemioterapia arteriosa nel trattamento dei gliomi maligni." Rivista di Neuroradiologia 7, no. 1_suppl (1994): 193–95. http://dx.doi.org/10.1177/19714009940070s139.
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Smaltino, F., R. Ruggiero, F. Fortunato, O. Catalano, and A. Frusciante. "La radiochirurgia stereotassica dei gliomi ad alto grado." Rivista di Neuroradiologia 7, no. 1_suppl (1994): 263–68. http://dx.doi.org/10.1177/19714009940070s151.
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Scerrati, M., P. Montemaggi, R. Roselli, M. Iacoangeli, A. Pompucci, and G. F. Rossi. "La brachiterapia interstiziale nel trattamento dei gliomi cerebrali." Rivista di Neuroradiologia 7, no. 1_suppl (1994): 275–76. http://dx.doi.org/10.1177/19714009940070s153.
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Piana, C., U. Pasquini, F. Menichelli, M. De Nicola, F. Bevilacqua, and U. Salvolini. "Chemioterapia endoarteriosa con ACNU (Nimustin) nei gliomi cerebrali maligni." Rivista di Neuroradiologia 5, no. 4_suppl (1992): 83–89. http://dx.doi.org/10.1177/19714009920050s410.
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Piana, C., U. Pasquini, F. Menichelli, M. De Nicola, and F. Bevilacqua. "Chemioterapia endoarteriosa con ACNU (Nimustin) nei gliomi cerebrali maligni." Rivista di Neuroradiologia 7, no. 1_suppl (1994): 189–91. http://dx.doi.org/10.1177/19714009940070s138.
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Ruggiero, G., A. Bacci, and R. Ricci. "Identificazione della natura istologica deigliomi cerebrali con tomografia computerizzata." Rivista di Neuroradiologia 2, no. 3 (1989): 267–71. http://dx.doi.org/10.1177/197140098900200308.
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Gli autori si propongono di verificare l'utilità rispettiva della biopsia e della radiologia per identificare il grado di malignità dei gliomi cerebrali. L'esame critico della letteratura dimostra che la biopsia effettuata su materiale chirurgico è più affidabile di quella sterotassica, ma che comunque essa non è esente da errori tecnici o diagnostici e da pericoli. La TC è utile e non inferiore, anzi non raramente superiore, alla RM. In una ricerca personale condotta su 123 casi verificati istologicamente, la TC, riesaminata dallo stesso neuroradiologo senza conoscenza della diagnosi, senza e con conoscenza della sintomatologia cliniCa, ha permesso l'identificazione precisa (gradi I-IV della scala di Kernohan) nel 42,8% e l'indicazione più generica di «benignità» (gradi I e II) e malignity (grado III e IV) nell'83%. Questi risultati sono stati ottenuti con esami eseguiti con vari tipi di apparecchi e miglioreranno sicuramente con l'utilizzo di macchine moderne e di una tecnica corretta: ricostruzione su tre piani, sezioni sottili; analisi densitometrica; proiezione extracranica38. Per conseguenza gli Autori propongono di eliminare la biopsia e classificare i gliomi cerebrali soltanto neuroradiologicamente (TC), in due tipi: Tipo B («benigno»), Tipo M (maligno).
Dissertations / Theses on the topic "Gliomi"
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Redaelli, Marco. "Herpes virus bovino di tipo 4 come vettore per la terapia genica dei gliomi." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3426019.
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Gliomas are considered among the most puzzling problems of medicine due to the complexity of their anatomic localization, and the lack of a real therapeutic treatment. The main topic of this work concerns the possibility to use bovine herpesvirus type 4 (BoHV-4) as a vector for gene therapy for the treatment of glioma, and that the cAMP-dependent protein kinases (PKA) pathway as a possible target for such therapy.
This study is based on a research project that involved both University of Padova and University of Parma.
Here BoHV-4 to is shown to infect rat glioma cells in vitro and in vivo, in addition, BoHV-4 can infect human immortalized glioma cells in vitro and human brain tumour primary cell cultures.
The study of the relationship between gliomas and the PKA pathway shows a peculiar distribution of the PKA regulatory subunits in glioma cells in mouse, rat and human. The present data suggest that the PKA pathway modulation may be targeted for the treatment of gliomas.
The present Study pave the way to the use of a safe and efficient BoHV-4-based vector for the delivery of therapeutic genes or for the targeting of specific abnormal pathways, like the PKA-mediated one, for the treatment of the hopeless high-grade glioma.<br>L’ipotesi alla base di questo lavoro è che vi sia la possibilità di impiegare quale vettore virale per la terapia genica dei gliomi l’herpesvirus bovino di tipo 4 (BoHV-4) e di determinare se la via di trasduzione del segnale mediata dalle protein chinasi AMPc-dipendenti (PKA) possa essere utilizzata come bersaglio terapeutico. Infatti i gliomi sono ritenuti essere uno dei più importanti e stimolanti problemi irrisolti della medicina. Questo sia per la evidente complessità della sede anatomica di insorgenza, sia per il fatto che, nonostante gli enormi sforzi in cui gli scienziati di tutto il mondo si sono profusi non si è ancora riusciti a giungere alla messa a punto di un protocollo curativo realmente efficace.
Il progetto di ricerca su cui si è basato il presente studio è il risultato della convergenza di due linee di ricerca preesistenti presso le Università di Padova e di Parma.
I risultati conseguiti hanno dimostrato la capacità di BoHV-4 di infettare in vitro e in vivo cellule di glioma di ratto. Inoltre tale capacità è stata confermata in vitro sia su cellule immortalizzate di glioma umano che su colture primarie di tumore cerebrale umano.
Per quanto riguarda lo studio della relazione tra PKA e tumori cerebrali, è stato in primo luogo rilevata una distribuzione peculiare delle diverse subunità regolatorie delle medesime che è caratteristica delle cellule di glioma. Inoltre diversi esperimenti suggeriscono che la modulazione di tale via possa essere impiegata per il trattamento dei gliomi oltre che per fini diagnostici.
Tutti i risultati ottenuti suggeriscono di proseguire ed ampliare il progetto facendo convergere entrambe le sue linee costituenti in un modello da poter esportare nella pratica clinica nel minor tempo possibile.
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COMI, ALESSANDRO. "Memoria verbale nei pazienti con glioma cerebrale." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/64636.
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Si sono studiati i correlati neurali dei sistemi di memoria verbale in pazienti con glioma cerebrale. Si tratta di pazienti sottoposti ad asportazione di lesioni cerebrali dell’emisfero dominante, in cui le funzioni mnestiche sono state valutate mediante prove specifiche prima e dopo l’intervento chirurgico, per verificare l’impatto funzionale dell’espanso e della rimozione della lesione. L’indagine anatomo-funzionale si è inoltre avvalsa delle tecniche di mappaggio cerebrale in awake surgery laddove l’intervento è stato eseguito in anestesia asleep-awake per la rimozione dei tumori estesi alle aree del linguaggio. Nel primo studio si esamina l’impatto della crescita tumorale sulla memoria verbale: le valutazioni neuropsicologiche effettuate pre-trattamento hanno permesso di identificare difficoltà conclamate o lievi compromissioni, che variano in funzione delle aree di infiltrazione tumorale; la prospettiva anatomo-clinica ha fornito una conferma dell’esistenza di sistemi di memoria verbale in distretti anatomo-funzionali differenti. Il secondo studio esamina i correlati neurali della memoria verbale a breve termine in un gruppo di pazienti sottoposti a mappaggio cerebrale in awake surgery: la stimolazione corticale e sottocorticale diretta ha permesso di identificare un circuito fronto-parietale coinvolto nei processi di MBT; l’analisi degli errori registrati durante i test intraoperatori ha permesso inoltre di distinguere il substrato neurale delle due componenti del circuito fonologico. Il terzo studio valuta gli effetti della lobectomia temporale sulla memoria a lungo termine; le prove mnestiche somministrate ad una settimana dall’intervento e dopo tre mesi hanno evidenziato prestazioni patologiche che non vanno incontro ad un rapido recupero nei pazienti che hanno subito la rimozione di un circuito cortico-sottocorticale esteso dalle regioni temporo-polari a quelle temporali mesiali; lo studio anatomico mediante voxel-based lesion-symptom mapping delle aree asportate ha permesso di verificare i correlati neurali di memoria semantica e apprendimento verbale. Questi risultati confermano che i pazienti con tumore cerebrali possono fornire dati interessanti nello studio dei deficit neuropsicologici.
