The regulatory networks were reverse engineered by ARACNe49 (link) from 20 different datasets: two B-cell context datasets profiled on Affymetrix HG-U95Av2 and HG-U133plus2 platforms, respectively; a high-grade glioma dataset profiled on Affymetrix HG-U133A arrays; and 17 human cancer tissue datasets profiled by RNASeq from TCGA (Table 1 ). The Affymetrix platform datasets were summarized by MAS5 (affy R-package50 ,51 (link)) using probe-clusters generated by the “cleaner” algorithm52 (link). Cleaner generates ‘informative’ probe-clusters by analyzing the correlation structure between probes mapping to the same gene and discarding non-correlated probes, which might represent poorly hybridizing or cross-hybridizing probes52 (link). The RNASeq level 3 data were downloaded from TCGA data portal, raw counts were normalized to account for different library size and the variance was stabilized by fitting the dispersion to a negative-binomial distribution as implemented in the DESeq R-package53 (link) (Bioconductor54 (link)). ARACNe was run with 100 bootstrap iterations using all probe-clusters mapping to a set of 1,813 transcription factors (genes annotated in Gene Ontology Molecular Function database (GO)55 (link) as GO:0003700—‘transcription factor activity’, or as GO:0004677—‘DNA binding’ and GO:0030528—‘Transcription regulator activity’, or as GO:0004677 and GO: 0045449—‘Regulation of transcription’), 969 transcriptional co-factors (a manually curated list, not overlapping with the transcritpion factor list, built upon genes annotated as GO:0003712—‘transcription cofactor activity’ or GO:0030528 or GO:0045449) or 3,370 signaling pathway related genes (annotated in GO Biological Process database as GO:0007165—‘signal transduction’ and in GO Cellular Component database as GO:0005622—‘intracellular’ or GO:0005886—‘plasma membrane’) as candidate regulators. Parameters were set to 0 DPI (Data Processing Inequality) tolerance and MI (Mutual Information) p-value threshold of 10−8. The regulatory networks based on ChIP experimental evidence were assembled from ChEA and ENCODE data. The mode of regulation was computed based on the correlation between TF and target gene expression as described below.
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Disorders
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Neoplastic Process
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Malignant Glioma
Malignant Glioma
Malignant Glioma: A type of primary brain tumor originating from glial cells, characterized by rapid, uncontrolled growth and invasiveness.
These tumors can be highly aggressive and pose significant challenges in treatment and management.
Optimizing research in this field is crucial for developing more effective therapies and improving patient outcomes.
PubCompare.ai's AI-driven platform can help researchers discover the best protocols, identify the most effective approaches, and leverage the power of artificial intelligence to advance Malignant Glioma research to the next level.
These tumors can be highly aggressive and pose significant challenges in treatment and management.
Optimizing research in this field is crucial for developing more effective therapies and improving patient outcomes.
PubCompare.ai's AI-driven platform can help researchers discover the best protocols, identify the most effective approaches, and leverage the power of artificial intelligence to advance Malignant Glioma research to the next level.
Most cited protocols related to «Malignant Glioma»
B-Lymphocytes
Biological Processes
Cellular Structures
DNA Chips
DNA Library
Gene Expression
Genes
HNF1A protein, human
Homo sapiens
Immune Tolerance
Malignant Glioma
Malignant Neoplasms
Plasma Membrane
Protoplasm
Signal Transduction
Tissues
Transcription, Genetic
Transcription Factor
High grade gliomas (HGGs) (WHO Grade III and IV) were requested from the St. Jude Children’s Research Hospital tissue resource core facility, and from the Institute of Cancer Research/Royal Marsden Hospital with approval for genome sequence analysis in accordance with St Jude Institutional Review Board (IRB) approval for the Pediatric Cancer Genome Project (PCGP), and the Clinical Research and Development Board of the Royal Marsden Hospital and the United Kingdom Children’s Cancer and Leukemia Group research ethics approval. Detailed clinicopathologic and sequencing information is in Supplementary Table 1 . There was a significant association between gender and tumor subtype, with 63% female DIPG patients and 63% male NBS-HGG patients (p=0.004).
