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> Disorders > Neoplastic Process > Astrocytoma, Anaplastic

Astrocytoma, Anaplastic

Astrocytoma, Anaplastic: A high-grade, rapidly growing form of astrocytic tumor.
These tumors are characterized by marked cellular pleomorphism, high mitotic activity, and areas of necrosis.
Astrocytoma, anaplastic is an aggressive malform of astocyte cells that can rapidly spread throughout the central nervous system.
Early detection and comprehensive treatment are critical for managing this type of brain cancer.

Most cited protocols related to «Astrocytoma, Anaplastic»

1
Molecular Profiling of Brain Tumors
DNA was extracted from samples of primary brain tumor and xenografts and from patient-matched normal blood lymphocytes obtained from the Tissue Bank at the Preston Robert Tisch Brain Tumor Center at Duke University and collaborating centers, as described previously.17 (link) All analyzed brain tumors were subjected to consensus review by two neuropathologists. Table 1 lists the types of brain tumors we analyzed. The samples from glioblastomas included 138 primary tumors and 13 secondary tumors. Of the 138 primary tumors, 15 were from patients under the age of 21 years. Secondary glioblastomas were categorized as WHO grade IV on the basis of histologic criteria but had been categorized as WHO grade II or III at least 1 year earlier. Of the 151 tumors, 63 had been analyzed in our previous genomewide mutation analysis of glioblastomas. None of the lower-grade tumors were included in that analysis.16 (link)
In addition to brain tumors, we analyzed 35 lung cancers, 57 gastric cancers, 27 ovarian cancers, 96 breast cancers, 114 colorectal cancers, 95 pancreatic cancers, and 7 prostate cancers, along with 4 samples from patients with chronic myelogenous leukemia, 7 from patients with chronic lymphocytic leukemia, 7 from patients with acute lymphoblastic leukemia, and 45 from patients with acute myelogenous leukemia. All samples were obtained in accordance with the Health Insurance Portability and Accountability Act. Acquisition of tissue specimens was approved by the institutional review board at the Duke University Health System and at each of the participating institutions.
Exon 4 of the IDH1 gene was amplified with the use of a polymerase-chain-reaction (PCR) assay and sequenced in DNA from the tumor and lymphocytes from each patient, as described previously.16 (link) In all gliomas and medulloblastomas without an R132 IDH1 mutation, exon 4 of the IDH2 gene (which contains the IDH2 residue equivalent to R132 of IDH1) was sequenced and analyzed for somatic mutations. In addition, we evaluated all astrocytomas and oligodendrogliomas of WHO grade I to grade III, all secondary glioblastomas, and 96 primary glioblastomas without R132 IDH1 mutations or R172 IDH2 mutations for alterations in the remaining coding exons of IDH1 and IDH2. All coding exons of TP53 and PTEN were also sequenced in the panel of diffuse astrocytomas, oligodendrogliomas, anaplastic oligodendrogliomas, anaplastic astrocytomas, and glioblastomas. EGFR amplification and the CDKN2A-CDKN2B deletion were analyzed with the use of quantitative real-time PCR in the same tumors.18 (link) We evaluated samples of oligodendrogliomas and anaplastic oligodendrogliomas for loss of heterozygosity at 1p and 19q, as described previously.15 (link),19 (link)
Yan H., Parsons D.W., Jin G., McLendon R., Rasheed B.A., Yuan W., Kos I., Batinic-Haberle I., Jones S., Riggins G.J., Friedman H., Friedman A., Reardon D., Herndon J., Kinzler K.W., Velculescu V.E., Vogelstein B, & Bigner D.D. (2009). IDH1 and IDH2 Mutations in Gliomas. The New England journal of medicine, 360(8), 765-773.
