TY - JOUR
T1 - Accumulation of the oxidative base lesion 8-hydroxyguanine in DNA of tumor-prone mice defective in both the Myh and Ogg1 DNA glycosylases
AU - Russo, Maria Teresa
AU - De Luca, Gabriele
AU - Degan, Paolo
AU - Parlanti, Eleonora
AU - Dogliotti, Eugenia
AU - Barnes, Deborah E.
AU - Lindahl, Tomas
AU - Yang, Hanjing
AU - Miller, Jeffrey H.
AU - Bignami, Margherita
PY - 2004/7/1
Y1 - 2004/7/1
N2 - The OGG1 and MYH DNA glycosylases prevent the accumulation of DNA 8-hydroxyguanine. In Myh
-/- mice, there was no time-dependent accumulation of DNA 8-hydroxyguanine in brain, small intestine, lung, spleen, or kidney. Liver was an exception to this general pattern. Inactivation of both MYH and OGG1 caused an age-associated accumulation of DNA 8-hydroxyguanine in lung and small intestine. The effects of abrogated OGG1 and MYH on hepatic DNA 8-hydroxyguanine levels were additive. Because there is an increased incidence of lung and small intestine cancer in Myh
-/-/Ogg1
-/- mice, these findings support a causal role for unrepaired oxidized DNA bases in cancer development.
AB - The OGG1 and MYH DNA glycosylases prevent the accumulation of DNA 8-hydroxyguanine. In Myh
-/- mice, there was no time-dependent accumulation of DNA 8-hydroxyguanine in brain, small intestine, lung, spleen, or kidney. Liver was an exception to this general pattern. Inactivation of both MYH and OGG1 caused an age-associated accumulation of DNA 8-hydroxyguanine in lung and small intestine. The effects of abrogated OGG1 and MYH on hepatic DNA 8-hydroxyguanine levels were additive. Because there is an increased incidence of lung and small intestine cancer in Myh
-/-/Ogg1
-/- mice, these findings support a causal role for unrepaired oxidized DNA bases in cancer development.
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U2 - 10.1158/0008-5472.CAN-04-0355
DO - 10.1158/0008-5472.CAN-04-0355
M3 - Article
C2 - 15231648
AN - SCOPUS:3042739635
VL - 64
SP - 4411
EP - 4414
JO - Journal of Cancer Research
JF - Journal of Cancer Research
SN - 0008-5472
IS - 13
ER -