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Malignant Peripheral Nerve Sheath Tumor

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Most cited protocols related to «Malignant Peripheral Nerve Sheath Tumor»

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Publication 2013
Cell Nucleus Cells LacZ Genes Malignant Peripheral Nerve Sheath Tumor Mitosis Mus Neoplasms Ovum Implantation Skin Transplantation, Autologous
More detailed information is available as Supp Data. In brief; MTS and clonogenicity assays were performed as previously described (26 ). Western blot analyses were performed by standard methods (26 ). ELISA HGF and VEGF levels were measured in MPNST cell conditioned media using enzyme-linked immunosorbent assay (ELISA). The assays were constructed and preformed following manufacturer’s instructions (R&D, Minneapolis, MN). Migration and invasion assays were conducted using modified Boyden chambers as previously described (27 (link)). qRTPCR for MMP2 was conducted as previously described (28 (link)).MET gene sequencing procedure and primers as well as siRNA and shRNA transfection and transduction procedures are detailed in Supp data.
Publication 2011
Biological Assay Cells Culture Media, Conditioned Enzyme-Linked Immunosorbent Assay Genetic Engineering Malignant Peripheral Nerve Sheath Tumor MMP2 protein, human Oligonucleotide Primers RNA, Small Interfering Short Hairpin RNA Transfection Vascular Endothelial Growth Factors Western Blot
Human NF1-related MPNST cell-lines ST88-14, T265, and S462 and non-NF1 sporadic human MPNST cell-lines STS26T and MPNST724 were maintained and propagated as previously described (18 (link)). Primary cultured normal human Schwann cells served as controls. The NF1-associated cell-line MPNST642 was established by us (Supp data); DNA fingerprinting (STR; Supp data) was conducted for all cell-lines <6mo prior to the conduct of the studies, confirming that no cross contamination has occurred. STS26T and MPNST724 cells were stably transfected to express GFP-LC3; over-expressing cells were FACS-sorted on the basis of GFP expression. HDAC inhibitors included PCI-24781 (Pharmacyclics, Sunnyvale, CA), suberoylanilide hydroxamic acid (SAHA) and MS-275 (Cayman Chemical, Ann Arbor, MI). Bafilomycin and chloroquine were obtained from Sigma (St Louis, MO). Commercially available antibodies were used for immunoblot or immunohistochemical detection of: acetylated H3, acetylated H4 (Millipore, Billerica, MA); acetylated tubulin (Sigma); caspase 3, LC3B (Cell Signaling, Danvers, MA); GFP, beclin, p53, actin (Santa Cruz, Santa Cruz, CA); IRGM, PARP (Abcam, Cambridge, MA); Ki-67 (MIB-1), vim (Dako, Carpenteria, CA); and S-100 (Biogenex, San Ramon, CA).
Publication 2010
Actins Antibodies Caimans Caspase 3 Cell Lines Cells Chloroquine Cultured Cells Histone Deacetylase Inhibitor Homo sapiens Immunoblotting Ki-67 Antigen Malignant Peripheral Nerve Sheath Tumor MS 27-275 PCI 24781 S100 Proteins Tubulin Vorinostat
Seven NTRK3-rearranged soft tissue spindle cell tumors other than classic IFS were retrieved from the consultation files of two of the authors (C.R.A., C.D.F.). The case selection for molecular investigation was based on the initial reported observations that the morphologic spectrum of kinase fusion-positive sarcomas includes tumors resembling fibrosarcomas (FSs) or MPNSTs. A large collection of these various morphologies was available in our consultation files from prior molecular studies, which were previously screened and lacked abnormalities in NTRK1/2, BRAF, and RAF1 genes.1 (link),3 (link) Clinical data, including age, gender, anatomic site, and gross features of tumors were retrieved from pathology reports. All tumors had been surgically removed and hematoxylin and eosin-stained slides from resection specimens were reviewed by two of us (A.S., C.R.A.). Tumors were graded according to the FNCLCC grading system. IHC for CD34, S100, SOX10, pan-TRK (TRK-ABC), and H3K27me3 was performed according to standardized procedures on automated platforms. Staining was performed on a Leica-Bond-3 (Leica, Buffalo Grove, Illinois) or a Ventana Benchmark (Ventana Medical Systems, Tucson, Arizona) automated immunostaining platform using a heat-based antigen retrieval method and high pH buffer.