Publication 2009
7-chloro-8-hydroxy-1-(3'-iodophenyl)-3-methyl-2,3,4,5-tetrahydro-1H-3-benzazepine Anaplastic Oligodendroglioma Astrocytoma Astrocytoma, Anaplastic Biological Assay BLOOD Brain Neoplasms Brain Tumor, Primary CDKN2A Gene Chronic Lymphocytic Leukemia Colorectal Carcinoma Deletion Mutation Diploid Cell EGFR protein, human Ethics Committees, Research Exons Gastric Cancer Genes Glioblastoma Glioma Grade II Astrocytomas Heterografts IDH2, human Leukemia, Myelocytic, Acute Leukemias, Chronic Granulocytic Loss of Heterozygosity Lung Cancer Lymphocyte Malignant Neoplasm of Breast Medulloblastoma Mutation Neoplasms Neuropathologist Oligodendroglioma Ovarian Cancer Pancreatic Cancer Patients Polymerase Chain Reaction Precursor Cell Lymphoblastic Leukemia Lymphoma Prostate Cancer PTEN protein, human Real-Time Polymerase Chain Reaction Tissues TP53 protein, human
2
Childhood Cancer Epidemiology: Pooled Analysis
Data were combined from five previous studies in which the incident cases of childhood cancer were identified from the population-based cancer registries of five states: California, Minnesota, New York (excluding New York City), Texas, and Washington. Cases were diagnosed between 1980 and 2004. The details of each state's selection and inclusion criteria have been previously reported 14 (link). Children up to age 14 years at diagnosis were included except in California where only cases less than 5 years of age were included (the CA study was originally designed to study early childhood cancers only). Cases were matched to birth certificates using probabilistic or sequential deterministic record linkage. Controls were randomly selected from each state's birth registry, in ratios to cases varying from 1:1 to 1:10 (differed by state). They were matched on date of birth in all states and also matched on sex in California and Texas. Any subject reported to have Down syndrome was excluded (n=100). Because subjects diagnosed before age 28 days were excluded in some of the states, this criterion was applied to all cases for consistency.
We classified the cancers according to the International Classification of Childhood Cancer (ICCC-3) and examined all groups with at least 200 cases 15 (link). We made one exception to this rule in order to examine the 109 cases of chronic myeloproliferative diseases (CMD) because of our interest in leukemia sub-types. Wilms tumors and retinoblastoma were further examined by unilateral and bilateral occurrence. Additionally we examined the CNS tumors by type to reflect clinically relevant biological differences using categories previously developed 16 . We classified pilocytic astrocytomas, astrocytomas not otherwise specified, and other grade I and II gliomas into the low grade glioma category. Malignant gliomas, anaplastic astrocytomas, and other grade III and IV gliomas were grouped into the high grade glioma category. Other separate categories included medulloblastomas, primitive neuroectodermal tumors (PNET), ependymomas, and intracranial/intraspinal germ cell tumors.
Odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression (SAS version 9.1). The individual matching of the California cases and controls was broken to allow the use of this procedure. The other states used frequency matching. We examined birth order in four categories: first, second, third, and fourth or more. In the multivariable analyses we adjusted for matching and pooling variables (state, sex, year of birth), maternal race, maternal age, singleton vs. multiple birth, gestational age, and birth weight (all categorized as shown in Table 2). We also stratified the analyses for the leukemia sub-types by age at diagnosis (0-4 years, 5-9 years, 10-14 years).
Von Behren J., Spector L.G., Mueller B.A., Carozza S.E., Chow E.J., Fox E.E., Horel S., Johnson K.J., McLaughlin C., Puumala S.E., Ross J.A, & Reynolds P. (2010). Birth order and Risk of Childhood Cancer: A Pooled Analysis from Five U.S. States. International journal of cancer. Journal international du cancer, 128(11), 2709-2716.
Publication 2010
Astrocytoma Astrocytoma, Anaplastic Biopharmaceuticals Birth Weight Central Nervous System Neoplasms Child Childbirth Diagnosis Down Syndrome Ependymoma Gestational Age Glioma Leukemia Malignant Glioma Malignant Neoplasms Medulloblastoma Mothers Multiple Birth Offspring Myeloproliferative Disorders Nephroblastoma Neuroectodermal Tumor, Primitive Pilocytic Astrocytoma Retinoblastoma Tumor, Germ Cell
3
In Silico Comparison of Brain Tumor SAGE Data
The Table 1 list the SAGE Genie's library name, Gene Expression Omnibus (GEO) [29 ] accession code and size of all used libraries.
