Astrocytoma Drug Discovery Service

Creative Biolabs has accumulated years of experience and global resources in the field of neuroscience. We provide one-stop solutions with advanced technologies and cutting-edge platforms, which enable researchers to shed light on the pathogenesis of astrocytoma and therefore explore novel therapeutic strategies for astrocytoma and other gliomas.

Astrocytoma is a common primary brain tumor that arises from astrocytes, which belongs to the type of glioma. There is a genetic susceptibility to astrocytoma development. Genetic diseases such as Turcot syndrome, p53 mutations, and neurofibromatosis type 1 (NF1) increase the risk of the onset of astrocytoma. In addition, being exposed to ionizing radiation enhances the risk of central nervous system malignancy. Current clinical interventions for astrocytoma are combined with tumor resection, radiotherapy, and chemotherapy. However, present therapeutic methods seem to be less effective to improve the survival of patients. Creative Biolabs has established an advanced brain tumor platform to accelerate research from mechanisms to preclinical studies.

Mechanism of Action Studies of Astrocytoma

Astrocytoma is intimately associated with genetic mutations, including mutations of isocitrate dehydrogenase (IDH1), ATRX, BRAF, TP53, and NOTCH genes (Killela, 2014). Astrocytoma is characterized by an increase in vascularity, which is induced by hypoxia as well as vascular endothelial growth factor (VEGF) and EGF. EGF is also involved in downstream signaling transduction including the phosphatidylinositol-3-kinase/RhoA/C (PI3K/RhoA/C) pathway and the mitogen-activated protein kinase/extracellular regulated kinase (MAPK/ERK) pathway. Besides, neuron glial antigen 2 (NG2)/chondroitin sulphate proteoglycan 4 (CSPG4) protein is involved in the extracellular regulation of the neuronal network, while signal-regulated kinases 1 and 2 (ERK1/2) and protein kinase C-alpha (PKCα) are intracellular regulators responsible for cell proliferation, survival, migration, invasion, cytoskeletal reorganization as well as chemo-resistance. In addition, astrocytoma may use neurotransmitters, such as acetylcholine, as autocrine signaling molecules to enhance tumor growth.

Fig.1 Schematic diagram detailing the currently identified aberrations in the MAPK pathway genes thought to be responsible for the development of pilocytic astrocytomas. (Penman, 2015)

Astrocytoma Solutions at Creative Biolabs

Besides traditional clinical interventions for astrocytoma combined with tumor resection, radiotherapy, and chemotherapy, Creative Biolabs is committed to assisting in the development of emerging therapeutic strategies for astrocytoma.

• Peptides as anticancer agents
• Peptides promote the reduction of tumor growth.
• Peptides act as molecular carriers promoting drug translocation across the blood-brain barrier to target glioma-specific receptors in the brain.
• Promising molecular targets: namely CXXR4, EGFR, AKT, VEGFR-2, MEK/ERK, integrins, MDGI, tenascin-C, neuropilin-1, etc.
• Immunotherapy
• NG2/CSPG4 as a promising tumor-associated antigen for antibody-based immunotherapy in patients with malignant astrocytoma.
• Prion protein (PrP^C)-targeting therapeutic
• PrP^C contributes to the multipotency, invasiveness, and tumorigenicity of cancer stem cells.
• Inhibition of cell growth and induce programmed cell death processes
• Proteasome inhibitors.
• Antineoplastic antibiotics.
• Protein translation inhibitor.

Creative Biolabs provides one-stop solutions for astrocytoma studies. A variety of in vitro, in vivo, and ex vivo services with stable astrocytoma cell cultures, brain slices, and animal models are available. We also offer reliable development and discovery services for astrocytoma research and development with advanced technologies and research platforms. The information about our platform for astrocytoma translational research and integrated research is below.

To learn more details about preclinical glioblastoma drug discovery solutions, please don't hesitate to contact us.

References

1. Killela, P. J.; et al. The genetic landscape of anaplastic astrocytoma. Oncotarget. 2014, 5(6): 1452.
2. Penman, C. L.; et al. Current understanding of BRAF alterations in diagnosis, prognosis, and therapeutic targeting in pediatric low-grade gliomas. Frontiers in oncology. 2015, 5: 54.