Publication 2019
Antigens Body Regions BRAF protein, human Buffaloes Buffers Cells Congenital Abnormality Eosin Fibrosarcoma Genes Hematoxylin Malignant Peripheral Nerve Sheath Tumor Neoplasms Operative Surgical Procedures Phosphotransferases Raf1 protein, human S100 Proteins Sarcoma Soft Tissue Neoplasms SOX10 Transcription Factor
Ben-Men-1 benign meningioma cells have been described (15 (link)). Malignant meningioma KT21-MG1 and IOMM-Lee cells (8 (link),9 (link)) were kindly provided by Dr. Anita Lal, University of California, San Francisco. HE1-1 is an adenovirus E1-transformed human embryonic kidney cell line (unpublished), and HMS-97 is a human malignant schwannoma cell line (26 (link)). All cell lines and primary human meningeal cells (ScienCell) were grown in Dulbecco’s modified eagle medium with 10% fetal bovine serum (Invitrogen). AR-42 and AR-12 were supplied by Arno Therapeutics and formulated into rodent chow (Research Diets) to deliver about 25mg/kg/day and 100mg/kg/day, respectively (21 (link)–23 (link)). Also, AR-42 was dissolved in dimethylsulfoxide (DMSO) for in vitro experiments.
Publication 2012
Adenovirus Vaccine AR-12 compound Benign Meningioma Cell Line, Transformed Cell Lines Cells Diet Eagle Embryo Fetal Bovine Serum HDAC-42 Homo sapiens Kidney Malignant Meningioma Malignant Peripheral Nerve Sheath Tumor Meninges Multiple Endocrine Neoplasia Type 1 Rodent Sulfoxide, Dimethyl Therapeutics

Most recents protocols related to «Malignant Peripheral Nerve Sheath Tumor»

All investigations involving human subjects were performed after approval by an institutional review board and in accordance with the principles of ethical research guidelines described in the U.S. Common Rule. Informed written consent was obtained from each subject. The Dana-Farber Cancer Institute Institutional Review Board (IRB) determined that this research met the criteria for exemption from IRB review and was categorized as Secondary Use research.
The GeM Consortium is composed of investigators from academic centers and hospitals (“member sites”) with eligible subjects and existing tissue banking protocols with consent for biospecimen and clinical data collection; genetic testing, including but not limited to whole-genome/exome sequencing; sharing of specimens/data with outside institutions, researchers, etc. The GeM coordinating center at Boston Children's Hospital (BCH) coordinated sharing of retrospectively collected specimens from existing tumor banks and pathology archives at member sites to perform molecular characterization of MPNST and related tumors.
All specimens and data were stripped of Protected Health Information using the Safe Harbor Method and coded. The prefix of each tumor sample ID included in the final cohort in Fig. 1 (n = 95) is an abbreviation of the member site that contributed the required specimens for analysis: Royal National Orthopaedic Hospital at University College, London (“ROY,” n = 43), Moffitt Cancer Center, Tampa (“MOF,” n = 12), Mount Sinai Hospital, Toronto (“TOR,” n = 9), Massachusetts General Hospital, Boston (“MGH,” n = 8), Washington University School of Medicine, St. Louis (“WUS,” n = 6), Nagoya University, Nagoya (“NAG,” n = 4), Boston Children's Hospital/Dana-Farber Cancer Institute, Boston (“BCH,” n = 3), New York University Langone Medical Center, New York (“NYU,” n = 3), Huntsman Cancer Institute at University of Utah, Salt Lake City (“HCI,” n = 1), Lifespan Laboratories, Rhode Island Hospital, Providence (“LIF,” n = 1).
The coordinating center at BCH received coded material from the following types of biospecimens: MPNSTs (both sporadic and NF1-related); precursor and other lesions, such as benign, atypical, and PN; metastatic and local recurrence neurofibroma; related specimens such as peripheral blood or tissue for germline comparison, and normal nerve where available. Subjects with tumors that were unrelated to MPNST or neurofibroma and subjects with specimens of insufficient quality and/or quality for pathology interpretation were excluded from this study.
