scholarly journals Altered Elemental Distribution in Male Rat Brain Tissue as a Predictor of Glioblastoma Multiforme Growth—Studies Using SR-XRF Microscopy

2022 ◽  
Vol 23 (2) ◽  
pp. 703
Author(s):  
Karolina Planeta ◽  
Zuzanna Setkowicz ◽  
Mateusz Czyzycki ◽  
Natalia Janik-Olchawa ◽  
Damian Ryszawy ◽  
...  
Keyword(s):  
Glioblastoma Multiforme ◽  
Rat Brain ◽  
Tumor Development ◽  
Primary Brain Tumor ◽  
New Drugs ◽  
Male Rat ◽  
Elemental Distribution ◽  
Strongly Correlated ◽  
Average Survival ◽  
Glioma Growth

Glioblastoma multiforme (GBM) is a particularly malignant primary brain tumor. Despite enormous advances in the surgical treatment of cancer, radio- and chemotherapy, the average survival of patients suffering from this cancer does not usually exceed several months. For obvious ethical reasons, the search and testing of the new drugs and therapies of GBM cannot be carried out on humans, and for this purpose, animal models of the disease are most often used. However, to assess the efficacy and safety of the therapy basing on these models, a deep knowledge of the pathological changes associated with tumor development in the animal brain is necessary. Therefore, as part of our study, the synchrotron radiation-based X-ray fluorescence microscopy was applied for multi-elemental micro-imaging of the rat brain in which glioblastoma develops. Elemental changes occurring in animals after the implantation of two human glioma cell lines as well as the cells taken directly from a patient suffering from GBM were compared. Both the extent and intensity of elemental changes strongly correlated with the regions of glioma growth. The obtained results showed that the observation of elemental anomalies accompanying tumor development within an animal’s brain might facilitate our understanding of the pathogenesis and progress of GBM and also determine potential biomarkers of its extension. The tumors appearing in a rat’s brain were characterized by an increased accumulation of Fe and Se, whilst the tissue directly surrounding the tumor presented a higher accumulation of Cu. Furthermore, the results of the study allow us to consider Se as a potential elemental marker of GBM progression.

scholarly journals GLEJAK WIELOPOSTACIOWY – POSTĘP WIEDZY NA TEMAT PATOGENEZY NOWOTWORU

2016 ◽  
Vol 60 (2) ◽  
Author(s):  
Paweł Wańkowicz ◽  
Przemysław Nowacki
Keyword(s):  
Glioblastoma Multiforme ◽  
Genetic Disorders ◽  
Primary Brain Tumor ◽  
Malignant Tumours ◽  
Current State ◽  
Multi Stage ◽  
Average Survival ◽  
The Central Nervous System ◽  
Stage Process

Glioblastoma multiforme is a particularly malignant form of primary brain tumor. This cancer represents 12–15% of all brain tumors. Despite advances in neurosurgery, radiation and chemotherapy, the average survival rate is only from 12.1 to 14.6 months. Glioblastoma multiforme is characterized by its diverse histological and cellular features. Like other malignant tumours, it is formed in a multi -stage process of somatic cell transformations, accumulating several genetic disorders. The last decade was a period of particular interest in stem cells. These cells have so far been identified in a variety of primary tumours in the brain. They are probably responsible for the recurrence and progression of cancer. Given the current state of knowledge, it is likely that modifications to the previously used morphological classification of tumours of the CNS will be made by the WHO, as well as the extension of its molecular criteria. In particular, such strategies are awaited for Glioblastoma multiforme – the most malignant primary tumor of the central nervous system, with so far very poor prognosis.