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VILLANI, UMBERTO. "Dall'imaging di microstruttura alla connettività strutturale: l'utilizzo della risonanza magnetica di diffusione per investigare l'impatto dei gliomi sul cervello umano." Doctoral thesis, Università degli studi di Padova, 2022. http://hdl.handle.net/11577/3450310.
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La Risonanza magnetica di diffusione (dMRI) sta diventando lo strumento più adatto per indagare la microstruttura del cervello umano in vivo.
Modellando le proprietà della diffusione dell’acqua nei tessuti cerebrali, è infatti possibile ottenere delle misure simili a quelle derivate dall’istologia, come la densità di fibre, la loro conformazione e la loro direzione di propagazione, in maniera non invasiva.
In più, misure locali di integrità e di orientazione della materia bianca possono essere usate da algoritmi di trattografia per ricostruire globalmente il percorso seguito dalle fibre in tutto il cervello, permettendo di studiare come le varie regioni corticali sono connesse.
Nonostante ciò, l’utilizzo della dMRI deve essere condotto con attenzione in presenza di patologie che alterano drasticamente la fisiologia del cervello, come nel caso dei tumori cerebrali.
La varietà di microambienti cellulari che caratterizza questo tipo di patologie invalida alcune ipotesi sul quale si fondano i modelli di microstruttura basati sulla dMRI. In più, il processo di ricostruzione della trattografia nel cervello presenta particolari difficoltà tecniche nelle regioni affette dalla patologia.
Date queste limitazioni, vi è del valore nell’utilizzare tecniche basate sulla dMRI in questo complesso ambiente patologico?
Negli ultimi tre anni, ho avuto modo di esplorare diverse di queste metodologie in una popolazione di pazienti con tumore cerebrale. La presente tesi vorrebbe quindi essere una sintesi di questo lavoro, che costituisce una base verso l’integrazione di tecniche di diffusione avanzate all’interno della pratica neuro-oncologica.
Nella sua interità, la tesi presenta tre lavori, organizzati come segue:
La prima parte presenta uno studio analitico su due noti modelli di microstruttura, Neurite Orientation Dispersion and Density Imaging (NODDI) e la Spherical Mean Technique. Questo lavoro è volto alla quantificazione della bontà del fit e precisione parametrica delle due tecniche all’interno della lesione tumorale. Alcuni lavori, concentrati principalmente su NODDI, usano queste tecniche come modelli di segnale e non biofisici, cercando di trovare biomarker capaci di caratterizzare aspecificamente il tessuto patologico. L’analisi qui svolta supporta i risultati di letteratura da un punto di vista tecnico, senza considerazioni sul significato biologico di questi modelli.
La seconda parte contiene uno studio di confronto tra due diversi metodi per la quantificazione di regioni di materia bianca sconnessa a causa del tumore. Due categorie di approcci qui sono stati studiati: approcci diretti, e approcci indiretti. I primi fanno uso della trattografia singolo-soggetto per investigare quali fasci di fibre siano affetti nel loro decorso dalla presenza del tumore. I secondi invece non hanno bisogno di acquisizioni dMRI, e utilizzano un atlante normativo di fasci di materia bianca per investigare, probabilisticamente, quali di questi potrebbero essere affetti data la locazione e l'estensione della zona tumorale. Utilizzando noti strumenti di analisi dell’immagine, i due approcci vengono qui confrontati, discutendo pregi e difetti di ciascun metodo.
Nella terza e ultima parte della tesi, viene studiata la relazione tra alterazioni di matrici di connettività strutturale (SC) di pazienti tumorali e variazioni regionali di metabolismo misurate usando la Tomografia ad Emissione di Positroni (PET) con tracciante [18F]-FDG. All'interno di questo studio, viene prima proposta una procedura per la selezione dell’algoritmo di trattografia ottimale per le analisi. A seguire, viene sviluppata una metodologia statistica per rilevare le loro connessioni della matrice SC alterate dalla presenza del tumore. La presenza di queste alterazioni viene infine correlata con la PET, e si discutono i risultati ottenuti, ponendo particolare attenzione alle limitazioni di entrambe queste modalità di imaging.<br>Diffusion-based Magnetic Resonance Imaging (dMRI) is rapidly becoming the instrument of choice to probe the structure of the human brain in vivo.
By modelling the properties of water diffusion inside cerebral tissues, it is indeed possible to extract surrogates of histological measures, such as fibre density, conformation and preferential direction, in a non-invasive manner. Furthermore, local orientational features can be used to reconstruct axonal pathways that link different brain regions, allowing the study of how they are structurally connected. Nevertheless, the quantification of dMRI measures must be cautious when the physiological environment of brain tissues is drastically altered. Such is the case of brain tumours.
The microstructure of brain tumours is highly heterogeneous, being diverse between and inside specific types and malignancy grade. The wide spectrum of cellular environments they feature invalidates several hypotheses on which diffusion-based microstructure models are built and, contemporarily, poses difficulties in the process of tracking white matter in affected regions.
Given these limitations, are these techniques worth using in this complex pathological environment? During the last three years I explored several state of the art diffusion-based methodologies in a cohort of patients suffering from a range of brain tumours. Hence, this thesis strives to be a summary of this work, laying the foundation for future studies aiming to integrate the use of advanced dMRI in the clinical neuro-oncological practice. The thesis is divided in three main parts, which are organized as follows:
In the first part, an assessment is made whether two widely known diffusion advanced models, Neurite Orientation Dispersion and Density Imaging (NODDI) and the Spherical Mean Technique (SMT) are properly fitted in the tumoral lesion in terms of goodness-of-fit and parameter precision. Several works, concentrating mainly on NODDI, used such techniques not as biophysical models but as signal representations, trying to find biomarkers that differentiate more and less isotropic environments which contribute to the totality of the diffusion signal in ‘tumoral’ voxels. These studies were performed without first checking whether these diffusion metrics are mathematically reliable. This issue is here assessed from a technical point of view, without giving specific biophysical meaning to the models in exam inside the tumoral tissues
The second part features a comparison study between methods for the identification of structurally disconnected white matter (WM) in brain tumour patients. Here, two branches of methodologies were identified, namely direct and indirect approaches. The formers use single-subject tractography to directly investigate which fibre bundles may be affected by the presence of the tumour. The latters, instead, embed the focal lesion on a normative atlas of white matter tracts, identifying the probability of a WM voxel being disconnected by the pathology. Employing known image analysis metrics, both approaches are discussed, highlighting points of convergence, but also of disagreement, in terms of the physio-pathological information they can convey.
In the third and last part of this thesis, tumour-related anomalies of diffusion-based structural connectivity (SC) matrices are put in relationship with metabolic measures from [18F]-FDG PET. A procedure for tractography algorithm selection was firstly performed, and after the SC quantification, a statistical method of detecting altered connections in the tumour-affected SC matrix is presented. Within such a framework, the amount of affected SC entries was eventually quantified in the available cohort of patients and put in relationship with standardized uptake values from PET. Finally, a discussion of the results of this association is provided, paying particular attention to the limitations of these imaging modalities in the brain oncological field.
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Sadeghi-Meibodi, Niloufar. "Image-based biomarkers for the invivo evaluation of human brain gliomas." Doctoral thesis, Universite Libre de Bruxelles, 2010. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209991.
