首页 » NTCC® SF7761 genomic DNA脑胶质瘤 SF7761细胞DNA标准品 BioVector NTCC质粒载体菌种细胞基因保藏中心

NTCC® SF7761 genomic DNA脑胶质瘤 SF7761细胞DNA标准品 BioVector NTCC质粒载体菌种细胞基因保藏中心

  • 价  格:¥98950
  • 货  号:SF7761 DNA
  • 产  地:北京
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NTCC®  SF7761 genomic DNA脑胶质瘤 SF7761细胞DNA标准品

NTCC® 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.
Overview 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.

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.
Background Information 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 (1).

A somatic mutation of histone H3.3 resulting in a lysine 27 to methionine substitution (H3.3K27M) occurs in 60% of DIPG (2). 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 (4). These epigenetic changes are thought to be important factors driving DIPG oncogenesis (2,3)

References
1. Schroeder KM et al. (2014) Pediatr. Res. 75(1-2): 205–209.

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