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FRANCESCO CAPPELLO

Cancer as a “Mitochondriopathy”.

  • Autori: Czarnecka, A.; MARINO GAMMAZZA, A.; DI FELICE, V.; Zummo, G.; Cappello, F.
  • Anno di pubblicazione: 2007
  • Tipologia: Articolo in rivista (Articolo in rivista)
  • Parole Chiave: mtDNA, mitochondria, cancer, prohibitin, homoplasmy

Abstract

Mitochondria are subcellular organelles, whose well-known function is to produce adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS). Alterations in respiratory activity and mtDNA appear to be a general feature of malignant cells. The presence of mtDNA mutations has been reported in various cancer cells, and the abundance of mtDNA damage is consistent with the intrinsic susceptibility to constitutive oxidative stress. Research about the functional aspects of mtDNA mutations in cancer development and therapeutic response is likely to be fruitful and to have significant clinical and prognostic impact. Although many studies to date have been focused on the identification and characterization of altered mtDNA, it is not clear if these accumulated mutations are the cause or the consequence of the carcinogenic process. This article provides a brief summary of our current understanding of mitochondrial pathobiology in cancer development

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