For our aims, it is sufficient to focus the analysis at the tag level. Thus, we process the tag counts and let the identification of tag's best gene match as a posterior question that could be carefully done only to really interesting tags. We choose not to process tags whose counts appear only in libraries of one class. It is important to note that all libraries are from bulk material, without cell-lines, and came from patients with similar disease description. The normal libraries came from different normal regions of the brain.
We think that this data set is very illustrative since there are biological replicates in the tumor class allowing clear verification of within-class biological variability. On the other hand, taking only one kind of disease, astrocytoma grade III, instead of all brain tumors in the database, leads one to believe that the within-class variability is in fact due to biological diversity of the patients and not due to very distinct molecular profile of distinct brain tumors stored in SAGE Genie's database.
Therefore, we believe that this in silico comparison is well-suited to demonstrate the necessity of dealing with within-class effect, although it is not our aim here to make a detailed or biological analysis of brain tumor data.
Vêncio R.Z., Brentani H., Patrão D.F, & Pereira C.A. (2004). Bayesian model accounting for within-class biological variability in Serial Analysis of Gene Expression (SAGE). BMC Bioinformatics, 5, 119.
Publication 2004
Astrocytoma, Anaplastic Biopharmaceuticals Brain Brain Neoplasms cDNA Library Cell Lines Dietary Fiber Gene Expression Genes Neoplasms Patients
4
Glioma Tissue Microarray Repository
Formalin-fixed, paraffin-embedded (FFPE) gliomas were retrieved from pathology archives. Deidentified tissue microarrays (TMAs) were constructed from the gliomas. Three 2-mm diameter cores per tumor were obtained, with each core embedded in a separate TMA block. A total of 104 cases comprised the TMAs, including 9 nonneoplastic controls (cortical dysplasias), 9 grade II astrocytomas, 11 grade III astrocytomas, 12 anaplastic oligodendrogliomas, 16 grade II oligodendrogliomas, and 47 grade IV glioblastomas (GBMs).
Deidentified fresh glioma specimens were prospectively banked via snap-freezing in liquid nitrogen at the time of surgery. Each case was annotated with the corresponding pathologic diagnosis and IDH1/2 mutation status.
Gilbert M.R., Liu Y., Neltner J., Pu H., Morris A., Sunkara M., Pittman T., Kyprianou N, & Horbinski C. (2013). Autophagy and Oxidative Stress in Gliomas with IDH1 Mutations. Acta neuropathologica, 127(2), 221-233.
Publication 2013
Anaplastic Oligodendroglioma Astrocytoma, Anaplastic Cortical Dysplasia Diagnosis Formalin Glioblastoma Glioma Grade II Astrocytomas Microarray Analysis Mutation Neoplasms Nitrogen Oligodendroglioma Paraffin Tissues
5
Genotyping of Glioma and Control Subjects
Genotyping data comes from four groups of subjects, 622 high grade astrocytic glioma cases and 602 controls from AGS, 3390 controls from Illumina controls (iControls), and 70 glioblastoma cases from TCGA 4 (link) (Supplementary Table 1a) that passed quality control measures described below, including checks for relatedness and European ancestry. Details of subject recruitment for AGS have been provided previously 20 ,21 (link). Briefly, cases aged 20 or older, diagnosed with histologically confirmed incident gliomas (International Classification of Diseases for Oncology, morphology codes 9380–9481) were recruited from the local population based registry, the Northern California Rapid Case Ascertainment program and the University of California, San Francisco Neuro-oncology clinic between 1997 and 2006. Additional pathology reviews were conducted by specialty trained neuropathologists including Kenneth Aldape and Tarik Tihan. Glioblastoma, which is the diagnosis for the large majority (84%) of cases, is a diagnosis with good concordance between pathologists 22 (link). Although survival bias is a concern for studies of glioblastoma, we obtained blood from subjects within a median of 80 days from diagnosis. Nevertheless, the results may not apply to those with the most rapidly fatal forms of this disease. AGS controls aged 20 years or older from the same residential area as cases were identified using random digit dialing and were frequency matched to cases on age, gender and ethnicity. Consenting participants provided blood and/or buccal specimens and information during an in-person or telephone interview. Because of the large scale genotyping platform used, only subjects who provided blood specimens were included in the present analysis. We initially only included individuals who self-identified as white in the genotyping, but then used methods described below to verify European ancestry.
