Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 4411-4414 |
| Number of pages | 4 |
| Journal | Cancer Research |
| Volume | 64 |
| Issue number | 13 |
| DOIs | |
| Publication status | Published - Jul 1 2004 |
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ASJC Scopus subject areas
- Cancer Research
- Oncology
Cite this
Accumulation of the oxidative base lesion 8-hydroxyguanine in DNA of tumor-prone mice defective in both the Myh and Ogg1 DNA glycosylases. / Russo, Maria Teresa; De Luca, Gabriele; Degan, Paolo; Parlanti, Eleonora; Dogliotti, Eugenia; Barnes, Deborah E.; Lindahl, Tomas; Yang, Hanjing; Miller, Jeffrey H.; Bignami, Margherita.
In: Cancer Research, Vol. 64, No. 13, 01.07.2004, p. 4411-4414.Research output: Contribution to journal › Article
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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.
UR - http://www.scopus.com/inward/record.url?scp=3042739635&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3042739635&partnerID=8YFLogxK
U2 - 10.1158/0008-5472.CAN-04-0355
DO - 10.1158/0008-5472.CAN-04-0355
M3 - Article
VL - 64
SP - 4411
EP - 4414
JO - Journal of Cancer Research
JF - Journal of Cancer Research
SN - 0008-5472
IS - 13
ER -