The study cohort comprised 127 (57 DIPGs and 70 NBS-HGGs) tumors (54 DIPGs and 54 NBS-HGG with matching germline samples) from 118 patients in two cohorts: a cohort for whole genome sequencing (WGS, n=42, 20 DIPGs and 22 NBS-HGGs), a cohort for evaluating the frequency of abnormalities using whole exome sequencing (WES, n=80, 36 DIPGs and 44 NBS-HGGs). Six tumors including their matched germline samples, including two hypermutator tumors (SJHGG003_D and SJHGG111_D) and four non-hypermutator tumors (SJHGG003_A, SJHGG008_A, SJHGG019_E and SJHGG022_D) were sequenced by both whole genome and whole exome sequencing. Among these tumors, 75 (31 DIPGs and 44 NBS-HGGs) were characterized by RNA-seq. In addition, 12 tumors (3 DIPGs and 9 NBS-HGGs) were characterized by RNA-seq only for structural variant discovery.
Tumor was available from diagnosis and relapse in 5 cases (SJHGG019_E/S, SJHGG024_D/R, SJHGG033_D/R, SJHGG112_D/R, SJHGG115_D/R), or diagnosis and autopsy in 3 cases (SJHGG001_D/A, SJHGG002_D/A, SJHGG093_D/A). One patient developed two independent tumors, a hemispheric malignant glioneuronal tumor (SJHGG003_D), and then a subsequent independent DIPG (SJHGG003_A).
Histopathology was centrally reviewed by DWE, an experienced neuropathologist, and MRI images of DIPG cases were reviewed by a pediatric neuro-oncologist (AB). DNA and RNA was extracted as previously described 56 (link).
The study cohort comprised 127 (57 DIPGs and 70 NBS-HGGs) tumors (54 DIPGs and 54 NBS-HGG with matching germline samples) from 118 patients in two cohorts: a cohort for whole genome sequencing (WGS, n=42, 20 DIPGs and 22 NBS-HGGs), a cohort for evaluating the frequency of abnormalities using whole exome sequencing (WES, n=80, 36 DIPGs and 44 NBS-HGGs). Six tumors including their matched germline samples, including two hypermutator tumors (SJHGG003_D and SJHGG111_D) and four non-hypermutator tumors (SJHGG003_A, SJHGG008_A, SJHGG019_E and SJHGG022_D) were sequenced by both whole genome and whole exome sequencing. Among these tumors, 75 (31 DIPGs and 44 NBS-HGGs) were characterized by RNA-seq. In addition, 12 tumors (3 DIPGs and 9 NBS-HGGs) were characterized by RNA-seq only for structural variant discovery.
Tumor was available from diagnosis and relapse in 5 cases (SJHGG019_E/S, SJHGG024_D/R, SJHGG033_D/R, SJHGG112_D/R, SJHGG115_D/R), or diagnosis and autopsy in 3 cases (SJHGG001_D/A, SJHGG002_D/A, SJHGG093_D/A). One patient developed two independent tumors, a hemispheric malignant glioneuronal tumor (SJHGG003_D), and then a subsequent independent DIPG (SJHGG003_A).
Histopathology was centrally reviewed by DWE, an experienced neuropathologist, and MRI images of DIPG cases were reviewed by a pediatric neuro-oncologist (AB). DNA and RNA was extracted as previously described 56 (link).
Autopsy
Child
Congenital Abnormality
Diagnosis
dipinacoline glutamate
Ethics Committees, Research
Genome
Germ Line
Leukemia
Males
Malignant Glioma
Malignant Neoplasms
Neoplasms
Neuropathologist
Oncologists
Patients
Relapse
RNA-Seq
Tissues
Woman
Temozolomide (TMZ, Temodal®, SP Europe, Belgium) is an alkylating agent intended for the treatment of recurrent malignant glioma. In a dosage finding experiment we found a dose of 25 mg/kg body weight to be effective in suppressing adult neurogenesis by more than 80% after monocyclic (3 days) of treatment (Figure 1A ).