Recent Advances on Glioblastoma Multiforme and Nano-drug Carriers: A Review

2019 ◽  
Vol 26 (31) ◽  
pp. 5862-5874 ◽  
Author(s):  
Wang Liao ◽  
Shengnuo Fan ◽  
Yuqiu Zheng ◽  
Shaowei Liao ◽  
Ying Xiong ◽  
...  
Keyword(s):  
Stem Cells ◽  
Glioblastoma Multiforme ◽  
Self Assembly ◽  
Poor Prognosis ◽  
Drug Delivery Systems ◽  
Drug Carriers ◽  
Therapeutic Resistance ◽  
Average Survival ◽  
Nano Drug Delivery ◽  
New Development

Glioblastoma Multiforme (GBM) is the most frequent glioma with a poor prognosis. The mainstay treatment for GBM is chemotherapy, but the average survival of GBM remains unsatisfactory due to therapeutic resistance. Poor permeability restricted by the Blood Brain Barrier (BBB) and the presence of Glioblastoma Stem Cells (GSCs) remain as two problems for chemotherapy. Recently, nanocarriers have attracted much attention in the research of GBM, owing to their advantages in self-assembly, biosafety, release controllability, and BBB penetrability, making them promising candidates for GBM treatment. This article aims to review the biologic signatures of BBB and GSCs, as well as the new development of nano-drug delivery systems to facilitate our understanding of targeted treatment for GBM.

scholarly journals Friend or Foe: Paradoxical Roles of Autophagy in Gliomagenesis

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1411
Author(s):  
Don Carlo Ramos Batara ◽  
Moon-Chang Choi ◽  
Hyeon-Uk Shin ◽  
Hyunggee Kim ◽  
Sung-Hak Kim
Keyword(s):  
Brain Tumor ◽  
Glioblastoma Multiforme ◽  
Cancer Biology ◽  
Molecular Mechanisms ◽  
Primary Brain Tumor ◽  
Molecular Target ◽  
Therapeutic Strategies ◽  
Homeostatic Mechanism ◽  
Cellular Context ◽  
Cellular Components

Glioblastoma multiforme (GBM) is the most common and aggressive type of primary brain tumor in adults, with a poor median survival of approximately 15 months after diagnosis. Despite several decades of intensive research on its cancer biology, treatment for GBM remains a challenge. Autophagy, a fundamental homeostatic mechanism, is responsible for degrading and recycling damaged or defective cellular components. It plays a paradoxical role in GBM by either promoting or suppressing tumor growth depending on the cellular context. A thorough understanding of autophagy’s pleiotropic roles is needed to develop potential therapeutic strategies for GBM. In this paper, we discussed molecular mechanisms and biphasic functions of autophagy in gliomagenesis. We also provided a summary of treatments for GBM, emphasizing the importance of autophagy as a promising molecular target for treating GBM.

scholarly journals Phosphorous Magnetic Resonance Spectroscopy to Detect Regional Differences of Energy and Membrane Metabolism in Naïve Glioblastoma Multiforme

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2598
Author(s):  
Lisa Maria Walchhofer ◽  
Ruth Steiger ◽  
Andreas Rietzler ◽  
Johannes Kerschbaumer ◽  
Christian Franz Freyschlag ◽  
...  
Keyword(s):  
Glioblastoma Multiforme ◽  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Healthy Volunteers ◽  
Regional Differences ◽  
Primary Brain Tumor ◽  
Brain Parenchyma ◽  
Resonance Spectroscopy ◽  
31P Mrs ◽  
Diffusion Parameters

Background: Glioblastoma multiforme (GBM) is a highly malignant primary brain tumor with infiltration of, on conventional imaging, normal-appearing brain parenchyma. Phosphorus magnetic resonance spectroscopy (31P-MRS) enables the investigation of different energy and membrane metabolites. The aim of this study is to investigate regional differences of 31P-metabolites in GBM brains. Methods: In this study, we investigated 32 patients (13 female and 19 male; mean age 63 years) with naïve GBM using 31P-MRS and conventional MRI. Contrast-enhancing (CE), T2-hyperintense, adjacent and distant ipsilateral areas of the contralateral brain and the brains of age- and gender-matched healthy volunteers were assessed. Moreover, the 31P-MRS results were correlated with quantitative diffusion parameters. Results: Several metabolite ratios between the energy-dependent metabolites and/or the membrane metabolites differed significantly between the CE areas, the T2-hyperintense areas, the more distant areas, and even the brains of healthy volunteers. pH values and Mg2+ concentrations were highest in visible tumor areas and decreased with distance from them. These results are in accordance with the literature and correlated with quantitative diffusion parameters. Conclusions: This pilot study shows that 31P-MRS is feasible to show regional differences of energy and membrane metabolism in brains with naïve GBM, particularly between the different “normal-appearing” regions and between the contralateral hemisphere and healthy controls. Differences between various genetic mutations or clinical applicability for follow-up monitoring have to be assessed in a larger cohort.