We also assembled an independent control genotype dataset of 3390 non-redundant white controls from Illumina iControlDB (Illumina, Inc., San Diego, CA). The subjects are anonymous, with information only on their age, gender and ethnicity. The iControl data also included 262 HapMap samples [30 CEU parent-child trios (Utah residents with ancestry from northern and western Europe), 84 YRI (Yoruba in Ibadan, Nigeria) and 88 Chinese or Japanese] that we used to identify and remove subjects with evidence of non-European ancestry from our analysis. We checked for evidence of non-European ancestry (Supplementary Figure 2) and sample duplicates or related subjects (IBS > 1.6; Supplementary Figure 3) among AGS samples, TCGA, and iControls by performing Multi-dimensional scaling (MDS) analysis on 20 bootstrap samples of 1000 random autosomal bi-allelic SNPs. Following these quality assessment measures, we obtained a total of 3390 white controls from three different Illumina panels with up to 306,154 autosomal SNPs overlapping the HumanHap370duo panel used for the AGS subjects: Illumina HumanHap300 (n=336 subjects), HumanHap550v1 (n=1519), and HumanHap550v3 (n=1552).
We downloaded HumanHap550 platform genotyping data from blood specimen DNA and demographic data for 89 glioblastoma cases from the Cancer Genome Atlas (TCGA; http://cancergenome.nih.gov/)4 (link). Although 72 were identified as whites, our analyses showed that one had non-European ancestry (Supplementary Figure 3) and another appeared to duplicate an AGS case, leaving 70 TCGA cases.
Wrensch M., Jenkins R.B., Chang J.S., Yeh R.F., Xiao Y., Ballman K.V., Berger M., Buckner J.C., Chang S., Decker P.A., Giannini C., Halder C., Kollmeyer T.M., Kosel M.L., LaChance D.H., McCoy L., O’Neill B., Patoka J., Pico A.R., Prados M., Quesenberry C., Rice T., Rynearson A., Smirnov I., Tihan T., Wiemels J., Yang P, & Wiencke J.K. (2009). Variants in the CDKN2B and RTEL1 regions are associated with high grade glioma susceptibility. Nature genetics, 41(8), 905-908.
Publication 2009
Alleles Astrocytoma, Anaplastic BLOOD Cheek Child Chinese Diagnosis Ethnicity Europeans Fingers Genome Glioblastoma Glioma HapMap Japanese Malignant Neoplasms Neoplasms Neuropathologist Parent Pathologists Single Nucleotide Polymorphism TRIO protein, human White Person

Most recents protocols related to «Astrocytoma, Anaplastic»

1
Awake Surgery for Dominant and Non-Dominant Glioma
As an observational retrospective study, we reviewed a cohort of 80 patients who underwent awake surgery with intraoperative direct electrical mapping for dominant and nondominant hemispheres. All patients were treated at Department of Neurosurgery, Tangdu Hospital, Airforce Medical University, from January 2013 to December 2021. The inclusion criteria were (1) age ≥ 18 years, (2) newly diagnosed glioma, including astrocytoma, oligodendroglioma, anaplastic oligodendroglioma, anaplastic astrocytoma, anaplastic oligoastrocytoma, and glioblastoma, based on the WHO 2007 classification. The WHO 2016 classification was applied in 2017-2019 (31 cases), and the WHO 2021 classification of glioma was applied in 2021 (18 cases). The exclusion criteria included biopsy and incomplete MRI data calculating the tumor volume.
Demographic, clinical, and histological data were collected and analyzed from patients and neurocognitive and functional outcomes. The Institutional Review Board at Tangdu Hospital approved the study (TDLL-202210-18).
Wang Y., Guo S., Wang N., Liu J., Chen F., Zhai Y., Wang Y., Jiao Y., Zhao W., Fan C., Xue Y., Gao G., Ji P, & Wang L. (2023). The clinical and neurocognitive functional changes with awake brain mapping for gliomas invading eloquent areas: Institutional experience and the utility of The Montreal Cognitive Assessment. Frontiers in Oncology, 13, 1086118.
Publication 2023
Anaplasia Anaplastic Oligodendroglioma Astrocytoma Astrocytoma, Anaplastic Biopsy Electricity Ethics Committees, Research Glioblastoma Multiforme Glioma Mixed Oligodendroglioma-Astrocytoma Neurosurgical Procedures Oligodendroglioma Operative Surgical Procedures Patients
2
Precision Medicine for Pediatric Brain Cancers
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).