Consequently, to suppress adult neurogenesis, mice from the treatment group (TMZ) received injections of TMZ at 25 mg/kg (i.p., 2,5 mg/ml in 0.9% NaCl), whereas the control group (CTR) received sham injections of saline only. This regimen was given on the first three days of a week for 4 weeks to resemble paradigms used for glioma treatment in humans (Figure 1B ). Behavioral testing was performed 4 weeks after the final TMZ injection.
For adult-born granule cells to become recruitable the sequence of proliferation, differentiation and maturation requires approximately up to 28 days. Thus, suppressing adult neurogenesis for at least 4 weeks combined with a reconstitution period of 4 more weeks ensured that most of the cells borne immediately before onset of TMZ treatment would have been already used or eliminated by apoptosis. Using intercalating convalescence times, we minimized the risk of confounding side effects during behavioral testing.
It has recently been shown that 6–8 weeks old, adult generated granule cells become selectively recruited during acquisition of a spatial learning task [21] (link). Therefore, our primary aim was to minimize the number of potentially recruitable adult-born neurons exactly at that time, when the new granule cells should be of particularly high relevance for task acquisition. Because we suppressed proliferation for at least 4 weeks and behavioral testing began an additional 4 weeks later, at the time-point of the behavioral analysis the subpopulation of 5–7 week old adult generated neurons is primarily affected by TMZ. An immediate recovery of the stem cell niche seemed unlikely as it was found that after wiping out proliferation in the SGZ by irradiation reconstitution occurs only slow and on a prolonged timescale [38] (link). Consequently, at the time, when the mice were learning the water maze task only very few (or no) new granule cells were available to be functionally integrated into existing circuits.
Consequently, to suppress adult neurogenesis, mice from the treatment group (TMZ) received injections of TMZ at 25 mg/kg (i.p., 2,5 mg/ml in 0.9% NaCl), whereas the control group (CTR) received sham injections of saline only. This regimen was given on the first three days of a week for 4 weeks to resemble paradigms used for glioma treatment in humans (
For adult-born granule cells to become recruitable the sequence of proliferation, differentiation and maturation requires approximately up to 28 days. Thus, suppressing adult neurogenesis for at least 4 weeks combined with a reconstitution period of 4 more weeks ensured that most of the cells borne immediately before onset of TMZ treatment would have been already used or eliminated by apoptosis. Using intercalating convalescence times, we minimized the risk of confounding side effects during behavioral testing.
It has recently been shown that 6–8 weeks old, adult generated granule cells become selectively recruited during acquisition of a spatial learning task [21] (link). Therefore, our primary aim was to minimize the number of potentially recruitable adult-born neurons exactly at that time, when the new granule cells should be of particularly high relevance for task acquisition. Because we suppressed proliferation for at least 4 weeks and behavioral testing began an additional 4 weeks later, at the time-point of the behavioral analysis the subpopulation of 5–7 week old adult generated neurons is primarily affected by TMZ. An immediate recovery of the stem cell niche seemed unlikely as it was found that after wiping out proliferation in the SGZ by irradiation reconstitution occurs only slow and on a prolonged timescale [38] (link). Consequently, at the time, when the mice were learning the water maze task only very few (or no) new granule cells were available to be functionally integrated into existing circuits.
