Regulación diferencial de la vía EGFR/PI3K/AKT/PTEN en gliomas de alto y bajo grado en pacientes colombianos

Alveiro, Erira; Penagos, José; Zubieta, Camilo; Velandia, Fernando; Arboleda, Humberto; Arboleda, Gonzalo

doi:10.1016/s0123-9015(13)70182-3

Cited by 1 publication

(1 citation statement)

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“…It has been reported that glioblastomas have defects in apoptotic pathways including Bcl-2 [140,141] , which is also a downstream target of the PI3K/Akt pathway [142] . Cancer cells are protected from apoptosis by the up-regulation of various anti-apoptotic molecules such as Bcl-2, which has been reported to be overexpressed in glioblastoma [143,144] . The inhibition of Bcl-2 significantly diminishes cell viability and induces apoptotic cell death in vitro.…”

Section: Pi3k/akt/mtormentioning

confidence: 99%

Growth factors and kinases in glioblastoma growth

Peña-Ortiz¹,

Germán-Castelán²,

González-Arenas³

2016

Adv Mod Oncol Res

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Glioblastoma multiforme (GBM) is the most aggressive type of brain cancer, having the highest invasion, migration, proliferation, and angiogenesis rates. Several signaling pathways are involved in the regulation of these processes including growth factors and their tyrosine kinase receptors, such as vascular endothelial growth factor (VEGF), transforming growth factor beta (TGFβ), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and insulin-like growth factor-I (IGF-I). Different kinases and regulators also participate in signaling pathways initiated by growth factors, such as mitogen-activated kinases (MAPK), protein kinases C (PKC), phosphatidylinositol-3 kinases (PI3K), protein kinase B (PKB or Akt), glycogen synthase kinase 3β (GSK3β), the mTOR complex, and Bcl-2. In this review, we will focus on the role of these proteins as possible therapeutic targets in GBM.

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