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Gliomas constitute 36% of all primary brain tumors and 81% of all primary malignant brain tumors. The overall prognosis in patients with gliomas depends mainly on the location and histologic grade of the tumor.<p>The World Health Organization classification of gliomas is the primary basis for guiding therapy and assessing overall prognosis in gliomas. This classification system, based on histological features, often falls short of predicting therapeutic response of individual tumors within the same histological grade. Yet, it still remains the grading method for both research and clinical prospects.<p>Unlike any other organ the brain has multiple protective layers such as the skull that ensure a homeostatic environment. The resulting reduced access to the brain and the absence of plasmatic brain tumor markers bring neuroimaging in a central position in diagnosis and management of brain tumors. Moreover, neuroimaging has evolved from a purely morphologic investigation into a diagnostic tool that allows characterization of particular physical alterations within brain tissue. Understanding the relationship between the physical characteristics of tumor tissue, studied by MR imaging, and biological characteristics of the tumor is therefore important for the appropriate integration of neuroimaging in brain tumor management. The general objective of this work is to define the relationship between physiologybased MR imaging and biological features of glial tumors. Diffusion and perfusionweighted imaging, physiologybased MR techniques provide the data based on physical characteristics of the tissues. Diffusion weighted imaging (DWI) allows the measurement of water molecules diffusivity within the brain tissue by means of apparent diffusion coefficient (ADC) measurements. Perfusion weighted imaging (PWI) is based on changes of MR signal during the passage of contrast material through the intravascular space and allows hemodynamic measurements such as those of cerebral blood volume (CBV)within the brain tissue.<p>Highgrade diffuse gliomas are currently differentiated from low grade diffuse gliomas by increased cellularity with nuclear atypia, mitotic activity, endothelial proliferation and necrosis. Components of the extracellular matrix and angiogenesis constitute some other features of gliomas, which have established links with oncogenic processes that influence the proliferative and infiltrative potentials of these tumors. We have specifically targeted these features in our comparative studies with the working hypothesis that physiologybased MR measurements, obtained in vivo, might provide information that is pertinent in terms of tumor malignancy.<p>We chose to approach the biology of brain tumors in two ways: in vivo, by means of metabolic imaging techniques such as positron emission tomography (PET) and ex vivo, by means of histological and immunohistochemical analyses of tumor specimens.<p>Many studies have investigated the relation between ADC values and cellularity in gliomas. The underlining theory is based on the premise that water diffusivity within the 9 extracellular compartment is inversely related to the content and attenuation of the constituents of the intracellular space. Therefore when cellularity increases, intracellular space volume increases with a relative reduction of the extracellular space, leading to restricted diffusion of water molecules. However other factors may affect the value of ADC in gliomas such as the extracellular matrix which contains various amounts of hydrophilic macromolecules susceptible to change water molecules diffusivity. Hyaluronic acid is one highly hydrophilic component of the extracellular matrix of gliomas and its level of expression changes significantly during the progression to anaplasia in gliomas. Our hypothesis was that hyaluronan may influence ADC values in high and low grade gliomas.<p>We demonstrated a positive correlation between ADC values and the immunohistochemical level of hyaluronan in glial tumors.<p>Previous studies have confirmed the utility of positron emission tomography using C11 Methionine (PETMET) as a prognostic tool in patients with gliomas. Higher MET uptake is associated with greater proliferative potential and a higher level of malignancy in gliomas.<p>The increased aminoacid uptake in gliomas seems to reflect increased transport mediated by aminoacid carriers located in the endothelial cell membrane. Our hypothesis was that CBV measurements, index of tumor vascularity, may be related to tumor aminoacid metabolism.<p>We found a positive correlation between maximum CBV values and maximum MET uptake values in gliomas.<p>A limitation to these preliminary studies was lack of direct correlation between MRbased measurements and histologic and metabolic data. Indeed, glial tumors are known for their remarkable tissue heterogeneity across different grades, within the same grade, and even within a single given tumor. Therefore we used image coregistration and stereotactic biopsies to further assess the relationship between MRbased imaging data and both metabolic and histologic analysis.<p>The second part of our studies was based on measurements at the exact same localization on both MR and PET images where biopsy specimens were performed. We found a local relationship between CBV and MET uptake values. Both measurements correlated with mitotic activity and endothelial proliferation; two features of tumor aggressiveness.<p>In order to quantify tumor cellularity and tumor angiogenesis, we respectively measured cell density and vessel density using immunohistochemical markers to identify vessels. We found a regional relationship between CBV and cell density, as well as vessel density in gliomas whereas no correlation was found regionally between ADC and cell density.<p>We concluded that CBV measurements may be used locally as indices of angiogenesis and cellularity in gliomas; whereas local ADC measurements are more variable and may not be used as a marker of cellularity in heterogeneous tumors such as gliomas.<br>Doctorat en Sciences médicales<br>info:eu-repo/semantics/nonPublished
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Tartaglia, Sara. "NEUROFIBROMATOSI DI TIPO 1 E GENI MODIFICATORI PREDISPONENTI L’INSORGENZA DI TUMORI (GLIOMA DELLE VIE OTTICHE)." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3425628.
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Introduction. Neurofibromatosis type I, the most common form of Neurofibromatosis, presents with a wide phenotypic variability, both inter- and intra-familiar; a comparative analysis between type/site of mutation and phenotype cannot identify a correlation between genotype and clinical features in affected patients. Pilocytic astrocytomas (PAs) are the tumors that occur most often in NF1 patients; they affect children and young adults and occur preferentially along the optic pathway. These tumors are defined as Grade I gliomas (low-grade) and their growth is slow, but a small number of these tumors continue to grow, behave in an aggressive fashion and cause loss of vision or hypothalamic dysfunction. It is not known which changes determine whether an NF1-associated pilocytic astrocytoma will remain stable or exhibit a clinical progression: genetic alterations associated with NF1-associated optic glioma pathogenesis have not been well characterized.
Aim of the study. The aim of the study was to analyze a group of NF1 patients affected with optic glioma and a group of patients affected with optic glioma in which the diagnosis of NF1 was excluded, in order to evaluate the presence of specific mutations in the NF1 gene and in the tumor-suppressor gene CDKN2A; to analyze polymorphisms in the tumor-suppressor genes CDKN2A and TP53, that are reported in the literature to be associated with risk and tumor progression, in the study patients and in a healthy control group; to evaluate results with statistical methods; to establish if the glioma formation is associated with some specific mutations or polymorphisms in the studied genes.
Materials and methods. A mutation/SNP screening in NF1, CDKN2A and TP53 genes was performed in 25 NF1 patients affected with optic glioma diagnosis and 21 non-NF1 patients affected with optic glioma. Blood samples were obtained after informed consent from all of the patients and a control group of 50 unrelated adult healthy individuals from the Padova Clinical Genetic Service database. Mutation analysis was done by DHPLC after amplification by PCR of all the exons of NF1 and CDKN2A genes, in all of the patients, and direct sequencing of the samples showing some alteration at the DHPLC analysis. The SNPs analysis was done in CDKN2A and TP53 genes in all the patients and in the control group by RFLP and HRMA, respectively, after amplification by PCR of the target sequences.
Results. Mutation scanning in the NF1 gene by DHPLC analysis has identified mutations in 60% of the NF1 patients with optic glioma diagnosis. A preferential type of nucleotidic alteration was not observed but the majority (67%) of them causes the formation of a truncated protein. No mutations were found in the non-NF1 patients with optic glioma diagnosis. These results confirm the lack of a genotype–phenotype (optic glioma) correlation in patients affected with NF1. Mutation scanning in the CDKN2A gene by DHPLC analysis has identified two nucleotidic alterations in three NF1 patients: the G442A polymorphism in exon 2, known in the literature, and a new substitution in 3’ UTR of the gene (C520G) that could represent a new polymorphism. SNPs analysis (C500G and C540T in 3’ UTR of CDKN2A gene and IVS 6+62 G/A and 12256 G/C, in the promoter region of the TP53 gene) was done by two different techniques: RFLP and HRMA, respectively. We have compared the two methods and define that HRMA is a better instrument for SNPs analysis because of its sensitivity and specificity and because it is a cost-effective and simple post-PCR technique. A statistical analysis of allelic and genotypic frequences of the CDKN2A and TP53 genes polymorphisms in patients and control groups was done using the ?2 test. The results seem to suggest a non-association between the presence of these SNPs and an increased risk of optic glioma growth in the studied population (P>0,05). However the number of individuals analized is not sufficient for exhaustive conclusions. Future studies should be done with more polymorphisms and a larger patients group.
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Lilja, Åsa. "Psychoneurooncology psychological dynamics in glioma patients /." Lund : Dept. of Psychology, Lund University, 1992. http://books.google.com/books?id=SnZrAAAAMAAJ.
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Ouedraogo, Zangbewende guy. "Rôle de l'activation de STAT3 dans l'agressivité des glioblastomes. : Cancérologie expérimentale." Thesis, Clermont-Ferrand 1, 2014. http://www.theses.fr/2014CLF1MM26/document.
