DNA damage, aging, and cancer.

By Jan H. J. Hoeijmakers. New England Journal of Medicine, 2009

2,173 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/9ddf07f630e9c0df3616442a81f4de6b8adfcb46

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Citations in the corpus

The DNA Damage Response: Making it safe to play with knives (2010, background): “Instead, deficiency of NER factors in the XP syndrome is known to greatly increase the risk of skin cancer andmelanoma because of defective repair of UV lesions in skin cells following sun exposure (Hoeijmakers, 2009).”
The Oxygen Rich Postnatal Environment Induces Cardiomyocyte Cell Cycle Arrest Through DNA Damage Response (2014, neutral): “…and Heyman, 1974) and can cause cellular toxicity by promoting damage of proteins, nucleic acids, lipids, or DNA, such as oxidized base, single- or double-strand breaks, resulting in cell-cycle arrest, apoptosis, or cellular senescence (Hoeijmakers, 2009; Marnett et al., 2003; Moos et al., 2000).”
The DNA damage response and cancer therapy (2012, background): “For example, the ultraviolet component of sunlight can cause up to 1 × 10 5 DNA lesions per cell per da”
HBV cccDNA: viral persistence reservoir and key obstacle for a cure of chronic hepatitis B (2015, background): “96 Hence, all cells are equipped with a sophisticated DNA repair machinery whose >250 components serve to detect DNA damage, signal to halt the cell cycle and allow time for repair, and ﬁ x the damage; in metazoans, failed repair will usually induce apoptosis (or else may result in cancerous cells).”
The hallmarks of aging. (2013, background): “…in DNA repair mechanisms cause accelerated aging in mice and underlie several human progeroid syndromes, such asWerner syndrome, Bloom syndrome, xeroderma pigmentosum, trichothiodystrophy, Cockayne syndrome, and Seckel syndrome (Gregg et al., 2012; Hoeijmakers, 2009; Murga et al., 2009).”
The NAD+/sirtuin pathway modulates longevity through activation of mitochondrial UPR and FOXO signaling (2013, neutral): “DISCUSSION The progressive functional decline that happens during the normal aging process is associated with the accumulation of mutations in DNA (Hoeijmakers, 2009) and changes in metabolic rate and mitochondrial function (Houtkooper et al.”
Defective Mitophagy in XPA via PARP1 Hyperactivation and NAD+/SIRT1 Reduction (2014, background): “Accumulation of nuclear DNA damage has been associated with accelerated aging disorders and normal aging; however, theconnectionbetweenDNAdamageandneurodegeneration is less clear (Hoeijmakers, 2009; Rass et al., 2007).”
UV Radiation and the Skin (2013, neutral): “UV-induced photolesions in every skin cell [133].”
Stereospecific PARP trapping by BMN 673 and comparison with olaparib and rucaparib (2013, background): “A large number of SSBs are generated endogenously as well as BER intermediates (12, 13).”