Nonetheless, published data were consistent with associations between: (a) the OGG1 S326C variant and increased risk of various types of cancer; (b) the XRCC1R194W variant and reduced risk of various types of cancer; and (c) the BRCA2 N372H variant and increased risk of breast cancer.
In the multivariate Cox model, XRCC1 expression was independently associated with cancer specific [p = 0.038] and progression free survival [p = 0.003].
Base excision repair (BER) genes (X-ray repair cross complementing 1, XRCC1 and human 8-oxoguanine DNA glycosylase 1, OGG1) may play a key role in maintaining genome integrity and preventing cancer development.
Hence, we performed a meta-analysis to investigate the association between cancer susceptibility and XRCC1Arg194Trp (59,227 cases and 81,587 controls from 201 studies) polymorphism in different inheritance models.
DNA repair genes is a key factor for cancer susceptibility, and we conducted a case-control study to investigate the association of XRCC1 codons 194 (Arg to Trp), 280 (Arg to His) and 399 (Arg to Gln) with risk of NSCLC.
These data, using the classic skin carcinogenesis model, provide new insight on the role of the XRCC1 399 polymorphism in neoplasia and may help explain the conflicting results relating this polymorphism to cancer risk at various sites.
The combination of variant alleles at codon 399 and in position -77 could affect XRCC1 protein activity, impairing genome integrity and promoting cancer occurrence.
XRCC1-directed personalization of immune checkpoint inhibitor therapy may be feasible and warrants further investigation in breast cancer.<i>Cancer </i>.
A large-scale multicenter study of cancer patients with a high number of radiosensitive individuals is needed to clarify the value of rare polymorphic microsatellite repeats in XRCC1 and XRCC3 as a biomarker of clinical radiosensitivity or increased cancer risk.
These polymorphic variants in the DNA repair pathway genes, such as XRCC1, have been associated with susceptibility of several types of cancer including thyroid cancer.
Recently, three coding polymorphisms in X-ray cross-complementing group 1 (XRCC1) DNA repair gene have been identified, and it is possible that these polymorphisms may affect DNA repair capacity and thus modulate cancer susceptibility.
BACKGROUND Various studies have highlighted the link between polymorphisms in the XRCC1 gene (encoding X-ray repair cross-complementing group 1) with the incidence of decreased DNA repair capacity and an increased predisposition to cancer.
We focused on X-ray repair cross-complementing group 1 (XRCC1), Xeroderma pigmentosum D (XPD) and apurinic/apyrimidinic endonuclease (APE1) as these are most extensively studied in cancer.
XRCC1 194Trp/Trp was strongly significantly associated with an increased risk of HCC cancer when compared with the wide-type genotype (OR=2.26, 95% CI=(1.23-5.38).
Moreover, our work also points out the importance of new studies for Arg399Gln association in some cancer types, such as glioma, gastric cancer, and oral cancer, where at least some of the covariates responsible for heterogeneity could be controlled, to obtain a more conclusive understanding about the function of the XRCC1Arg399Gln polymorphism in cancer development.
However, in stratified analyses based on cancer site, a significant association was found between the XRCC1Arg194Trp polymorphism and oral cancer under the allelic, heterozygote, and dominant models.
Concurrent effects of ABCB1 C3435T, ABCG2 C421A, and XRCC1Arg194Trp genetic polymorphisms with risk of cancer, clinical output, and response to treatment with imatinib mesylate in patients with chronic myeloid leukemia.
These results also indicated that a joint effect between PARP-1 Val762Ala and XRCC1Arg399Gln could be involved in the risk of cancer development (OR = 3.53, 95% CI = 1.30-9.59).