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Les gliomes sont des tumeurs du système nerveux central. Leur plus haut degré de malignité est le glioblastome (GBM), le plus fréquent des cancers du cerveau. Les patients atteints de GBM sont d’abord opérés (si possible) puis traités par la radiothérapie avec témozolomide concomitant et adjuvant. Ce traitement n’est cependant pas curatif, en partie en raison d’une radiorésistance primaire élevée des cellules de GBM. La voie de signalisation JAK/STAT3 (Janus Kinase/Signal Transducer and Activator of Transcription 3) semble contribuer à la gravité des GBM. STAT3 est une protéine intracellulaire de transduction du signal. Elle est activée par phosphorylation de ses résidus tyrosine 705 (pSTAT3-Y705) et sérine 727 (pSTAT3-S727). L’activation de la tyrosine 705 se produit en aval du signal induit par la liaison de la cytokine interleukine 6 (IL-6) à son complexe récepteur transmembranaire gp130-IL-6Rα. Les mécanismes d’activation de la sérine 727 sont moins bien caractérisés. Le rôle de l’activation de STAT3 dans la radiorésistance des GBM a été ici étudié. Une évaluation du niveau basal de pSTAT3-Y705, pSTAT3-S727 et de la radiorésistance intrinsèque a été faite sur un panel de 15 lignées de GBM humain. L’activation de STAT3 dans les lignées cellulaires de gliomes a été évaluée par western blot et la radiorésistance par la survie cellulaire à l’irradiation. En plus de la description de l’état basal d’activation de STAT3 dans les lignées cellulaires de gliomes, cette étude a mis en évidence pour la première fois, une corrélation de pSTAT3-S727 avec la radiorésistance intrinsèque des GBM. Une stratégie de blocage pharmacologique de STAT3 nous a permis d’identifier le Gö6976 comme inhibant la phosphorylation Y705 de STAT3 dans les cellules de GBM. Celui-ci s’est avéré inhiber aussi la phosphorylation S727 mais seulement dans les lignées de GBM pSTAT3-Y705 négatives. Le traitement par le Gö6976 ralentit la croissance des cellules de GBM, indépendamment du statut d’activation de STAT3. De façon intéressante, le Gö6976 a montré un pouvoir radiosensibilisant très significatif sur les lignées pSTAT3-Y705 négatives, ce qui est concordant avec la baisse du niveau de pSTAT3-S727. La pertinence de ces résultats est confortée par un marquage immunohistochimique sur des échantillons cliniques de GBM, montrant la présence à des degrés variables de pSTAT3-S727 dans toutes les cellules cancéreuses de tous les patients. En parallèle, une étude in vitro des fonctions de pSTAT3-S727 utilisant des dominants positif et négatif est en cours. En somme, nous avons démontré que pSTAT3-S727 participe à la radiorésistance intrinsèque et que pSTAT3-Y705 est un marqueur prédictif négatif de la réponse des cellules de GBM au Gö6976 à la fois comme inhibiteur de pSTAT3-S727 et radiosensibilisant. L’ensemble de nos résultats conforte l’intérêt d’une inhibition spécifique de pSTAT3-S727 pour radiosensibiliser les GBM et ainsi améliorer le traitement des patients<br>Gliomas are tumors of the central nervous system. The highest degree in glioma malignancy is Glioblastoma (GBM) that is the most frequent of the brain cancers. GBM patients are treated by surgery at first (if it is possible), followed by radiotherapy and concomitant and adjuvant temozolomide. However, this treatment is not curative in part because GBM cells display an outstanding primary radioresistance. The JAK/STAT3 (Janus Kinase/Signal Transducer and Activator of Transcription 3) signaling pathway seems to be involved in the GBM aggressiveness. STAT3 is an intracellular signal transducer protein. It is activated by phosphorylation on its tyrosine 705 (pSTAT3-Y705) and serine 727 (pSTAT3-S727) residues. The tyrosine 705 activation is produced downstream the signal induced by the binding of interleukine-6 (IL-6) cytokine to its gp130-IL-6Rα transmembrane receptor complex. The mechanisms of the serine 727 phosphorylation are less characterized. The role of STAT3 activation in the radioresistance of GBM was studied here. Basal levels of pSTAT3-Y705, pSTAT3-S727 and intrinsic radioresistance were evaluateded in a panel of 15 GBM cel lines. Activation of STAT3 in the glioma cell lines was assessed by western blotting and radioresistance through cell surviving fraction to irradiation. In addition to the description of the basal activation of STAT3 in the glioma cell lines, this study evidenced, for the first time, a correlation between pSTAT3-S727 and GBM intrinsic radioresistance. Using a pharmacological inhibition strategy, we identified Gö6976 as a chemical blocking Y705 phosphorylation of STAT3 in GBM cells. Gö6976 also inhibited pSTAT3-S727 but only in the pSTAT3-Y705-negative cell lines. Treating GBM cell with Gö6976 slowed their growth regardless of STAT3 activation status. Interestingly, Gö6976 showed a highly significant radiosensitizing effect on pSTAT3-Y705-negative cell lines that was consistent with the down-modulation of pSTAT3-S727. The relevance of these results is strengthened by immunohistochemical assay performed of GBM clinical samples that showed a variable level of pSTAT3-S727 positive staining in all tumor cells of all the patients. Furthermore, we are currently running on an in vitro study of the pSTAT3-S727 biological function by the mean of STAT3 dominant positive and dominant negative proteins. In summary, we showed that pSTAT3-S727 is involved in the intrinsic radioresistance and that pSTAT3-Y705 is a negative predicting marker of GBM cell response to Gö6976 as both a pSTAT3-S727 inhibitor and a radiosensitizer. Altogether, our results strengthen the clinical relevance of a specific inhibition of pSTAT3-S727 to radiosensitize GBM and then improve the patient treatment
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Selek, Laurent. "Traitement intra-tumoral des gliomes malins par infusion convective de bevacizumab, développement d'un modèle de gliome chez le gros animal, étude anatomique de la diffusion convective dans un encéphale humain." Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAS040/document.
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Les gliomes de haut-grades sont des les tumeurs primitives les plus fréquentes du système nerveux central. Le traitement de cette pathologie associe chirurgie, radiothérapie et chimiothérapie. Les principales faiblesses de ces traitements sont le caractère infiltrant de la tumeur au sein d’un parenchyme hautement fonctionnel, l’existence de la barrière hémato-encéphalique limitant le passage trans-vasculaire de la chimiothérapie et la radiorésistance naturelle des cellules gliomateuses.Parmi les stratégies proposées pour outre-passer cette barrière hémato-encéphalique, une injection directe au sein du parenchyme a été évoquée. Afin d’optimiser cette délivrance le concept d’infusion convective a été développé, il s’agit d’une injection intra-parenchymateuse à un débit lent et contrôlé.Le bevacizumab est un anticorps dirigé contre le VEGF-A, un des principaux facteurs angiogéniques. Le but de ce traitement est de lutter contre l’ angiogénèse et de freiner la croissance tumorale.Dans un premier temps, la pharmacocinétique d’une injection intracérébrale de bevacizumab a été étudiée en comparaison avec une administration systémique plus classique. Les résultats permettent de mettre en évidence une concentration locale équivalente avec des concentrations systémiques beaucoup plus faibles avec une injection intra-tumorale. Un point important de cette étude est que la concentration dans l’hémisphère controlatéral à l’injection est aussi importante que lors d’une injection systémique.Puis l’efficacité d’une injection intratumorale de bevacizumab a été comparée à un traitement systémique sur un modèle de gliome chez la souris. L’efficacité du traitement est claire sur la survie de l’animal avec un avantage pour une injection intratumorale par rapport à une injection systémique. D’un point de vue microscopique cet avantage de survie peut être corrélé à une angiogénèse et une prolifération tumorale moins importante an cas d’injection directe au sein de la tumeur.Contrairement aux études pré-cliniques chez les rongeurs, les principaux essais cliniques n’ont pas permis de mettre en évidence un avantage d’une injection intra-tumorale directe. Principalement du à une mauvaise délivrance liée à des fuites et des reflux. Une des limites du modèle petit animal est l’absence de sillon cortical, vecteur de fuite. Le développement d’un modèle de gliome anatomiquement pertinent permettrait de simuler au mieux ces fuites et simultanément la mise au point de technologies de délivrance implantable à l’échelle humaine. Nous avons donc développé le premier modèle de gliome chez le porc. L’immunotolérance a été induite par un traitement par ciclosporine, des cellules de gliomes humains U87 et G6 ont été implantés, permettant se développer des tumeurs.Afin de dépister une mauvaise délivrance et anticiper les fuites ou les reflux, nous avons étudié les profils de pression le long de la ligne d’injection corrélés à l’existence de fuites ou de reflux. Nous avons pu identifier un profil pressionnel typique d’une injection de qualité. Les injections ne répondant pas à ces critères ont systématiquement conduits à des fuites ou reflux.L’étape suivante a été l’injection au sein d’une tumeur chez des porcs grâce à un système innovant implanté. Cette injection a été possible sans complication infectieuse avec une bonne tolérance locale et neurologique.La dernière étape de ce travail est l’étude anatomique de la diffusion d’un colorant injecté par une