ArticleNucleic acids research2001
Suppression of gene amplification and chromosomal DNA integration by the DNA mismatch repair system.
Article in Nucleic acids research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
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- A Review of Research Progress in Multidrug-Resistance Mechanisms in Gastric Cancer.OncoTargets and therapy · 2020Review
- Induction/reversal of drug resistance in gastric cancer by non-coding RNAs (Review).International journal of oncology · 2019Review
- The emerging role of long non-coding RNAs in the drug resistance of colorectal cancer.International journal of clinical and experimental pathology · 2018Review
- Long non-coding RNAs in anti-cancer drug resistance.Oncotarget · 2017Review
- Met promotes the formation of double minute chromosomes induced by Sei-1 in NIH-3T3 murine fibroblasts.Oncotarget · 2016Article
- Downregulation of GSK3β by miR-544a to maintain self-renewal ability of lung caner stem cells.Oncology letters · 2014Article
- Methotrexate induces oxidative DNA damage and is selectively lethal to tumour cells with defects in the DNA mismatch repair gene MSH2.EMBO molecular medicine · 2009Article
- Human MutL-complexes monitor homologous recombination independently of mismatch repair.DNA repair · 2009Article
- Assessing metabolic stress and autophagy status in epithelial tumors.Methods in enzymology · 2009Article
- Autophagy suppresses tumor progression by limiting chromosomal instability.Genes & development · 2007Article
- Repression of mutagenesis by Rad51D-mediated homologous recombination.Nucleic acids research · 2006Article
- Illegitimate DNA integration in mammalian cells.Gene therapy · 2003Review
- Article
- High rate of CAD gene amplification in human cells deficient in MLH1 or MSH6.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mismatch repair (MMR)-deficient cells are shown to produce >15-fold more methotrexate-resistant colonies than MMR normal cells. The increased resistance to methotrexate is primarily due to gene amplification since all the resistant clones contain double-minute chromosomes and increased copy numbers of the DHFR gene. In addition, integration of linearized or retroviral DNAs into chromosomes is also significantly elevated in MMR-deficient cells. These results suggest that in addition to microsatellite instability and homeologous recombination, MMR is also involved in suppression of other genome instabilities such as gene amplification and chromosomal DNA integration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.