Comprehensive clinical and pathology report data for each participant were collected by the international MPNST Registry at Washington University School of Medicine (WUSM). Data include demographic information, disease course, tumor size/anatomic location, histologic/immuno-histochemical characteristics, diagnostic imaging, surgical procedures, systemic treatment information, neoadjuvant therapy, toxicity, clinical outcomes, and survival.
Publication 2023
Blood Disease Progression Ethics Committees, Research Exome Genome Germ Line Malignant Neoplasms Malignant Peripheral Nerve Sheath Tumor Neoadjuvant Therapy Neoplasms Neoplasms by Site Nervousness Neurofibroma Operative Surgical Procedures Recurrence Sodium Chloride, Dietary Specimen Collection Tissues
FFPE tissue blocks were collected for each fresh-frozen tumor which underwent multiomic profiling and were used for pathology review, IHC (MYF-4, H3K7me3, S100, and Sox10) and additional molecular characterization [i.e., ploidy assay and multiregional whole-exome sequencing (WES)]. FFPE H&E slides from available blocks were reviewed by a pathologist to identify the block most representative (i.e., morphologically similar) to the frozen material which underwent multiomic profiling. These H&E sections were digitally scanned (40×) at each pathology hub by the Deep Lens Biomedical Imaging Team and uploaded to the VIPER digital pathology platform (Deep Lens, Inc.). Multiregional 500× exome sequencing was performed on 5 samples each from 36 FFPE NF1-related MPNST specimens to assess intratumor heterogeneity.
Publication 2023
Biological Assay Fingers Freezing Genetic Heterogeneity Lens, Crystalline Malignant Peripheral Nerve Sheath Tumor MYOG protein, human Neoplasms Pathologists S100 Proteins SOX10 Transcription Factor Tissues
Survival analysis was performed using the Cox proportional-hazards model as implemented in the R package survival (version 2.30; ref. 93 ). Significance was assessed by the likelihood ratio test using a cutoff for a statistical significance of 0.05. We considered only MPNSTs with conventional histology for survival analysis. The proportional-hazards assumption was tested using the cox.zph function from the R package survival (93 ).
Publication 2023
Malignant Peripheral Nerve Sheath Tumor
Distinct KrasG12D and KrasG12DSetd2–/– mouse lung tumors were dissected and minced into pieces in Trizol (Thermo Fisher Scientific). The minced tumor tissues were then put in Lysing Matrix D tubes (MP Biomedicals) in Trizol and homogenized by FastPrep-24 homogenizer (MP Biomedicals). Total RNA was extracted and cleaned up using RNeasy Mini Kit (Qiagen). Library preparation and sequencing were performed by the Integrated Genomics Operation Core Facility at MSKCC. After RiboGreen quantification and quality control of Agilent BioAnalyzer, 6–15 ng of total RNA underwent amplification (12 cycles) using the SMART-Seq V4 (Clontech) ultra low–input RNA kit for sequencing. In total, 10 ng of amplified cDNA was used to prepare Illumina HiSeq libraries with the Kapa DNA library preparation chemistry (Kapa Biosystems) using 8 cycles of PCR. Samples were barcoded and run on a HiSeq 4,000 in a 50 bp/50 bp paired end run, using the TruSeq SBS Kit v3 (Illumina). On average, 60 million paired reads were generated per sample, and the percentage of mRNA bases was 73% on average. Raw reads were trimmed and filtered for quality using Trimmomatic (53 (link)). Processed reads were then aligned against the mm10 version of the mouse genome using STAR (60 (link)). For each RefSeq annotated gene, reads overlapping with exon regions were counted using HTSeq (61 (link)). Gene-level differential expression analysis was conducted using DESeq2 (62 (link)).