technique d’infusion convective. Cette étude s’intéressait notamment à la diffusion depuis la corona-radiata vers les différentes voies de substance blanche. La diffusion est anisotrope le long des fibres de substance blanche cependant la diffusion suit des voies différentes en fonction de la position du cathéter par rapport à elle. L’injection semble ouvrir des voies d’impédances rhéologiques faibles préférentielles nécessitant une adaptation anatomique aux voies qui seront la cible du traitement<br>High grade gliomas are the most frequent primitive central nervous system tumor. The standard treatment is an association of surgery, radiotherapy and chemotherapy. The mains issues with these treatments are the infiltrative properties of the tumour in a highly functional parenchyma, the blood-brain barrier limiting the transvascular transport of chemotherapy and the inherent radioresistance of glioma cells.Upon different strategy to overpass the blood-brain barrier, a direct injection in the brain was advocated. In order to maximize this delivery, the concept of convection enhanced delivery was developed; it consists in a direct injection in the parenchyma with a low flow-rate.Bevacizumab is an anti-VEGF A antibody, VEGF is one of the most important angiogenic factors. The goal of this treatment is to inhibit the angiogenesis and slow down the tumor growth.We propose to study the use of this antibody in a direct intra-cerebral infusion.First, we focalize on the pharmacokinetic properties of an intratumoral injection by convection –enhanced delivery compared to a systemic administration. This shows an equivalent intratumoral concentration with systemic concentrations significantly lower with the intra-tumoral injection. An important result is the similar concentration in the controlateral hemisphere with the two routes of infusion. Convection-enhanced delivery is suitable to carry far from the infusion site high molecular weight proteins. An intra-tumoral bevacizumab may theoretically provide similar efficiency with less systemic side-effect.Then, the efficiency of an intra-tumoral infusion of bevacizumab is compared to a systemic injection on a mouse glioma model. In terms of survival the intra-tumoral treatment is significantly more efficient with an important decrease of angiogenesis and tumoral proliferation.If convection-enhanced delivery rodent study were promising, clinical trials failed to show any efficiency of intra-tumoral injection mainly due to inadequate delivery secondary to backflows and leakages. One of the limits of the rodent model is the absence of cortical sulci, main leakage provider. The development of a model anatomically relevant could simulate real conditions of injection and develop implantable device of injection in realistic conditions. We have developed the first induced model of glioma in a large animal. We choose the pig for the similarity of its brain anatomy and its size. The animals have been treated with ciclosporin to induce an immunosuppression, human glioma cells have been implanted, leading to the development of brain tumor.We have studied the pressure on the infusion line and correlate it to backflow and leakage. We have identified a pattern of pressure for successful infusion. Different pressure pattern have systematically led to backflow or leakage. These pressures criteria could permit to us an early detection of inadequate infusion to replace the catheter and avoid the failure of precedent clinical trials.Next step have been the intra-tumoral injection via an implanted device on pig glioma model. No infectious complication has been related with a good local and neurologic tolerance. The injections have led to a relevant diffusion through the tumor with a rapid flow to the periphery due to the interstitial pressure gradient between the tumor and the periphery.Last step of this work have been the anatomical study of a dye distribution by convection-enhanced delivery in a human encephalon. Indeed if pig brain is similar to human brain, human white matter structure is unique. This work is focalized on the diffusion from the corona-radiata to the main white matter tracts. The distribution is anisotropic following white matter but the diffusion is different depending on the position of the catheter. The infusion seems to open low rheological impedance paths the position of the catheter have to be adapted to the white matter tract to target
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Azar, Safa. "Tumeurs cérébrales de bas grade : élaboration de modèles in vitro et in vivo pour le développement de thérapies innovantes." Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT017.
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Les gliomes diffus de bas grades sont des tumeurs qui affectent des régions fonctionnelles du cerveau chez des jeunes patients. Malgré leur faible taux de prolifération ces tumeurs peuvent dégénérer en des tumeurs plus agressives après leurs exérèses. Le gène IDH1 est très fréquemment muté dans les DLGG. Cette mutation confère à l’enzyme isocitratedeshydrogénase (IDH1) la propriété de produire du 2-OH-glutarate (2-HG) au lieu de l’α-cétoglutarate (α-KG). L’oncométabolite 2HG rentre alors en compétition avec l’α-KG pour les enzymes de déméthylation conduisant à une hyperméthylation de l’ADN et de l’histone H3 concourant à un blocage de la différenciation cellulaire. Mon projet de thèse consiste à la caractérisation des cellules tumorales et la compréhension des voies de signalisation impliquées dans la progression tumorale ainsi que l’identité du microenvironnement tumoral. Les récepteurs tyrosine kinase, PDGFRα et EGFR, sont abondamment exprimés par les cellules tumorales mais ne sont pas activés. En revanche, une forte phosphorylation de la protéine Erk p42/44 a été détectée dans les tumeurs. Cette phosphorylation a une double origine : les cellules tumorales et leur environnement. L’utilisation d’une série de marqueurs m’a permis de mieux définir l’état de différenciation des cellules tumorales et de mettre en évidence une préférence pour l’expression de Sox8 dans les oligodendrogliomes tandis que Sox9 est prédominant dans les astrocytomes. Dans une seconde partie, j’ai mis au point des méthodes pour la culture des gliomes diffus de bas grade et isolé cinq lignées de gliomes portant la mutation récurente IDH1 R132H. Récemment, la société Agios a identifié des inhibiteurs très spécifiques (notamment l’AGI-5198) de l’enzyme mutée IDH1 qui, utilisés dans un modèle de gliome murin, provoquent une déméthylation des histones H3K9me3 associées à une augmentation de l’expression de gènes de différenciation ainsi qu’à une réduction de la masse tumorale. A contrario, j’ai montré que l’AGI-5198 augmente la croissance cellulaire sur les lignée de patients, modifie la migration cellulaire ainsi que différentes voies de signalisation.Ces travaux apportent un nouvel éclairage sur le phénotype des cellules tumorales, leur diversité et les mécanismes moléculaires régissant leur prolifération<br>Low grade gliomas are low proliferating tumors affecting functional regions of young patients. In most cases, they tend to transform into a more malignant state following surgery. These tumors carry a key mutation in isocitrate dehydrogenase (70-80% of DLGG). Gliomas with IDH1 mutation have improved prognosis compared togliomaswith wild type IDH1. IDH1 protein acquires the ability to convert α-Ketoglutarate (α-KG) to 2-OH-glutarate (2-HG). The new onco-metabolite can interfere with the normal function of α-KG, leading to a general hypermethylation of the genome, thus inducing a blockage of the cellular differentiation. Very good reviews on the molecular mechanisms underlying high grade glioma invasion already exist but little is known about the cellular and molecular mechanisms in diffuse low grade gliomas. To that end, I characterized the profile of IDH1 mutated cells in the different types of DLGG. I have demonstrated that the tyrosine kinase, PDGFRα and EGFR receptors are abundantly expressed by tumor cells eventhough they are not activated. In contrast, a strong phosphorylation of Erk p42 / 44 proteins was detected in these tumors. This phosphorylation has a dual origin: tumor cells and their environment. The use of a series of markers allowed me to better define the state of differentiation of cancerous cells and to demonstrate a preferential expression of Sox8 in oligodendrogliomas while Sox9 is predominant in astrocytomas. In a second time, I have developed a method for the culture of low-grade diffuse gliomas and isolated five cell lines carrying the recurrent mutation IDH1 R132H. Recently Agios has identified very specific inhibitors (particularly AGI-5198) of the mutated IDH1 enzyme which, used in a murine glioma model, contributed to the demethylation of H3K9me3 histones with an increased expression of differentiation related genes as well as a reduction of the tumor mass. On the contrary, I have shown that AGI-5198 increases cell growth of patient cell lines, modifies the cellular migration and various signaling pathways.These studies shed new light on the phenotype of tumor cells, their diversity and The molecular mechanisms governing their proliferation
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Bruyère, Céline. "Caractérisation du rôle des chémokines de type CXCL dans le comportement biologique de deux types de cancers naturellement résistants à l'apoptose, le cancer de l'oesophage et le gliome." Doctoral thesis, Universite Libre de Bruxelles, 2011. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209819.