Adult
Alkylating Agents
Apoptosis
Bears
Body Weight
Cells
Childbirth
Cytoplasmic Granules
Glioma
Homo sapiens
Malignant Glioma
MAZE protocol
Mus
Neurogenesis
Neurons
Population Group
Radiotherapy
Saline Solution
Sodium Chloride
Stem Cell Niche
Temodal
Treatment Protocols
Adult
Autopsy
Becaplermin
Biopsy
Buffers
Cell Culture Techniques
Cells
Culture Media, Serum-Free
Deoxyribonuclease I
dipinacoline glutamate
Enzymes
Erythrocytes
Ethics Committees, Research
Glioma
Hemoglobin, Sickle
Heparin
HEPES
Homo sapiens
Liberase
Malignant Glioma
matrigel
Myelin
Neoplasms
Oligodendroglioma
PDGF AA
Serum
Short Tandem Repeat
Stem, Plant
Stem Cells
Sterility, Reproductive
Sucrose
Tissues
Pediatric high grade gliomas (pHGG), including diffuse intrinsic pontine glioma (DIPG), are among the most lethal types of cancer occurring in children [[1] (link), [2] (link)]. Major advances in our understanding of the biology of the disease have been made in the past years. These advances include the discovery that these tumors are often driven by unique epigenetic events which are not seen in their adult counterparts, most importantly caused by mutations in the gene encoding Histone 3 [[3] (link), [4] (link)]. Besides being important for the development of a therapy for these diseases, the discovery of the unique epigenetic profile of pHGG and DIPG makes these tumors useful models for the study of epigenetic regulation of gene expression in general. However, research into these tumors and their epigenetic landscape has been hampered by the difficulty with which the tumor cells can be genetically modified. For unknown reasons, primary cultures of pHGG and DIPG cells are impervious to the introduction of genetic modifications by retro- or lentiviral transduction using standard laboratory techniques, which have been around since 1996 [5 (link)]. So far, only a few successful stable transductions of pHGG/DIPG cells have been reported [[6] (link), [7] (link), [8] (link), [9] ]. As primary pHGG and DIPG cells are generally cultured as neurospheres in serum-free medium, we hypothesized that this culture methodology is, at least partially, responsible for their resistance to retro- and lentiviral transduction, possibly as a result of the stem-like phenotype these cells adopt under serum-free conditions [[10] (link), [11] (link), [12] (link)]. Alternatively, it is possible that fetal bovine serum (FBS) contains components that render cells susceptible to viral infection via unknown mechanisms. In line with this hypothesis, we successfully introduced genes in primary pHGG and DIPG cells by exposing these cells to FBS for a short period of time during the lentiviral transduction protocol. Hereby, we report the first reliable and reproducible lentiviral transduction protocol for primary pHGG and DIPG cells, allowing researchers to study their unique biological background and epigenetic landscape in more detail than before. This protocol has already been used to transduce primary DIPG neurospheres for use in a recent study by our group [13 (link)].
Adult
Biopharmaceuticals
Cells
Child
Diffuse Intrinsic Pontine Glioma
Fetal Bovine Serum
Gene Editing
Genes
Histones
Malignant Glioma
Malignant Neoplasms
Mutation
Neoplasms
Phenotype
Serum
Stem, Plant
Therapeutics
Virus Diseases
Vision
Most recents protocols related to «Malignant Glioma»
Patients were enrolled on the PRecISion Medicine for Children with Cancer clinical trial (NCT03336931), as part of the Australian Zero Childhood Cancer (ZERO) Precision Medicine Program. ZERO is an Australian national paediatric precision medicine program currently focused on real time recruitment and analysis of patients with high-risk paediatric cancers (< 30% chance of survival). Informed consent was provided by the parents/legal guardian for participants under the age of 18 years and by participants over the age of 18 years15 (link). Eighty-nine patients diagnosed with brain tumours were enrolled on the ZERO clinical trial from September 2017 until May 2020. Amongst these patients, 28 were diagnosed with a H3K27M DMG and 39 with other high-grade glioma lacking the H3K27M mutation (HGG), including WHO grade III anaplastic astrocytoma and grade IV glioblastomas (GBM) irrespective of their anatomical location or their molecular profile besides the absence of H3K27M mutation15 (link). Out of the five cases presented in this study, two cases, zcc120 and zcc183 were previously reported in part15 (link).
The molecular profiling platform consisted of germline and tumour whole genome sequencing (WGS) associated with matched germline DNA WGS, tumour only RNA-sequencing and tumour DNA Infinium MethylationEPIC array (Illumina). DNA and RNA were extracted from fresh, fresh frozen or cryopreserved tumour tissue and matched germline samples (from either fresh, cryopreserved or fresh frozen peripheral blood or skin) at the Children’s Cancer Institute (Australia), as described previously15 (link). WGS was conducted at the Kinghorn Centre for Clinical Genomics at the Garvan Institute of Medical Research (Australia), DNA methylation array performed by the Australian Genome Research Facility and transcriptome sequencing performed at Murdoch Children’s Research Institute (Australia).