scholarly journals 5′-AMP-activated protein kinase activity is elevated early during primary brain tumor development in the rat

2010 ◽  
Vol 128 (9) ◽  
pp. 2230-2239 ◽  
Author(s):  
Taichang Jang ◽  
Joy M. Calaoagan ◽  
Eunice Kwon ◽  
Steven Samuelsson ◽  
Lawrence Recht ◽  
...  
Keyword(s):  
Brain Tumor ◽  
Protein Kinase ◽  
Kinase Activity ◽  
Tumor Development ◽  
Primary Brain Tumor ◽  
Protein Kinase Activity ◽  
Amp Activated Protein Kinase

Celecoxib and radioresistant glioblastoma-derived CD133+ cells: improvement in radiotherapeutic effects

2011 ◽  
Vol 114 (3) ◽  
pp. 651-662 ◽  
Author(s):  
Hsin-I Ma ◽  
Shih-Hwa Chiou ◽  
Dueng-Yuan Hueng ◽  
Lung-Kuo Tai ◽  
Pin-I Huang ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Critical Role ◽  
Tumor Development ◽  
Primary Brain Tumor ◽  
Scid Mice ◽  
Therapeutic Effects ◽  
Glioblastoma Cells ◽  
Source Case ◽  
Cox 2

Object Glioblastoma, the most common primary brain tumor, has a poor prognosis, even with aggressive resection and chemoradiotherapy. Recent studies indicate that CD133+ cells play a key role in radioresistance and recurrence of glioblastoma. Cyclooxygenase-2 (COX-2), which converts arachidonic acid to prostaglandins, is over-expressed in a variety of tumors, including CD133+ glioblastomas. The COX-2–derived prostaglandins promote neovascularization during tumor development, and conventional radiotherapy increases the proportion of CD133+ cells rather than eradicating them. The aim of the present study was to investigate the role of celecoxib, a selective COX-2 inhibitor, in enhancing the therapeutic effects of radiation on CD133+ glioblastomas. Methods Cells positive for CD133 were isolated from glioblastoma specimens and characterized by flow cytometry, then treated with celecoxib and/or ionizing radiation (IR). Clonogenic assay, cell irradiation, cell cycle analysis, Western blot, and xenotransplantation were used to assess the effects of celecoxib alone, IR alone, and IR with celecoxib on CD133+ and CD133− glioblastoma cells. Three separate xenotransplantation experiments were carried out using 310 severe combined immunodeficient (SCID) mice: 1) an initial tumorigenicity evaluation in which 3 different quantities of untreated CD133– cells or untreated or pretreated CD133+ cells (5 treatment conditions) from 7 different tumors were injected into the striatum of 2 mice (210 mice total); 2) a tumor growth study (50 mice); and 3) a survival study (50 mice). For these last 2 studies the same 5 categories of cells were used as in the tumorigenicity (untreated CD133– cells, untreated or pretreated CD133+ cells, with pretreatment consisting of celecoxib alone, IR alone, or IR and celecoxib), but only 1 cell source (Case 2) and quantity (5 × 104 cells) were used. Results High levels of COX-2 protein were detected in the CD133+ but not the CD133− glioblastoma cells. The authors further demonstrated that 30 μM celecoxib was able to effectively enhance the IR effect in inhibiting colony formation and increasing IR-mediated apoptosis in celecoxib-treated CD133+ glioblastoma cells. Furthermore, reduction in radioresistance was correlated with the induction of G2/M arrest, which was partially mediated through the increase in the level of phosphorylated-cdc2. In vivo xenotransplant analysis further confirmed that CD133+-associated tumorigenicity was significantly suppressed by celecoxib treatment. Importantly, pretreatment of CD133+ glioblastoma cells with a combination of celecoxib and IR before injection into the striatum of SCID mice resulted in a statistically significant reduction in tumor growth and a statistically significant increase in the mean survival rate of the mice. Conclusions Celecoxib combined with radiation plays a critical role in the suppression of growth of CD133+ glioblastoma stemlike cells. Celecoxib is therefore a radiosensitizing drug for clinical application in glioblastoma.

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