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Le glioblastome qui correspond au stade de malignité le plus élevé des gliomes est associé à un très mauvais pronostic car il envahit le parenchyme cérébral de manière diffuse, ce qui rend son exérèse complète généralement impossible, et il résiste aux traitements conventionnels en raison de sa résistance intrinsèque aux stimuli pro-apoptotiques. Le cancer de l’œsophage est également un cancer très agressif car invasif et résistant également aux stimuli pro-apoptotiques. <p>Les chémokines sont des cytokines chémotactiques responsables de la migration des leucocytes et exprimées en réponse à des cytokines inflammatoires, à des facteurs de croissance et à des stimuli pathogènes. De nombreux cancers possèdent un réseau complexe de ces chémokines. Les chémokines de type CXCL et plus particulièrement CXCL8 et CXCL12 sont impliquées dans la biologie des gliomes et du cancer de l’oesophage. Au cours de mon travail de thèse de doctorat, nous avons étudié l’expression des 15 chémokines CXCL et des 9 récepteurs aux chémokines CXCL dans divers modèles de gliomes et de cancers de l’œsophage. Cette étude menée par RT-PCR nous a permis de mettre en évidence la présence d’un patron d’expression complexe de ces chémokines CXCL dans les divers modèles analysés. Nous avons observé une expression plus importante des chémokines CXCL pro-angiogéniques par rapport aux chémokines anti-angiogéniques dans ces deux types de cancers. Nous avons également pu mettre en évidence une implication potentielle des chémokines CXCL2, CXCL3 et CXCL8 dans l’acquisition de la résistance au traitement par témozolomide des gliomes d’origine astrogliale. <p>Les glioblastomes et les cancers de l’œsophage étant deux types de cancers résistants aux stimuli pro-apoptotiques, et le témozolomide étant la seule molécule dotée de bénéfices thérapeutiques réels dans le cas du glioblastome, nous avons également testé le témozolomide dans nos modèles de cancer de l’œsophage in vitro et in vivo. Nous avons pu ainsi montrer un bénéfice thérapeutique réel apporté par cette molécule in vivo sur des animaux immunodéficients greffés avec des cellules humaines de carcinome épidermoïde de l’œsophage. Ce bénéfice thérapeutique peut être expliqué en partie par différents mécanismes d’action tels que l’induction de processus soutenus d’autophagie suivis par de l’apoptose mais également par des effets anti-angiogéniques. Enfin, nous avons pu montrer que la diminution d’expression même transitoire de la chémokine CXCL2 dans nos modèles in vitro de glioblastome et de carcinome épidermoïde de l’œsophage entraîne une diminution de la croissance de ces populations cellulaires cancéreuses, suggérant un rôle important de cette chémokine dans la biologie de ces deux types de cancers. Enfin, nous avons démontré un effet anti-angiogénique in vivo pour le témozolomide dans un modèle de xénogreffes de cancers oesophagiens humains chez la souris immunodéficiente.<p><p>En conclusion, l’ensemble de nos résultats suggèrent que le témozolomide, bien qu’il devienne bientôt un générique sous sa forme d’administration i.v. (la forme orale étant déjà générique), pourrait représenter une molécule d’intérêt pour combattre le cancer de l’œsophage, comme on le sait déjà depuis 2005 en ce qui concerne les glioblastomes. Nos résultats montrent ensuite l’importance du patron d’expression des chémokines CXCL dans la biologie des cellules gliales tumorales et des cellules cancéreuses de l’œsophage. Enfin, nos résultats montrent que le témozolomide détruit en partie ce réseau de chémokines CXCL au sein de ces deux types de cancers.<p><br>Doctorat en Sciences biomédicales et pharmaceutiques<br>info:eu-repo/semantics/nonPublished
Books on the topic "Gliomi"
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S, Berger Mitchel, and Wilson Charles B. 1929-, eds. The gliomas. W.B. Saunders, 1999.
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1924-, Suzuki Jirō, ed. Treatment of glioma: With 137 figures. Springer-Verlag, 1988.
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Yamanaka, Ryuya, ed. Glioma. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3146-6.
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Karim, A. B. M. F., and Edward R. Laws, eds. Glioma. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84127-9.
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G, Broggi, and Gerosa M. A, eds. Cerebral gliomas: Proceedings of the International Workshop on Brain Tumors, held in Santa Margherita Ligure, Italy, 20-22 June 1988. Excerpta Medica, 1989.
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Pope, Whitney B., ed. Glioma Imaging. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-27359-0.
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Barańska, Jolanta, ed. Glioma Signaling. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-4719-7.
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Barańska, Jolanta, ed. Glioma Signaling. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-30651-9.
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1935-, Voth D., Krauseneck P, and Mainzer Herbsttagung (4th : 1983 Oct. 13-15), eds. Chemotherapy of gliomas: Basic research, experiences, and results. De Gruyter, 1985.
Find full textBook chapters on the topic "Gliomi"
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Quinones, Addison, and Anne Le. "The Multifaceted Glioblastoma: From Genomic Alterations to Metabolic Adaptations." In The Heterogeneity of Cancer Metabolism. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_4.
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AbstractGlioblastoma multiforme (GBM) develops on glial cells and is the most common as well as the deadliest form of brain cancer. As in other cancers, distinct combinations of genetic alterations in GBM subtypes induce a diversity of metabolic phenotypes, which explains the variability of GBM sensitivity to current therapies targeting its reprogrammed metabolism. Therefore, it is becoming imperative for cancer researchers to account for the temporal and spatial heterogeneity within this cancer type before making generalized conclusions about a particular treatment’s efficacy. Standard therapies for GBM have shown little success as the disease is almost always lethal; however, researchers are making progress and learning how to combine therapeutic strategies most effectively. GBMs can be classified initially into two subsets consisting of primary and secondary GBMs, and this categorization stems from cancer development. GBM is the highest grade of gliomas, which includes glioma I (low proliferative potential), glioma II (low proliferative potential with some capacity for infiltration and recurrence), glioma III (evidence of malignancy), and glioma IV (GBM) (malignant with features of necrosis and microvascular proliferation). Secondary GBM develops from a low-grade glioma to an advanced-stage cancer, while primary GBM provides no signs of progression and is identified as an advanced-stage glioma from the onset. The differences in prognosis and histology correlated with each classification are generally negligible, but the demographics of individuals affected and the accompanying genetic/metabolic properties show distinct differentiation [3].
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Karim, A. B. M. F., and J. H. Kralendonk. "Pitfalls and Controversies in the Treatment of Gliomas." In Glioma. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84127-9_1.
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Pozza, F., F. Colombo, C. Marchetti, and G. Chierego. "Stereotactic External Radiotherapy for Gliomas: Technique, Dosimetry, Results." In Glioma. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84127-9_10.
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Bleehen, N. M. "Hypoxic Cell Sensitizers in the Management of Brain Tumours." In Glioma. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84127-9_11.
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Rao, B. R., N. C. A. Roelvink, and B. J. Slotman. "Role of Steroid Hormones in Gliomas." In Glioma. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84127-9_12.
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Rutten, E. H. J. M. "Radiation Injury to the Brain." In Glioma. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84127-9_13.
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van der Kogel, A. J. "Clinical Implications of Radiobiological Studies on CNS Tolerance." In Glioma. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84127-9_14.
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Áfra, D., and W. Müller. "Recurrent Low-Grade Gliomas: Dedifferentiation and Prospects of Reoperation." In Glioma. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84127-9_15.
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Larson, D. A., P. K. Sneed, and P. H. Gutin. "Interstitial Brachytherapy for Recurrent Malignant Gliomas." In Glioma. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84127-9_16.
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Thomas, D. G. T. "Chemotherapy for Cerebral Gliomas: Current Status and Future Perspectives." In Glioma. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84127-9_17.
Full textConference papers on the topic "Gliomi"
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Karlović-Vidaković, Marijana. "SUVREMENE NEURORADIOLOŠKE METODE PRIKAZA INTRAAKSIJALNIH TUMORA MOZGA." In Okrugli sto “Tumori centralnog nervnog sistema”. Academy of Sciences and Arts of Bosnia and Herzegovina, 2021. http://dx.doi.org/10.5644/pi2021.197.02.
