Our results suggest that XPD G751A, hOGG1C326G and XRCC4 G1394T gene polymorphisms might play an important role in colorectal carcinogenesis and increase the risk of developing CRC in the Chinese Han population.
Mth1/Ogg1-double knockout mice increased GO accumulation in the genome, but exhibited little susceptibility to spontaneous tumorigenesis, thus revealing that accumulation of GO in cellular genomes induces MUTYH-dependent cell death.
The present study was aimed to explore whether the hOGG1 gene variants play an important role in the carcinogenesis of epithelial ovarian cancer (EOC).
In addition, we show that loss of TSC2 in kidney tumor of Eker rat is associated with loss of OGG1 and accumulation significant levels of oxidative DNA damage 8-oxo-deoxyguanine suggesting that TSC2 and OGG1 play a major role in renal tumorigenesis.
The authors found that the ERCC2 Asp312Asn AA, MSH2 IVS1 + 9G > C CC, OGG1 Ser326Cys GG and CG + GG, and OGG1 748-15C > G GG and CG + GG genotypes were significantly associated with an increased risk of GB carcinogenesis (odds ratio [OR], 2.1, 1.8, 2.5, 1.8, 2.0, and 1.6, respectively).
Damage to DNA may lead to carcinogenesis but is repaired through activation of pathways involving polymorphic enzymes, including human 8-oxoguanine glycosylase 1 (OGG1).
Loss of heterozygosity at the 8-oxoG-DNA glycosylase (OGG1) allele is found in human kidney clear cell carcinoma identifying loss of OGG1 function as a possible contributor to tumorigenesis in the kidney.
Enhancement of lung carcinogenesis initiated with 4-(N-hydroxymethylnitrosamino)-1-(3-pyridyl)-1-butanone by Ogg1 gene deficiency in female, but not male, mice.
Damage to DNA may lead to carcinogenesis but is repaired through activation of pathways involving polymorphic enzymes, including human 8-oxoguanine glycosylase 1 (hOGG1), X-ray repair cross-complementing 1 (XRCC1), and xeroderma pigmentosum group D (XPD).
The DNA damage repair genes, mutY and mutM, prevent G to T mutations caused by reactive oxygen species in Escherichia coli, but it has remained debatable whether deficiencies in their mammalian counterparts, Myh and Ogg1, are directly involved in tumorigenesis.
We herein review that MTH1, MUTYH and OGG1 play important roles in mammalian cells avoiding an accumulation of oxidative DNA damage, both in the nuclear and mitochondrial genomes, thereby suppressing carcinogenesis and cell death.
To test the involvement of hOGG1 mutation in colon carcinogenesis, we analysed the genetic changes of hOGG1 and the activity of oh8Gua glycosylase in 15 paired normal and tumorous colon specimens.
Repair activities of some mutated and polymorphic OGG1 proteins are lower than those of wild-type OGG1-type la-Ser326 protein and, thus, could be involved in human carcinogenesis.
The frequent allelic imbalance and suppression of the hOGG1 gene thus imply that repair for oxidative DNA damages may be relevant in future studies on head and neck squamous carcinogenesis.