SCC126M
SF7761 Human DIPG H3.3-K27M Cell Line
Human
Synonyme(s) :
Diffuse intrinsic pontine glioma cells
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A propos de cet article
UNSPSC Code:
41106514
NACRES:
NA.81
eCl@ss:
32011203
Biological source:
human
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Laissez-nous vous aiderNom du produit
SF7761 Human DIPG H3.3-K27M Cell Line, SF7761 pediatric diffuse intrinsic pontine glioma (DIPG) cell line harbors the histone H3.3 Lys 27-to-methionine (K27M) mutation and can support research and drug development efforts targeting DIPG.
biological source
human
technique(s)
cell culture | mammalian: suitable
Quality Level
General description
Diffuse intrinsic pontine gliomas (DIPG) are highly aggressive and difficult to treat tumors arising in the ventral pons of the brain stem. Despite therapeutic advances, DIPG is incurable and most patients, primarily children, die within 2 years of diagnosis. DIPG is one of the leading causes of death in children with brain tumors .
A somatic mutation of histone H3.3 resulting in a lysine 27 to methionine substitution (H3.3K27M) occurs in 60% of DIPG . In H3.3K27M DIPG patient samples, levels of H3K27 dimethylation (H3K27me2) and trimethylation (H3K27me3) are reduced globally. Expression of H3.3K27M was also shown to be associated with increased levels of H3K27 acetylation (H3K27ac) and recruitment of bromodomain proteins at sites of active transcription . These epigenetic changes are thought to be important factors driving DIPG oncogenesis
A somatic mutation of histone H3.3 resulting in a lysine 27 to methionine substitution (H3.3K27M) occurs in 60% of DIPG . In H3.3K27M DIPG patient samples, levels of H3K27 dimethylation (H3K27me2) and trimethylation (H3K27me3) are reduced globally. Expression of H3.3K27M was also shown to be associated with increased levels of H3K27 acetylation (H3K27ac) and recruitment of bromodomain proteins at sites of active transcription . These epigenetic changes are thought to be important factors driving DIPG oncogenesis
SF7761 is a human glioma cell line derived by surgical biopsy from a young female H3.3K27M DIPG patient (5). The tumor cells were immortalized with hTERT (human telomerase ribonucleoprotein reverse transcriptase) using retroviral transduction. SF7761 cells are tumorigenic in athymic rodents with the tumor cells recapitulating the infiltrative growth of human brainstem gliomas (5, 6).
IMPORTANT NOTE: SF7761 are grown as neurospheres in suspension culture. Neurospheres are to be passaged using gentle mechanical trituration when they reach diameters of 200-500 um or through enzymatic dissociation.
IMPORTANT NOTE: SF7761 are grown as neurospheres in suspension culture. Neurospheres are to be passaged using gentle mechanical trituration when they reach diameters of 200-500 um or through enzymatic dissociation.
Application
Research Category
Cancer
Oncology
Cancer
Oncology
Subject to local law, this product is intended to be sold for internal in vitro research use only subject to terms and conditions found here: www.sigmaaldrich.com/restrictedcelluse. This product may not be: re-engineered or copied; used to make derivatives, modifications or functional equivalents; used to obtain patents or other IP claiming use of the product; used to develop, test, or manufacturer a commercial product; used as a component in a commercial product; resold or licensed; used in any clinical applications or trials; or used in humans. A license or limited commercial use agreement is required for use by any for-profit entity, use in services, and use in sponsored academic research. For information regarding any such use, please contact licensing@milliporesigma.com.
Biochem/physiol Actions
Cancer Cells
Preparation Note
Store in liquid nitrogen. The cells can be cultured for at least 10 passages after initial thawing without significantly affecting the cell marker expression and functionality.
Analysis Note
• Each vial contains ≥ 200 viable neurospheres.
• Cells are tested negative for HPV-16, HPV-18, Hepatitis A, C, Herpesvirus type 6, 7, 8 and HIV-1 & 2 viruses by PCR.
• Cells are negative for mycoplasma contamination.
• Each lot of cells is genotyped by STR analysis to verify the unique identity of the cell line.
• Cells are tested negative for HPV-16, HPV-18, Hepatitis A, C, Herpesvirus type 6, 7, 8 and HIV-1 & 2 viruses by PCR.
• Cells are negative for mycoplasma contamination.
• Each lot of cells is genotyped by STR analysis to verify the unique identity of the cell line.
Classe de stockage
12 - Non Combustible Liquids
wgk
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificats d'analyse (COA)
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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.
Kui-Ming Chan et al.
Genes & development, 27(9), 985-990 (2013-04-23)
Recent studies have identified a Lys 27-to-methionine (K27M) mutation at one allele of H3F3A, one of the two genes encoding histone H3 variant H3.3, in 60% of high-grade pediatric glioma cases. The median survival of this group of patients after
Kristin M Schroeder et al.
Pediatric research, 75(1-2), 205-209 (2013-11-07)
Diffuse intrinsic pontine glioma (DIPG) is a high-grade glioma that originates in the pons and is seen exclusively in children. Despite numerous efforts to improve treatment, DIPG remains incurable with 90% of children dying within 2 y of diagnosis, making
Rintaro Hashizume et al.
Journal of neuro-oncology, 110(3), 305-313 (2012-09-18)
Diffuse intrinsic pontine gliomas arise almost exclusively in children, and despite advances in treatment, the majority of patients die within 2 years after initial diagnosis. Because of their infiltrative nature and anatomic location in an eloquent area of the brain
Therapeutic targeting of polycomb and BET bromodomain proteins in diffuse intrinsic pontine gliomas.
Andrea Piunti et al.
Nature medicine, 23(4), 493-500 (2017-03-07)
Diffuse intrinsic pontine glioma (DIPG) is a highly aggressive pediatric brainstem tumor characterized by rapid and uniform patient demise. A heterozygous point mutation of histone H3 occurs in more than 80% of these tumors and results in a lysine-to-methionine substitution
Rintaro Hashizume et al.
Nature medicine, 20(12), 1394-1396 (2014-11-18)
Pediatric brainstem gliomas often harbor oncogenic K27M mutation of histone H3.3. Here we show that GSKJ4 pharmacologic inhibition of K27 demethylase JMJD3 increases cellular H3K27 methylation in K27M tumor cells and demonstrate potent antitumor activity both in vitro against K27M
Contenu apparenté
Numéro d'article de commerce international
| Référence | GTIN |
|---|---|
| SCC126 | 04054839354779 |
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