ArticleMolecular and cellular biology1995
An XPG DNA repair defect causing mutagen hypersensitivity in mouse leukemia L1210 cells.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 30 citations in OpenAlex.
- Xpg limits the expansion of haematopoietic stem and progenitor cells after ionising radiation.Nucleic acids research · 2016Article
- DNA-damage response gene polymorphisms and therapeutic outcomes in ovarian cancer.The pharmacogenomics journal · 2013Article
- Down-regulation of the nucleotide excision repair gene XPG as a new mechanism of drug resistance in human and murine cancer cells.Molecular cancer · 2010Article
- Nucleotide excision repair and cancer.Journal of molecular histology · 2006Review
- Preclinical perspectives on platinum resistance.Drugs · 2000Review
- Molecular cloning and structural analysis of the functional mouse genomic XPG gene.Mammalian genome : official journal of the International Mammalian Genome Society · 1996Article
- Combination effects of poly(ADP-ribose) polymerase inhibitors and DNA-damaging agents in ovarian tumor cell lines--with special reference to cisplatin.Journal of cancer research and clinical oncology · 1996Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the most widely used antitumor drugs is cis-diamminedichloroplatinum(II) (cisplatin), and mechanisms of cisplatin resistance have been investigated in numerous model systems. Many studies have used mouse leukemia L1210/0 as a reference wild-type cell line, and cisplatin-resistant subclones have been derived from it. Increased DNA excision repair capacity is thought to play a key role in the acquired cisplatin resistance, and this has influenced development of drugs for clinical trials. We report here that the L1210/0 line is in fact severely deficient in nucleotide excision repair of damaged DNA in vivo and in vitro. L1210/0 cell extracts could be complemented by extracts from repair-defective human xeroderma pigmentosum (XP) or rodent excision repair cross-complementing (ERCC) mutant cells, except for XPG/ERCC5 mutants. Purified XPG protein could restore repair proficiency to L1210/0 extracts. Expression of mouse XPG mRNA was similar in all L1210 lines studied, suggesting a point mutation or small alteration of XPG in L1210/0 cells. The DNA repair capacity of a cisplatin-resistant subline, L1210/DDP10, is similar to that of type culture collection L1210 cells and to those of other normal mammalian cell lines. Nucleotide excision repair of DNA is thus clearly important in the intrinsic cellular defense against cisplatin. However, in contrast to what is generally believed, enhancement of DNA repair above the normal level in these rodent cells does not appear to be a mechanism of acquired resistance to the drug.
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