SciELO - Scientific Electronic Library Online

vol.26 número1Evaluación de la mutación A3243G del ADN mitocondrial en pacientes con diferentes subtipos de migrañaEpilepsia refractaria índice de autoresíndice de materiabúsqueda de artículos
Home Pagelista alfabética de revistas  

Servicios Personalizados




Links relacionados

  • En proceso de indezaciónCitado por Google
  • No hay articulos similaresSimilares en SciELO
  • En proceso de indezaciónSimilares en Google


Acta Neurológica Colombiana

versión impresa ISSN 0120-8748


CARDONA, Andrés Felipe et al. Genomic value of isocitrate-dehydrogenase (IDH1/2) in glioma origin and progression (ONCOLGroup). Acta Neurol Colomb. [online]. 2010, vol.26, n.1, pp.22-33. ISSN 0120-8748.

SUMMARY Heterozygous mutations in the gene encoding isocitrate dehydrogenase (IDH) occur in gliomas, but their mechanistic role in tumor development is unknown. Tumor-derived IDH mutations impair the enzyme's affinity for its substrate and dominantly inhibit wild-type IDH1 activity through the formation of catalytically inactive heterodimers. Forced expression of mutant IDH1 in cultured cells reduces formation of the enzyme product, α-ketoglutarate (α-KG), and increases the levels of hypoxia-inducible factor subunit 1 (HIF-1α, a transcription factor that facilitates tumor growth when oxygen is low and whose stability is regulated by α-KG. HIF-1α levels were higher in human gliomas harboring an IDH1 mutation than in tumors without a mutation, thus, IDH1/2 contributes to tumor progression in part through induction of the HIF-1 pathway. Numerous independent research groups had demonstrated the role of IDH mutations as a prognostic marker, especially for those patients with low grade gliomas and secondary glioblastomas with oligodendroglial pattern. This knowledge indicates great opportunities to improve diagnostic and therapeutic strategies for gliomas, which are not currently targeted at the specific molecular alterations. This paper presents a detailed review of the role of the IDH gene mutations in progression and manteinance of gliomas, and explores some therapeutic options directed against this environment.

Palabras clave : mutation; isocitrate dehydrogenase; hypoxia-inducible factor; glioma.

        · resumen en Español     · texto en Español     · Español ( pdf )