Previous studies have reported that the Asp1104His polymorphism in Xeroderma Pigmentosum complementation group G (XPG) was associated with the susceptibility to colorectal cancer (CRC), although the results were inconsistent.
These results suggest that the XPG-TFIIH complex is involved in transcription elongation and that defects in this association may partly account for Cockayne syndrome in XP-G/CS patients.
The Xeroderma pigmentosum complementation group G (XPG) rs2296147T>C polymorphism is suspected to associate with the clinical outcomes of cancer patients.However, the results are inconsistent.
The control mice, in which one-half of Xpg genomic DNA fragment was replaced with a normal Xpg cDNA fragment, had a normal growth rate, a normal life span, normal sensitivity to UV light, and normal DNA repair ability, indicating that the Xpg gene partially replaced with the normal cDNA fragment retained normal functions.
The xeroderma pigmentosum group G (XPG or ERCC5) and group F (XPF or ERCC4) play an important role in DNA repair, and produce dual incision 3' and 5' to the damaged nucleotide fragment.
We hypothesize that genetic polymorphisms in DNA repair gene XPA (xeroderma pigmentosum group A) and XPG (xeroderma pigmentosum group G) (ERCC5, excision repair cross-complementation group 5), which result in inter-individual differences in DNA repair efficiency, may predict clinical response to platinum agents in advanced non-small cell lung cancer (NSCLC) patients.
XPG (CC) combined with XPA (TC/CC) genotypes showed an independent role for TTP (relative risk, RR = 6.38; p = 0.0001) and survival (RR = 34; p = 0.0005).
Microinjection of ERCC5 cDNA specifically restored the defect of xeroderma pigmentosum group G cells (XP-G) as measured by unscheduled DNA synthesis, and XP-G cells stably transformed with ERCC5 cDNA showed nearly normal UV resistance.
These findings suggest that genetic variation in XPG/ERCC5 may not affect the risk of SCCHN, although rs4150351 C variant genotypes were associated with an increased expression of XPG/ERCC5 mRNA and nonsignificantly decreased risk of SCCHN.
DNA was extracted from blood samples and 15 common nonsynonymous SNPs in seven-nucleotide excision repair genes [XPC, RAD23B (hHR23B), CSB (ERCC6), XPD (ERCC2), CCNH, XPF (ERCC4), and XPG (ERCC5)] were genotyped.
We found that in vivo knock down of Xeroderma pigmentosum, complementation group G (Xpg) causes elevation of HSC numbers after IR treatment, while numbers of haematopoietic progenitors are elevated to a lesser extent.
Excision repair cross-complementing 1 (ERCC1), Xeroderma pigmentosum group G (XPG), and breast cancer 1 (BRCA1) are involved in DNA damage repair, whereas ribonucleotide reductase M1 (RRM1) is implicated in DNA synthesis.
We conducted a perspective study to investigate whether the expression of excision repair cross-complementing 1 (ERCC1), xeroderma pigmentosum group G (XPG), breast cancer 1 (BRCA1), and ribonucleotide reductase M1 (RRM1) is correlated with clinical outcome of non-small cell lung cancer (NSCLC).
The xeroderma pigmentosum group G (XPG or ERCC5) and group F (XPF or ERCC4) play an important role in DNA repair, and produce dual incision 3' and 5' to the damaged nucleotide fragment.
We applied our newly CRISPR/Cas9 generated human <i>XPF</i> knockout cell line with complete loss of XPF and primary fibroblasts from an XP-G patient (XP20BE) to analyze until now uncharacterized spontaneous mRNA splice variants of these two endonucleases.
Excision repair cross-complementing 1 (ERCC1), Xeroderma pigmentosum group G (XPG), and breast cancer 1 (BRCA1) are involved in DNA damage repair, whereas ribonucleotide reductase M1 (RRM1) is implicated in DNA synthesis.
These results suggest that the XPG-TFIIH complex is involved in transcription elongation and that defects in this association may partly account for Cockayne syndrome in XP-G/CS patients.
Similar differences were observed in overall survival, with median survival not reached for patients with low BRCA1, regardless of XPG levels, or for patients with intermediate/high BRCA1 and high XPG.