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Primarni tumori mozga predstavljaju aproksimativno 2% od ukupnog broja tumora s godišnjom incidencijom 6-7/100.000 stanovnika u Europi. Najčešći su u dobi 45-70 godina života. U dječjoj dobi čine do 25% od ukupnog broja tumora. Incidencija intraaksijalnih tumora mozga je 2-3/100.000 od kojih su najčešći gliomi, koji čine oko 50% svih gliomskih tumora. Višeslojna kompjuterizirana tomografija (MSCT) prva je dijagnostička metoda izbora kada postoji sumnja na tumor mozga radi njezine široke dostupnosti i kratkog vremena trajanja snimanja. Superiorna je u mogućnosti prikaza intratumorskih kalcifikata kao i destrukcije okolnog koštanog tkiva. Sukladno recentnoj klasifikaciji tumora centralnog nervnog sustava (CNS), karakteristike i stupanj malignosti tumora izravno su povezane s molekularnom biologijom tumorskog tkiva. Stoga je magnetna rezonancija (MR) neuroradiološka metoda izbora u suvremenoj dijagnostici intraaksijalnih tumora mozga koja se koristi upotrebom standardnih i naprednih tehnika snimanja. Mogućnost visoke tkivne diferencijacije i prostorne rezolucije komparativna je prednost MR pretrage, čija je uloga pouzdana dijagnostika i klasifikacija tumora. Uređaji visoke rezolucije poput 3 Tesla MR uređaja, omogućavaju detaljnu analizu tumora, točnu lokalizaciju, identifikaciju granica i anatomskih odnosa tumora s okolnim strukturama, uključujući prikaz vaskulariziranosti tumora i prekida integriteta krvno-moždane barijere, te nazočnost nekroze tumorskog tkiva, intratumorskog krvarenja i intrakranijskog kompresijskog učinka. U novije se vrijeme posebno ističe uloga metaboličkih i funkcijskih dijagnostičkih pretraga poput MR spektroskopije, MR perfuzije,diffusion- weighted imaging (DWI) i diffusion tensor imaging (DTI) koje su sve više zastupljene u prosudbi stupnja malignosti tumorskog tkiva. Navedene neuroradiološke dijagnostičke metode predstavljaju značajan doprinos u planiranju neurokirurškog i onkološkog liječenja i prognozi tumorske bolesti.
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FELIN, CAROLLINA DANEZI, GIULLIANO DANEZI FELIN, GIANCARLLO DANEZI FELIN, FELLIPE DANEZI FELIN, and IZABELLA PAZ DANEZI FELIN. "GENÉTICA MOLECULAR DOS GLIOMAS CEREBRAIS: IMPORTÂNCIA NA CLASSIFICAÇÃO, SOBREVIDA E TRATAMENTO." In I Congresso Nacional de Pesquisas e Estudos Genéticos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/geneticon/9009.
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Introdução: No Brasil os gliomas representam 42% dos tumores cerebrais. Originam-se do parênquima cerebral e tem comportamento variado. Os de alto grau são agressivos e tem sobrevida média global de 15 meses. Os de baixo grau tem sobrevida de 2-5 anos, podem recidivar ou progredir para piores graus. Objetivos: Identificar a genética molecular dos gliomas e sua importância na classificação, sobrevida e tratamento desses tumores. Metodologia: Revisão de literatura através de pesquisa na base de dados MEDLINE, via PubMed, utilizando os termos: “glioma” [and] “molecular genetics” [and] “therapy”. Aplicados os filtros de busca: “textos completos gratuitos”, “dados associados” e “últimos 5 anos”. Foram encontrados 22 resultados e incluídos 6 para esse estudo. Os critérios de elegibilidade foram todos os artigos coincidentes com tema proposto conforme os filtros e termos de busca. Excluiu-se 16 artigos por não contemplarem os critérios elegíveis. Realizada extração de dados, análise dos resultados e redação dessa revisão. Resultados: No contexto do glioma estão os seguintes tumores: astrocitoma, oligodendroglioma, glioblastoma multiforme e ependimoma. Há marcadores genéticos específicos que caracterizam os astrocitomas de acordo com os graus de I até IV. Os glioblastomas secundários apresentam mutações nos genes IDH1 ou IDH2 diferentemente da apresentação primária. Os astrocitomas e os oligodendrogliomas podem expressar mutações dos genes IDH1 ou IDH2. Os oligodendrogliomas frequentemente tem mutação IDH1/2 e codeleção 1p/19q, enquanto que os astrocitomas tem mutação dos genes ATRX, pTP53 e IDH1/2, sem a codeleção 1p/19q. A codeleção 1p/19q é característica dos tumores oligodendrogliais, útil no diagnóstico e também como preditor de melhor sobrevida e melhor resposta à radioterapia e à quimioterapia. A presença da mutação IDH1/2 relaciona o tumor a um melhor prognóstico e melhor resposta à quimioterapia. Existem quatro graus do ependimoma e nove subtipos moleculares distintos, determinado variabilidade genotípica e fenotípica, determinando tratamento e prognóstico diversos. Conclusão: Foi possível identificar que o perfil genético molecular dos gliomas é determinante tanto para subclassificar quanto para predizer sobrevida e tratamento, pois a genética molecular heterogênea dos gliomas mostrou caracterizar doenças com fenótipos distintos. O conhecimento da genética molecular pode abrir novas oportunidades de tratamento indicando estratégias mais específica de tratamento.
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Dutra, Milla Giancristofaro, Bernardo Valle Zanetti, Ana Luiza Badini Tubenchlak, et al. "Management of low-grade gliomas." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.052.
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Background: Gliomas are the most aggressive and prevalent primary malignant tumors of the central nervous system. For better mapping, they are subclassified into degrees in proportion to their malignancy. Although low-grade patients have a better prognosis, they are extremely heterogeneous. Since the high variability in the outcomes of the condition, it is essential to investigate the current therapeutic strategies available. Objective: Analyze the management of low-grade gliomas. Methods: In April 2021, a literature review was conducted on MEDLINE using the descriptors: “Glioma”, “Low Grade”; “Treatment”; as well as their variations obtained in MeSH. Controlled and randomized clinical trials carried out on humans in the last five years were included. Results: 63 articles were found and 10 of them were analyzed in this review. The research has shown that total tumor resection is the therapeutic modality that causes the greatest drop in the mortality rates. Furthermore, the greater the extraction, the greater the progression-free survival. In this way, for greater safety of large-scale surgeries, several intraoperative techniques have been developed. An example is the waking approach, which presents favorable long-term functional results and low failure rates. However, the isolated surgery is often not sufficiently curative. Therefore, it is necessary to complement radiotherapy and chemotherapy with temozolomide, associated with a 5 to 10 year survival rate when combined. Conclusions: Studies have shown that total resection of the tumor is the best way to manage low-grade gliomas, but it is often combined with temozolamide chemotherapy and radiotherapy for a better prognosis.
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Nascimento, Gabriela Oliveira do, Kevin Gustavo Dos Santos Silva, Lucas Aparecido Longhi de Andrade, and Jésus Faria Rosa Júnior. "O PAPEL DA BIÓPSIA NO CONTEXTO DA EPILEPSIA." In I Congresso Brasileiro de Estudos Patológicos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbesp/25.
