Increased mRNA expression levels of ERCC1, OGG1 and RAI in colorectal adenomas and carcinomas

We have examined mRNA expression of two DNA repair genes, ERCC1 and OGG1 as well as the putative apoptosis controlling gene RAI, in normal tissues and lesions from 36 cases with adenomas (mild/moderat n = 21 and severe n = 15, dysplasia) and 9 with carcinomas.Comparing expression levels of ERCC1, OGG1 and RAI between normal tissue and all lesions combined yielded higher expression levels in lesions, 3.3-fold higher (P = 0.005), 5.6-fold higher(P < 3·10-5) and 7.7-fold higher (P = 0.0005), respectively. The levels of ERCC1, OGG1 and RAI expressions when comparing lesions, did not differ between adenomas and CRC cases, P = 0.836, P = 0.341 and P = 0.909, respectively. When comparing expression levels in normal tissue, the levels for OGG1 and RAI from CRC cases were significantly lower compared to the cases with adenomas, P = 0.012 and P = 0.011, respectively.Our results suggest that increased expression of defense genes is an early event in the progression of colorectal adenomas to carcinomas.Most colorectal cancers (CRC) develop through multiple mutations in the normal colonic mucosa, and evolve through the adenoma-carcinoma sequence [1,2]. Various endogenous and exogenous agents from environmental exposures are constantly damaging DNA, and in combination with low DNA repair capacity this have been interpreted as increasing the likelihood of cancer development [3-7].The range of different DNA lesions is broad and there are different repair pathways depending on the nature of the damage. Nucleotide excision repair (NER) will repair bulky adducts [8] while base excision repair (BER) is responsible for the repair of base damage and single strand breaks [9]. Only a few studies have to our knowledge studied DNA repair expression of nucleotide excision repair (NER) and base excision repair (BER) genes in CRC. Even less is known about the level and significance of DNA repair expression during the formation of adenomas and the transition period in the adenoma-carcinoma seque