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Insulin-mediated signaling promotes proliferation and survival of glioblastoma through Akt activation.

Gong Y, Ma Y, Sinyuk M, Loganathan S, Thompson RC, Sarkaria JN, Chen W, Lathia JD, Mobley BC, Clark SW, Wang J
Neuro Oncol. 2016 18 (1): 48-57

PMID: 26136493 · PMCID: PMC4677408 · DOI:10.1093/neuonc/nov096

Metabolic complications such as obesity, hyperglycemia, and type 2 diabetes are associated with poor outcomes in patients with glioblastoma. To control peritumoral edema, use of chronic high-dose steroids in glioblastoma patients is common, which can result in de novo diabetic symptoms. These metabolic complications may affect tumors via profound mechanisms, including activation of insulin receptor (InsR) and the related insulin-like growth factor 1 receptor (IGF1R) in malignant cells.

MeSH Terms (17)

Animals Antigens, CD Brain Neoplasms Cell Proliferation Cell Survival Female Glioblastoma Humans Insulin Insulin-Like Growth Factor I Insulin-Like Growth Factor II Mice, Nude Proto-Oncogene Proteins c-akt Receptor, Insulin Receptors, Somatomedin Signal Transduction Tumor Cells, Cultured

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