Additional cohorts were used in this study from Mondal et al.7 (link) GSE140124 (N = 9 H3-WT cases) and Castel et al.6 (link) E-MTAB-8888 (N = 14 H3-WT and N = 25 H3.3-K27M and H3.1-K27M mutant cases).
The molecular profiling platform consisted of germline and tumour whole genome sequencing (WGS) associated with matched germline DNA WGS, tumour only RNA-sequencing and tumour DNA Infinium MethylationEPIC array (Illumina). DNA and RNA were extracted from fresh, fresh frozen or cryopreserved tumour tissue and matched germline samples (from either fresh, cryopreserved or fresh frozen peripheral blood or skin) at the Children’s Cancer Institute (Australia), as described previously15 (link). WGS was conducted at the Kinghorn Centre for Clinical Genomics at the Garvan Institute of Medical Research (Australia), DNA methylation array performed by the Australian Genome Research Facility and transcriptome sequencing performed at Murdoch Children’s Research Institute (Australia).
Additional cohorts were used in this study from Mondal et al.7 (link) GSE140124 (N = 9 H3-WT cases) and Castel et al.6 (link) E-MTAB-8888 (N = 14 H3-WT and N = 25 H3.3-K27M and H3.1-K27M mutant cases).
Anaplasia
Astrocytoma, Anaplastic
BLOOD
Brain Neoplasms
Child
DNA Chips
Freezing
Genome
Germ Line
Glioblastoma
Legal Guardians
Malignant Glioma
Malignant Neoplasms
Methylation
Mutation
Neoplasms
Parent
Patients
Precision Medicine
RNA, Neoplasm
Skin
Tissues
The package "ggpubr" (https://CRAN.R-project.org/package=ggpubr ) was used to analyze the different PCOLCE expression levels among the different glioma grades. These samples were obtained from TCGA database and compared to normal samples that were obtained from the GTEx database (https://commonfund.nih.gov/gtex ). We further confirmed PCOLCE levels in normal and high-grade glioma (HGG) samples using the Human Protein Atlas (HPA) (http://www.proteinatlas.org ).
Glioma
Malignant Glioma
NR4A2 protein, human
Protocol full text hidden due to copyright restrictions
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Infantile Neuroaxonal Dystrophy
Malignant Glioma
Neoplasms
Patients
Radiotherapy
Recurrence
We retrospectively analyzed 4 adult patients with H3F3A-mutant M-HGGs who underwent radiotherapy at Xuanwu Hospital, Capital Medical University from August 2020 to December 2021. A series of 16 adult patients with M-HGGs without H3F3A mutation was used as a comparative group. Cases with solitary high-grade glioma were excluded. The patients underwent at least 6 months of postoperative follow-up. The cases were classified according to the 2016 WHO classification of CNS tumors.9 (link)
The M-HGGs are defined as 2 or more lesions on magnetic resonance imaging (MRI). The clinical, radiologic and pathological data were reviewed. This study was reviewed and approved by the Ethics Committee of Xuanwu Hospital, Capital Medical University.
The extent of resection was classified as gross total resection (GTR), subtotal resection (STR), and biopsy. Postoperative radiotherapy was performed with the volume-modulated arc therapy (VMAT) technique based on the recommendations for high-grade glioma target delineation in the 2020 version of the National Comprehensive Cancer Network (NCCN) guidelines. Chemotherapy was given using the Stupp protocol.
Histological pathology is the result of hematoxylin and eosin (HE) staining and immunohistochemical staining, and antibodies are routinely detected, including IDH1, P53, Ki-67, and H3 K27 M. H3 G34R/V was partially detected. The molecular data included IDH1/2, TERT, MGMT promoter methylation, and partial H3 G34 or H3 K27 detection. Mutational analysis of IDH1/2, H3 G34 and H3 K27 was performed using polymerase chain reaction and Sanger sequencing. MGMT promoter methylation was assessed by pyrosequencing.