Ajuyah P., Mayoh C., Lau L.M., Barahona P., Wong M., Chambers H., Valdes-Mora F., Senapati A., Gifford A.J., D’Arcy C., Hansford J.R., Manoharan N., Nicholls W., Williams M.M., Wood P.J., Cowley M.J., Tyrrell V., Haber M., Ekert P.G., Ziegler D.S, & Khuong-Quang D.A. (2023). Histone H3-wild type diffuse midline gliomas with H3K27me3 loss are a distinct entity with exclusive EGFR or ACVR1 mutation and differential methylation of homeobox genes. Scientific Reports, 13, 3775.
Publication 2023
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
3
Prognostic Analysis of Glioma Subtypes
To determine the correlation between single gene expression and clinical characteristics and prognosis of glioma patients, we conducted univariate and multivariate independent prognostic analysis on gene expression profile, clinical profile, and survival profile in CGGA and GSE43378 by Cox regression method using survival R package. The clinical profile of glioma patients in CGGA and GSE43378 are shown in Table 1. We further screened out clinical characteristics relating to glioma prognosis and determined the prognostic value of the single gene, p<0.05 was considered statistically significant.

Clinical Characteristics of Patients with Glioma in CGGA and GSE43378

ParametersCGGA (N=749)GSE43378 (N=50)
Age
<=41, n (%)342(45.7)12(24.0)
>41, n (%)407(54.3)38(76.0)
Gender
Female, n (%)307(41.0)16(32.0)
Male, n (%)442(59.0)34(68.0)
Radio
No, n (%)124(16.6)–
Yes, n (%)625(83.4)–
Chemo
No, n (%)229(30.6)–
Yes, n (%)520(69.4)–
Histology
Astrocytoma (A), n (%)75(10.0)5(10.0)
Anaplastic astrocytoma (AA), n (%)75(10.0)7(14.0)
Anaplastic oligodendroglioma (AO), n (%)37(04.9)4(08.0)
Anaplastic oligoastrocytoma (AOA), n (%)128(17.1)2(04.0)
Oligodendroglioma (O), n (%)39(05.2)–
Oligoastrocytoma (OA), n (%)104(13.9)–
Glioblastoma (GBM), n (%)291(38.9)32(64.0)
PRS_type
Primary, n (%)502(67.0)–
Recurrent, n (%)222(29.7)–
Secondary, n (%)25(03.3)–
Grade
WHO II, n (%)218(29.1)5(10.0)
WHO III, n (%)240(32.0)13(26.0)
WHO IV, n (%)291(38.9)32(64.0)
IDH_mutation
Wildtype, n (%)339(45.3)–
Mutant, n (%)410(54.7)–
1p19q_codeletion
Non-codel, n (%)594(79.3)–
Codel, n (%)155(20.7)–
Survival state
Live, n (%)293(39.1)8(16.0)
Dead, n (%)456(60.9)42(84.0)
Zhang J.J., Zhang Y., Chen Q., Chen Q.N., Yang X., Zhu X.L., Hao C.Y, & Duan H.B. (2023). A Novel Prognostic Marker and Therapeutic Target Associated with Glioma Progression in a Tumor Immune Microenvironment. Journal of Inflammation Research, 16, 895-916.
Publication 2023
Anaplasia Anaplastic Oligodendroglioma Astrocytoma, Anaplastic Gene Expression Gene Expression Profiling Genes Glioblastoma Multiforme Glioma Males Mixed Oligodendroglioma-Astrocytoma Oligodendroglioma Patients Prognosis
4
Anaplastic Astrocytoma Cell Culture Protocol
The research was performed on the human anaplastic astrocytoma SW1783 cell line, which was obtained from ATCC (HTB-13™, Manassas, VA, USA). Cells were cultured in DMEM supplemented with FBS (final concentration 10%), penicillin G (10,000 U/mL), neomycin (10 μg/mL), and amphotericin B (0.25 mg/mL) at 37 °C and humidified 5% CO2 atmosphere.
