Brain Tumor Dissociation Kit

Brain Tumor Dissociation Kit

The Brain Tumor Dissociation Kit (P) has been developed specifically for the gentle and effective tissue dissociation of human and mouse brain tumors, such as glioblastoma multiforme or medulloblastoma. Since tumor tissue can be sticky, it is recommended to use the kit in combination with the gentleMACS™ Dissociator or the gentleMACS Octo Dissociator. In less than an hour, the tissue dissociation procedure efficiently yields high numbers of viable cells. Dissociated cells are immediately ready for further applications, such as cell culture, flow cytometry, molecular applications, or for cell isolation using MACS
®
Technology.

Background information

The quality of starting material is important for any experiment, and a perfect single-cell suspension is a prerequisite for many downstream applications. Glioblastoma, neuroblastoma, medulloblastoma, xenograft brain tumor samples can be effectively dissociated into single-cell suspensions using the Brain Tumor Dissociation Kit (P) and a gentleMACS™ Dissociator.
The Brain Tumor Dissociation Kit (P) is based on papain. The antigens GLAST (ACSA-1) and PSA-NCAM used to identify some neural populations are sensitive to papain. Immune cell epitopes are also sensitive to papain. If preservation of these antigen epitopes is required for downstream applications, it is more suitable to use in this case the Tumor Dissociation Kit, mouse (# 130-096-730) or Tumor Dissociation Kit, human (# 130-095-929) depending on the species from where the tumor originated.
  • Selected references

    1. Környei et al. (2007) Astroglia-derived retinoic acid is a key factor in glia-induced neurogenesis. FASEB J. 21: 2496-2509
    2. Santagata, S. et al. et al. (2014) Intraoperative mass spectrometry mapping of an onco-metabolite to guide brain tumor surgery. Proc. Natl. Acad. Sci. U.S.A. 111: 11121-11126
    3. Skog, J. et al. (2008) Glioblastoma microvesicles transport RNA and proteins that promote tumour growth and provide diagnostic biomarkers. Nat. Cell Biol. 10(12): 1470-1476
    4. Kijima, N. et al. (2012) CD166/activated leukocyte cell adhesion molecule is expressed on glioblastoma progenitor cells and involved in the regulation of tumor cell invasion. Neuro-oncology 14: 1254-1264
    5. Janiszewska, M. et al. (2012) Imp2 controls oxidative phosphorylation and is crucial for preserving glioblastoma cancer stem cells. Genes Dev. 26: 1926-1944
    6. Piao, Y. et al. (2012) Glioblastoma resistance to anti-VEGF therapy is associated with myeloid cell infiltration, stem cell accumulation, and a mesenchymal phenotype. Neuro-oncology 14: 1379-1392
    7. Golebiewska, A. et al. (2013) Side population in human glioblastoma is non-tumorigenic and characterizes brain endothelial cells. Brain 136: 1462-1475
    8. Piao, Y. et al. (2013) Acquired resistance to anti-VEGF therapy in glioblastoma is associated with a mesenchymal transition. Clin. Cancer Res. 19: 4392-4403
    9. Zeiner, P. S. et al. (2014) MIF receptor CD74 is restricted to microglia/macrophages, associated with a M1-polarized immune milieu and prolonged patient survival in gliomas. Brain Pathol. 25: 491-504
  • Selected references

  • Brochures and posters

  • Scientific posters

Product options: 1
for 25
preparations
EUR 240.00

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