Accumulation of the oxidative base lesion 8-hydroxyguanine in DNA of tumor-prone mice defective in both the Myh and Ogg1 DNA glycosylases

Maria Teresa Russo; Gabriele De Luca; Paolo Degan; Eleonora Parlanti; Eugenia Dogliotti; Deborah E. Barnes; Tomas Lindahl; Hanjing Yang; Jeffrey H. Miller; Margherita Bignami

doi:10.1158/0008-5472.CAN-04-0355

Accumulation of the oxidative base lesion 8-hydroxyguanine in DNA of tumor-prone mice defective in both the Myh and Ogg1 DNA glycosylases

Maria Teresa Russo, Gabriele De Luca, Paolo Degan, Eleonora Parlanti, Eugenia Dogliotti, Deborah E. Barnes, Tomas Lindahl, Hanjing Yang, Jeffrey H. Miller, Margherita Bignami

A.O.U. San Martino - IST, Istituto Nazionale Ricerca sul Cancro (GENOVA)

Research output: Contribution to journal › Article › peer-review

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	https://doi.org/10.1158/0008-5472.CAN-04-0355
Publication status	Published - Jul 1 2004

ASJC Scopus subject areas

Cancer Research
Oncology

Access to Document

10.1158/0008-5472.CAN-04-0355

Cite this

@article{138d482d7c3f4f3898d32d8b1a253e2b,

title = "Accumulation of the oxidative base lesion 8-hydroxyguanine in DNA of tumor-prone mice defective in both the Myh and Ogg1 DNA glycosylases",

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.",

author = "Russo, {Maria Teresa} and {De Luca}, Gabriele and Paolo Degan and Eleonora Parlanti and Eugenia Dogliotti and Barnes, {Deborah E.} and Tomas Lindahl and Hanjing Yang and Miller, {Jeffrey H.} and Margherita Bignami",

year = "2004",

month = jul,

day = "1",

doi = "10.1158/0008-5472.CAN-04-0355",

language = "English",

volume = "64",

pages = "4411--4414",

journal = "Journal of Cancer Research",

issn = "0008-5472",

publisher = "American Association for Cancer Research Inc.",

number = "13",

}

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

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 -

Accumulation of the oxidative base lesion 8-hydroxyguanine in DNA of tumor-prone mice defective in both the Myh and Ogg1 DNA glycosylases

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this