Progression-free survival (PFS) was defined as the time from surgery to progression. Overall survival (OS) was defined as the time from surgery to death from any cause or to the date of the last visit. Follow-up was mainly performed through outpatient and telephone visits. Clinical characteristics were described using descriptive statistics, while survival analysis comprised the median PFS estimation, the median OS estimation, the Kaplan–Meier curve, and the log-rank test using GraphPad Prism.9 (link)
A p-value <0.05 was considered statistically significant.
The M-HGGs are defined as 2 or more lesions on magnetic resonance imaging (MRI). The clinical, radiologic and pathological data were reviewed. This study was reviewed and approved by the Ethics Committee of Xuanwu Hospital, Capital Medical University.
The extent of resection was classified as gross total resection (GTR), subtotal resection (STR), and biopsy. Postoperative radiotherapy was performed with the volume-modulated arc therapy (VMAT) technique based on the recommendations for high-grade glioma target delineation in the 2020 version of the National Comprehensive Cancer Network (NCCN) guidelines. Chemotherapy was given using the Stupp protocol.
Histological pathology is the result of hematoxylin and eosin (HE) staining and immunohistochemical staining, and antibodies are routinely detected, including IDH1, P53, Ki-67, and H3 K27 M. H3 G34R/V was partially detected. The molecular data included IDH1/2, TERT, MGMT promoter methylation, and partial H3 G34 or H3 K27 detection. Mutational analysis of IDH1/2, H3 G34 and H3 K27 was performed using polymerase chain reaction and Sanger sequencing. MGMT promoter methylation was assessed by pyrosequencing.
Progression-free survival (PFS) was defined as the time from surgery to progression. Overall survival (OS) was defined as the time from surgery to death from any cause or to the date of the last visit. Follow-up was mainly performed through outpatient and telephone visits. Clinical characteristics were described using descriptive statistics, while survival analysis comprised the median PFS estimation, the median OS estimation, the Kaplan–Meier curve, and the log-rank test using GraphPad Prism.9 (link)
A p-value <0.05 was considered statistically significant.
Adult
Antibodies
Biopsy
Central Nervous System Neoplasms
Disease Progression
Eosin
Ethics Committees, Clinical
Hematoxylin
Malignant Glioma
Malignant Neoplasms
Methylation
Mutation
O(6)-Methylguanine-DNA Methyltransferase
Operative Surgical Procedures
Outpatients
Patients
Pharmacotherapy
Polymerase Chain Reaction
prisma
Radiotherapy
TERT protein, human
Therapeutics
The differential expression of the target single gene in normal brain, low-grade glioma, and high-grade glioma tissues was verified by immunohistochemical experiments. This experiment was approved by the Ethics Committee of the First Hospital of Shanxi Medical University and complied with the Declaration of Helsinki. Five normal brain tissues were collected from patients with traumatic brain injury or epilepsy, 10 postoperative tissues from patients with low-grade glioma, and 10 postoperative tissues from patients with high-grade glioma. After routine paraffin embedding, tissue sections were taken, placed on slides, deparaffinized, and rehydrated. After antigen retrieval and endogenous peroxidase blockade, they were then exposed to monogenic polyclonal antibodies (bs-13168R, Bioss) and enzyme-labeled IgG polymers. Diaminobenzidine (DAB) chromogenic solution and hematoxylin were used as a counterstain to visualize the presence of antibodies. Immunohistochemical image analysis was performed using the Scanscope digital pathology scanning system from Aperio, USA, and the expression of FCGBP in tissues was quantified by Cytoplasmic V2 software with Cytoplasm H-Score. Cytoplasm H-Score was obtained by multiplying the percentage of positive cells by the staining intensity score.
