Oxidative Stress in Cancer-Prone Genetic Diseases in Pediatric Age: The Role of Mitochondrial Dysfunction.
Serafina PerroneFederica LottiUrsula GeronziElisa GuidoniMariangela LonginiGiuseppe BuonocorePublished in: Oxidative medicine and cellular longevity (2016)
Oxidative stress is a distinctive sign in several genetic disorders characterized by cancer predisposition, such as Ataxia-Telangiectasia, Fanconi Anemia, Down syndrome, progeroid syndromes, Beckwith-Wiedemann syndrome, and Costello syndrome. Recent literature unveiled new molecular mechanisms linking oxidative stress to the pathogenesis of these conditions, with particular regard to mitochondrial dysfunction. Since mitochondria are one of the major sites of ROS production as well as one of the major targets of their action, this dysfunction is thought to be the cause of the prooxidant status. Deeper insight of the pathogenesis of the syndromes raises the possibility to identify new possible therapeutic targets. In particular, the use of mitochondrial-targeted agents seems to be an appropriate clinical strategy in order to improve the quality of life and the life span of the patients.
Keyphrases
- oxidative stress
- dna damage
- papillary thyroid
- end stage renal disease
- diabetic rats
- ischemia reperfusion injury
- chronic kidney disease
- induced apoptosis
- squamous cell
- cell death
- ejection fraction
- systematic review
- newly diagnosed
- reactive oxygen species
- prognostic factors
- case report
- peritoneal dialysis
- lymph node metastasis
- early onset
- squamous cell carcinoma
- copy number
- cancer therapy
- patient reported outcomes
- heat shock
- drug delivery
- signaling pathway
- young adults
- patient reported