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Introdução: A epilepsia, doença que afeta aproximadamente 50 milhões de pessoas no mundo, é caracterizada pela ocorrência imprevisível de convulsões, geradas por disparos de neurônios. As crises ocorrem pela perda de neurônios gabaérgicos ou hiperexcitação dos glutamatérgicos, o que gera hiperexcitabilidade do sistema nervoso central, determinando manifestações clínicas espectrais. A doença é manifestação de diversas outras, como encefalite e malformação arteriovenosa. Na histopatologia, costuma-se encontrar: displasia cortical, com lesões microscópicas diversas; esclerose hipocampal, com perda segmentar de neurônios e gliose; e encefalite de Rasmussen, com inflamação crônica. Apesar de ser utilizada em poucos casos, é preciso esclarecer o papel da biópsia na epilepsia. Objetivo: Analisar o papel da biópsia na epilepsia por meio de uma revisão sistemática da literatura disponível. Material e métodos: No site Descritores em Ciências da Saúde (DeCS) foram definidos os descritores "Epilepsy" e “Biopsy”. No PubMed e Scielo foi realizada uma pesquisa com tais descritores associados. Foram selecionados apenas ensaios clínicos randomizados, revisões sistemáticas e metaanálises. Não foi estabelecido critérios quanto ao ano de publicação. Os resultados foram analisados qualitativamente quanto às possíveis aplicações da biópsia no contexto da epilepsia. Resultados: Foram encontrados 11 artigos, dos quais 7 artigos foram elegíveis, sendo 3 ensaios clínicos, 3 revisões e 1 meta-análise. Dos excluídos, um era levantamento, outro estudo transversal, outro não randomizado e outro não detalhou metodologia. Apesar de correlacionarem biópsia e craniotomia e citarem biópsia para neoplasias do sistema nervoso central, nenhuma associou o procedimento à epilepsia. Um ensaio clínico citou biópsia como forma de diagnóstico de neurocisticercose, também sem associar à epilepsia. Outro ensaio avaliou o diagnóstico para lesões cerebrais por biópsia estereotáxica guiada por espectroscopia por Ressonância Nuclear Magnética, apesar de não associar esses meios de diagnóstico à epilepsia. A meta-análise indicou que três dos pacientes avaliados que possuíam glioma angiocêntrico foram submetidos à biópsia e não apresentaram recorrência de convulsões. Conclusão: Há poucos estudos sobre a aplicação da biópsia na epilepsia. Porém, a literatura disponível já demonstra a importância da biópsia para doenças que cursam com epilepsia, tais como lesões cerebrais e glioma angiocêntrico.
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Ul Ain, Qurat, Iqra Duaa, Komal Haroon, Faisal Amin, and Muhammad Zia ur Rehman. "MRI Based Glioma Detection and Classification into Low-grade and High-Grade Gliomas." In 2021 15th International Conference on Open Source Systems and Technologies (ICOSST). IEEE, 2021. http://dx.doi.org/10.1109/icosst53930.2021.9683838.
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Grossauer, Stefan, Katharina Koeck, Malek Chouchane, Joanna J. Phillips, Claudia K. Petritsch, and Theodore Nicolaides. "Abstract 143: MAPK pathway blockade effects on glioma stem cells and immunotherapy in BRAFV600Emutant gliomas." 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.am2018-143.
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Duarte, Fernanda, Aristófanes C. Silva, Marcelo Gattass, and Antonino C. dos S. Neto. "Classificação de Gliomas Utilizando Índices de Biodiversidade e de Diversidade Filogenética em Imagens por Ressonância Magnética Através de uma Abordagem Radiomics." In Anais do Simpósio Brasileiro de Computação Aplicada à Saúde. Sociedade Brasileira de Computação - SBC, 2019. http://dx.doi.org/10.5753/sbcas.2019.6239.
Full textAbstract:
Gliomas estão entre os tumores cerebrais malignos mais comuns. Eles podem ser classificados entre gliomas de baixo e alto grau e sua identificação precoce é fundamental para o direcionamento do tratamento apli- cado. Utilizando uma abordagem radiomics, o presente trabalho propõe o uso de ı́ndices de biodiversidade e de diversidade filogenética, definidos no campo da biologia, no problema de classificação de gliomas. O método proposto apre- sentou resultados promissores, com AUC, acurácia, sensibilidade e especifici- dade de 0,926, 0,902, 0,962 e 0,733, respectivamente.
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Sharma, Puja, Brian Koons, and Amrinder S. Nain. "Blebbing Dynamics, Single Cell Force Measurements, and the Influence of Cytochalasin D on Glioblastoma Multiforme Cells Using STEP Fibers." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93105.
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Classified as a grade IV tumor of the central nervous system, Glioblastoma multiforme (GBM) arises from the glia. A poor understanding of tumor metastasis and limited treatment options have led to increase in deaths of patients suffering from GBM. Studying glioma behavior using aligned structures that mimic native glioblastoma metastatic path is challenging. In this study, we utilize a previously described non-electrospinning platform to manufacture aligned 3D structures called STEP nanonets that not only allows the study of individual cell-nanofiber interaction, but also allows the calculation of migratory forces using beam mechanics. In particular, the blebbing dynamics, force generation, and the effect of an actin disruptor, Cytochalasin D have been investigated on a glioma cell line (DBTRG, Denver Based Tumor Research Group). It was observed that cell pulled onto the nanofibers causing measurable deflections when they were in spread and non-blebbing conditions. In non-spread configurations while attached to fibers, the cells acquired spherical configurations and resumed blebbing. The average migratory force generated by cells exposed to DMSO (control, 1:1000 dilution) using nanonets of 2μm by 400nm fibers was 0.58±0.06nN. Actin disruptor, Cytochalasin D severely compromised the ability of the glioma cells to migrate causing no deflection of the fibers. Forces exerted by tumor cells on their native microenvironment affects their ability to metastasize, invade and proliferate. While the result presents actin disruptor as a potential target to minimize metastasis, the influence of other cytoskeleton disruptors can also be studied using the platform. Moreover, the results obtained from the study can be utilized to better understand the individual cell – nanofibers interaction which can shed light on how cells interact with their native environment during metastasis.
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Kijewska, Magdalena A., Malgorzata Sielska, Renata Polakowska, Zbigniew Korwek, Aleksandra Ellert-Miklaszewska, and Bozena Kaminska. "Abstract C230: Osteopontin as a driving force of glioma-related inflammation and a candidate for therapeutic targeting in malignant gliomas?" In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c230.
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Fujita, Mitsugu, Stacy A. Decker, Flavia Popescu, et al. "Abstract 1359: COX2 blockade suppresses glioma-genesis by promoting anti-glioma immunosurveillance." In 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.am10-1359.
Full textReports on the topic "Gliomi"
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Keating, Amy. Targeting Pediatric Glioma with Apoptosis and Autophagy Manipulation. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada567861.
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Keating, Amy. Targeting Pediatric Glioma with Apoptosis and Autophagy Manipulation. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada614915.
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Zhang, Hui-Mei, Xiao-Bing Huo, Hua-Long Wang, and Chen Wang. Recurrent glioma and radiation necrosis: a meta-analysis of MRI diagnosis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.12.0028.
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Becher, Oren, and Alex Chung. Genetically Engineered Mouse Model of Diffuse Intrinsic Pontine Glioma as a Preclinical Tool. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada569511.
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Becher, Oren. Genetically Engineered Mouse Model of Diffuse Intrinsic Pontine Glioma as a Preclinical Tool. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada620002.
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Chen, Qian, Yuhua Hu, Haihua Zhan, and Yawei He. The diagnostic value of miR-221/222 in glioma : a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.3.0064.
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Yang, Chao, Tao-junjin Lu, Jie Wang, Qing Zhang, Ze-Fen Wang, and Zhi-Qiang Li. Association of systemic immune-inflammation index with grade and prognosis in glioma patients: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.4.0072.
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Gu, Xindong, Xining He, Hualong Wang, et al. Dynamic susceptibility contrast-enhanced perfusion-weighted imaging in differentiation between recurrence and pseudoprogression in high-grade glioma: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.2.0056.
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Hua, Rong, Yi-Bing Shi, Yu-Fei Fu, and Chen Wang. Diagnostic performance of dynamic susceptibility contrast-enhanced perfusion-weighted imaging in differentiating recurrence from radiation injury in postoperative glioma: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.11.0101.
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Mahmoudi, Farhad, Mahtab Mokarram, Sadegh Sabouhi, Sara Hashemi, Parastoo Saberi, and Hadi Zamanian. Application of digital health for improving medication adherence in MS patients. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.10.0058.
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Review question / Objective: The aim of this study is to evaluate the efficacy of digital health interventions in monitoring and improving medication adherence in Multiple Sclerosis patients. Condition being studied: Multiple sclerosis (MS) is the most prevalent chronic inflammatory disease of the central nervous system (CNS), which leads to focal lesions in the white matter, characterized by selective primary demyelination with partial preservation of axons and reactive astrocytic gliosis. The disease is thought to be due to a complex interaction between different genetic and environmental factors. The prevalence of MS is rising all over the world, due on one hand to earlier diagnosis and prolonged survival, and on the other to a true increase in incidence of the disease. The diagnosis of MS remains clinical despite recent advances in diagnostics and relies on demonstrating dissemination in space and time while excluding alternative diagnoses.