Excision repair cross-complementing factor 1 gene expression is a molecular marker associated with platinum based chemotherapy sensitivity.

A DNA excision repair protein.

ERCC-1 is a protein that in humans is encoded by the ERCC1 gene.

It is DNA excision repair protein.

ERCC1 forms the ERCC1-XPF enzyme complex that participates in DNA repair and DNA recombination.

The ERCC1-XPF nuclease also functions in pathways to repair double-strand breaks in DNA, and in the repair of crosslink damage that harmfully links the two DNA strands.

Cells with disabling mutations in ERCC1 are more sensitive than normal to particular DNA damaging agents, including ultraviolet (UV) radiation and to chemicals that cause crosslinking between DNA strands.

No human individuals have been found with complete (homozygous) deletion of ERCC1

Rare individuals harbor inherited mutations that impair the function of ERCC1.

ERCC1 was the first human DNA repair gene to be isolated by molecular cloning.

The human ERCC1 gene encodes the ERCC1 protein of 297 amino acids

ERCC1-XPF does not cut DNA that is exclusively single-stranded or double-stranded, but it cleaves the DNA phosphodiester backbone specifically at junctions between double-stranded and single-stranded DNA.

The ERCC1–XPF nuclease incises the damaged DNA strand.

The ERCC1 protein interacts with the XPA protein to coordinate DNA and protein binding.

Cells with mutant ERCC1–XPF are moderately more sensitive than normal cells to agents that cause double-stranded breaks in DNA.

Cells carrying mutations in ERCC1 or XPF are especially sensitive to agents that cause DNA interstrand crosslinks.

Interstrand crosslinks block the progression of DNA replication.

Cerebro-oculo-facio-skeletal syndrome is caused by ERCC1 mutations that cause cerebro-oculo-facio-skeletal syndrome.

Cerebro-oculo-facio-skeletal syndrome (COFS syndrome) is a rare recessive disorder in which affected individuals undergo rapid neurologic decline and indications of accelerated aging.

One mechanism of resistance to platinum chemotherapy drugs correlates with high ERCC1 activity.

Nucleotide excision repair is the primary DNA repair mechanism that removes the therapeutic platinum-DNA adducts from the tumor DNA.

ERCC1 activity levels, being an important part of the nucleotide excision repair common final pathway, as seen in patients with gastric, ovarian, colorectal and bladder cancers.

Surgically removed Non-small cell lung carcinoma (NSCLC) tumors that receive no further therapy have a better survival if ERCC1-positive than if ERCC1-negative.

Thus ERCC1 positivity is a favorable prognostic marker.

ERCC1-positive NSCLC tumors do not benefit from adjuvant platinum chemotherapy.

ERCC1-negative NSCLC tumors, prognostically worse without treatment, derive substantial benefit from adjuvant cisplatin-based chemotherapy.

High ERCC1 is thus a negative predictive marker, ref2242ing to how it will respond to a specific type of treatment.

ERCC1 protein expression is reduced or absent in 84% to 100% of colorectal cancers.

The promoter of ERCC1 is methylated in 38% of gliomas, resulting in reduced mRNA and protein expression.

Reduction of protein expression of ERCC1 in 84% to 100% of colon cancers indicates that reduced ERCC1 is one of the most frequent reductions of a DNA repair gene observed in a cancer.

Deficiency in ERCC1 protein expression appears to be an early event in colon carcinogenesis.

ERCC1 was found to be deficient in 40% of the crypts within 10 cm on each side of colonic adenocarcinomas.

There is a low level of protein expression of ERCC1 in 84% to 100% of sporadic colon cancers.

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