Prior to the experiment, SW1783 cells were seeded in 96-well microplates (3000 cells/well) and T-75 flasks (1 × 106 cells/flask), and preincubated for 48 h (37 °C, 5% CO2). Afterward, the medium was removed and the drug solutions, prepared in DMEM, were added. Following 48 h of treatment, cells cultured in flasks were detached by trypsinization, centrifuged, and resuspended in the medium for further analyses.
Maszczyk M., Banach K., Rok J., Rzepka Z., Beberok A, & Wrześniok D. (2023). Evaluation of Possible Neobavaisoflavone Chemosensitizing Properties towards Doxorubicin and Etoposide in SW1783 Anaplastic Astrocytoma Cells. Cells, 12(4), 593.
Publication 2023
Amphotericin B Astrocytoma, Anaplastic Atmosphere Cell Lines Cells Homo sapiens Neomycin Penicillin G Pharmaceutical Solutions
5
Cell Viability Assay for Anticancer Drugs
The viability of the cells was estimated using a WST-1 (4-[3-(4-iodophenyl)-2-(4-nitrophenyl)-2H-5-tetrazolio]-1,3-benzene disulfonate) colorimetric assay. This analysis is based on the action of mitochondrial dehydrogenases that catalyze the reduction of the WST-1 reagent. The amount of the product correlates with the number of metabolically active cells. Human anaplastic astrocytoma SW1783 cells were seeded at 3000 cells per well in 96-well microplates in a supplemented DMEM growth medium and incubated for 48 h at 37 °C and 5% CO2. Then, the medium was replaced with solutions of NEO (1–75 μM), doxorubicin (1–50 μM), etoposide (1–50 μM), irinotecan (1–50 μM), and NEO (25 μM, 75 μM) combined with doxorubicin (1 μM), etoposide (10 μM), and irinotecan (10 μM). After 48 h of incubation, 10 μL of WST-1 reagent was added to each well and after 1h of incubation, the absorbance of the samples was measured at 440 nm and, as a reference wavelength, 650 nm using an Infinite 200 PRO (TECAN, Männedorf, Switzerland) microplate reader. The controls were normalized to 100% for each assay, and the results were shown as the percentage of the controls.
Maszczyk M., Banach K., Rok J., Rzepka Z., Beberok A, & Wrześniok D. (2023). Evaluation of Possible Neobavaisoflavone Chemosensitizing Properties towards Doxorubicin and Etoposide in SW1783 Anaplastic Astrocytoma Cells. Cells, 12(4), 593.
Publication 2023
4-nitrophenyl Astrocytoma, Anaplastic Benzene Biological Assay Catalysis Cells Cell Survival Colorimetry Doxorubicin Etoposide Homo sapiens Irinotecan Mitochondrial Inheritance Oxidoreductase

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More about "Astrocytoma, Anaplastic"

Astrocytoma, anaplastic is a high-grade, rapidly growing form of astrocytic tumor characterized by marked cellular pleomorphism, high mitotic activity, and areas of necrosis.
This aggressive malformation of astocyte cells can quickly spread throughout the central nervous system, making early detection and comprehensive treatment critical for managing this type of brain cancer.
Synonyms for astrocytoma, anaplastic include anaplastic astrocytoma, grade III astrocytoma, and malignant astrocytoma.
Related terms include glioblastoma, oligodendroglioma, and ependymoma, which are other types of glial cell tumors.
The abbreviation 'AA' is commonly used to refer to astrocytoma, anaplastic.
Key subtopics in astrocytoma, anaplastic research include tumor biology, genetic alterations, tumor microenvironment, treatment strategies (such as surgery, radiation, and chemotherapy), and disease prognosis.
Researchers may utilize cell culture models like U87MG cells, which are a commonly used glioblastoma cell line, as well as culture media like DMEM, Ham's F-12, and MOGGCCM to study this cancer.
Growth factors like EGF may be investigated for their role in tumor progression, while preservatives like RNAlater can be used to stabilize RNA from tissue samples.
Antibiotics like penicillin and streptomycin are often included in cell culture conditions to prevent microbial contamination.
By leveraging a wide range of research tools and techniques, scientists can gain deeper insights into the complex biology of astrocytoma, anaplastic and develop more effective treatments for this devastating form of brain cancer.