About: DNA repair: Exploiting the Fanconi anemia parhway as a potential therapeutic target     Goto   Sponge   NotDistinct   Permalink

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  • DNA repair is an active cellular process to respond to constant DNA damage caused by metabolic processes and environmental factors. Since the outcome of DNA damage is generally adverse and long term effects may contribute to oncogenesis, cells have developed a variety of DNA repair mechanisms, which operate depending on the type of DNA damage inflicted. At least 15 Fanconi anemia (FA) proteins interact in a common pathway involved in homologous recombination. Inherited homozygous mutations in any of these FA genes cause a rare disease, Fanconi anemia, characterized by congenital abnormalities, progressive bone-marrow failure and cancer susceptibility. Heterozygous germline FA mutations predispose to various types of cancer. In addition, somatic FA mutations have been identified in diverse cancer types. Evidence exists that cells deficient in the FA pathway become dependent on alternative pathways for survival. Additional inhibition of such alternative pathways is thus expected to result in cell death, creating a relationship of synthetic lethality. Identifying these relationships can reveal yet unknown mechanisms of DNA repair and new targets for therapy.
  • DNA repair is an active cellular process to respond to constant DNA damage caused by metabolic processes and environmental factors. Since the outcome of DNA damage is generally adverse and long term effects may contribute to oncogenesis, cells have developed a variety of DNA repair mechanisms, which operate depending on the type of DNA damage inflicted. At least 15 Fanconi anemia (FA) proteins interact in a common pathway involved in homologous recombination. Inherited homozygous mutations in any of these FA genes cause a rare disease, Fanconi anemia, characterized by congenital abnormalities, progressive bone-marrow failure and cancer susceptibility. Heterozygous germline FA mutations predispose to various types of cancer. In addition, somatic FA mutations have been identified in diverse cancer types. Evidence exists that cells deficient in the FA pathway become dependent on alternative pathways for survival. Additional inhibition of such alternative pathways is thus expected to result in cell death, creating a relationship of synthetic lethality. Identifying these relationships can reveal yet unknown mechanisms of DNA repair and new targets for therapy. (en)
Title
  • DNA repair: Exploiting the Fanconi anemia parhway as a potential therapeutic target
  • DNA repair: Exploiting the Fanconi anemia parhway as a potential therapeutic target (en)
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  • DNA repair: Exploiting the Fanconi anemia parhway as a potential therapeutic target
  • DNA repair: Exploiting the Fanconi anemia parhway as a potential therapeutic target (en)
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  • RIV/00023001:_____/11:00002465!RIV13-AV0-00023001
http://linked.open...avai/riv/aktivita
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  • P(KJB502030901)
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  • 3
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  • 195101
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  • RIV/00023001:_____/11:00002465
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  • DNA damage, DNA repair, Fanconi anemia, Synthetic lethality Targeted therapy (en)
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  • CZ - Česká republika
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  • [E5D6D478DCCB]
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  • Physiological research
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  • 60
http://linked.open...iv/tvurceVysledku
  • Gallmeier, E.
  • Hucl, Tomáš
http://linked.open...ain/vavai/riv/wos
  • 000293138600006
issn
  • 0862-8408
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