Antibodies
Antigens
azo rubin S
Brain
Cytoplasm
Enzymes
Epilepsy
Ethics Committees, Clinical
Gene Expression
Glioma
Hematoxylin
Malignant Glioma
Patients
Peroxidase
Polymers
Tissues
Traumatic Brain Injury
Top products related to «Malignant Glioma»
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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DMEM (Dulbecco's Modified Eagle's Medium) is a cell culture medium formulated to support the growth and maintenance of a variety of cell types, including mammalian cells. It provides essential nutrients, amino acids, vitamins, and other components necessary for cell proliferation and survival in an in vitro environment.
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U87MG is a human glioblastoma cell line derived from a malignant brain tumor. It is a well-established model system used in cancer research and drug discovery studies.
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Streptomycin is a broad-spectrum antibiotic used in laboratory settings. It functions as a protein synthesis inhibitor, targeting the 30S subunit of bacterial ribosomes, which plays a crucial role in the translation of genetic information into proteins. Streptomycin is commonly used in microbiological research and applications that require selective inhibition of bacterial growth.
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Penicillin is a type of antibiotic used in laboratory settings. It is a broad-spectrum antimicrobial agent effective against a variety of bacteria. Penicillin functions by disrupting the bacterial cell wall, leading to cell death.
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Penicillin/streptomycin is a commonly used antibiotic solution for cell culture applications. It contains a combination of penicillin and streptomycin, which are broad-spectrum antibiotics that inhibit the growth of both Gram-positive and Gram-negative bacteria.
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Penicillin is a type of antibacterial drug that is widely used in medical and laboratory settings. It is a naturally occurring substance produced by certain fungi, and it is effective against a variety of bacterial infections. Penicillin works by inhibiting the growth and reproduction of bacteria, making it a valuable tool for researchers and medical professionals.
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DMEM/F12 is a cell culture medium developed by Thermo Fisher Scientific. It is a balanced salt solution that provides nutrients and growth factors essential for the cultivation of a variety of cell types, including adherent and suspension cells. The medium is formulated to support the proliferation and maintenance of cells in vitro.
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Streptomycin is a laboratory product manufactured by Merck Group. It is an antibiotic used in research applications.
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L-glutamine is an amino acid that is commonly used as a dietary supplement and in cell culture media. It serves as a source of nitrogen and supports cellular growth and metabolism.
More about "Malignant Glioma"
Malignant Glioma, also known as Glioblastoma Multiforme (GBM), is an aggressive type of primary brain tumor that originates from glial cells.
These tumors are characterized by rapid, uncontrolled growth and invasiveness, posing significant challenges in treatment and management.
Optimizing research in this field is crucial for developing more effective therapies and improving patient outcomes.
Researchers studying Malignant Glioma often utilize cell lines such as U87MG, which are derived from human glioblastoma cells.
These cell lines are commonly cultured in DMEM (Dulbecco's Modified Eagle Medium) or DMEM/F12 media, supplemented with essential nutrients like L-glutamine and antibiotics such as Penicillin and Streptomycin to prevent microbial contamination.
PubCompare.ai's AI-driven platform can help researchers discover the best protocols, identify the most effective approaches, and leverage the power of artificial intelligence to advance Malignant Glioma research to the next level.
By comparing published literature, pre-prints, and patents, researchers can optimize their experimental designs and streamline their investigations, ultimately leading to breakthroughs in the understanding and treatment of this devastating disease.
These tumors are characterized by rapid, uncontrolled growth and invasiveness, posing significant challenges in treatment and management.
Optimizing research in this field is crucial for developing more effective therapies and improving patient outcomes.
Researchers studying Malignant Glioma often utilize cell lines such as U87MG, which are derived from human glioblastoma cells.
These cell lines are commonly cultured in DMEM (Dulbecco's Modified Eagle Medium) or DMEM/F12 media, supplemented with essential nutrients like L-glutamine and antibiotics such as Penicillin and Streptomycin to prevent microbial contamination.
PubCompare.ai's AI-driven platform can help researchers discover the best protocols, identify the most effective approaches, and leverage the power of artificial intelligence to advance Malignant Glioma research to the next level.
By comparing published literature, pre-prints, and patents, researchers can optimize their experimental designs and streamline their investigations, ultimately leading to breakthroughs in the understanding and treatment of this devastating disease.