Differentially expressed genes detected by RNA-Seq (FDR < 0.05) were subjected to GSEA using the JAVA GSEA 3.0 program (63 (link)). The gene sets from the Molecular Signature Database (MSigDB) — including c2 (curated gene sets), c5 (GO gene sets), and c6 (oncogenic signatures gene sets) — were used for the analysis. The composite PRC2 signature was generated by merging the published PRC2 modules in liver cancer (20 (link)), MPNST (21 (link)), hESCs (25 (link)), hematopoietic stem cells (26 (link)), and neural progenitor cells (27 (link)). The KRAS signature was generated by merging the gene sets from MSigDB, including KRAS.600_UP.V1_UP, KRAS.600.LUNG.BREAST_UP.V1_UP, KRAS.BREAST_UP.V1_UP, KRAS.LUNG_UP.V1_UP, and KRAS.KIDNEY_UP.V1_UP. The PTEN_DN_UP signature was generated by merging PTEN_DN.V1_UP and PTEN_DN.V2_UP data sets from MSigDB.
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Publication 2023
Breast Cancer of Liver DNA, Complementary DNA Library Exons Gene Expression Profiling Genes Genome Human Embryonic Stem Cells K-ras Genes Kidney Lung Lung Neoplasms Malignant Peripheral Nerve Sheath Tumor Mus Neoplasms Neural Stem Cells Oncogenes Polycomb Repressive Complex 2 PTEN protein, human RNA, Messenger RNA-Seq Stem Cells, Hematopoietic Tissues trizol
All surgeries were performed by the multidisciplinary team for soft tissue sarcoma at Zhongshan Hospital Affiliated to Fudan University. Well differentiated liposarcoma and low-grade dedifferentiated liposarcoma are mainly local recurrences, so we implement a more aggressive surgical strategy (even if the surrounding organs of the tumor are not violated by the naked eye, they will be resected together); for high-grade dedifferentiated liposarcoma, If it is evaluated that there is the invasion of surrounding organs, complete radical resection should be attempted, and combined organ resection should also be performed; leiomyosarcoma often presents as a tumor with clear borders, and if the surrounding organs invade the adjacent units of the tumor, it should be preserved; for pleomorphic undifferentiated sarcoma, malignant peripheral nerve sheath tumor, and solitary fibrous tumor, complete resection with negative margins is enough.
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Publication 2023
Leiomyosarcoma Liposarcoma, Dedifferentiated Malignant Peripheral Nerve Sheath Tumor Neoplasms Operative Surgical Procedures Recurrence Sarcoma Surgical Margins Tumor, Solitary Fibrous Well Differentiated Liposarcoma

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More about "Malignant Peripheral Nerve Sheath Tumor"

Malignant Peripheral Nerve Sheath Tumor (MPNST) is a rare and aggressive type of soft tissue sarcoma that arises from the cells that surround peripheral nerves.
This complex condition, also known as neurofibrosarcoma or malignant schwannoma, is a subtype of peripheral nerve sheath tumors.
MPNST can occur sporadically or in individuals with neurofibromatosis type 1 (NF1), a genetic disorder characterized by the development of benign tumors called neurofibromas.
Patients with NF1 have an increased risk of developing MPNST, which can be a devastating complication of their disease.
The pathogenesis of MPNST is not fully understood, but it is believed to involve the loss of tumor suppressor genes, such as NF1 and TP53, which can lead to uncontrolled cell growth and tumor formation.
MPNST typically presents as a painless, rapidly growing mass, often in the extremities or trunk.
Diagnosis of MPNST often involves a combination of imaging studies, such as magnetic resonance imaging (MRI) and positron emission tomography (PET) scans, as well as biopsy to confirm the diagnosis.
Treatment typically involves a multimodal approach, including surgical resection, radiation therapy, and chemotherapy, depending on the stage and location of the tumor.
Researchers are actively investigating new treatment strategies for MPNST, including the use of targeted therapies, immunotherapy, and combination approaches.
Ongoing studies are exploring the use of agents like penicillin/streptomycin, SNF96.2, FBS, DMEM, Lipofectamine 2000, SNF02.2, Polybrene, CellTiter 96® AQueous One Solution Cell Proliferation Assay, Forskolin, and Puromycin in various experimental models and clinical trials.
By leveraging the latest research and data-driven insights from platforms like PubCompare.ai, researchers and clinicians can optimize their approach to understanding and managing this complex and challenging disease, ultimately improving outcomes for patients with Malignant Peripheral Nerve Sheath Tumor.