ArticleThe Journal of clinical investigation1996
Competency in mismatch repair prohibits clonal expansion of cancer cells treated with N-methyl-N'-nitro-N-nitrosoguanidine.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
53 citing papers in PubMed, 145 citations in OpenAlex.
- Evaluation of Mutation Risk Using Patient-Derived Organoids in Patients With Lynch Syndrome.International journal of cancer · 2026Article
- Inflammation Drives Phosphorylation and Acetylation of MutS Homolog 3 and Interaction with Cytosolic HDAC6.Journal of Cancer · 2026Article
- Serendipity Strikes: How Pursuing Novel Hypotheses Shifted the Paradigm Regarding the Genetic Basis of Colorectal Cancer and Changed Cancer Therapy.Digestive diseases and sciences · 2023Article
- Review article: Lynch Syndrome-a mechanistic and clinical management update.Alimentary pharmacology & therapeutics · 2022Review
- Aspirin and the chemoprevention of cancers: A mathematical and evolutionary dynamics perspective.Wiley interdisciplinary reviews. Systems biology and medicine · 2020Review
- Immunological Features with DNA Microsatellite Alterations in Patients with Colorectal Cancer.Journal of cancer immunology · 2020Article
- Tetranucleotide Microsatellite Mutational Behavior Assessed in Real Time: Implications for Future Microsatellite Panels.Cellular and molecular gastroenterology and hepatology · 2020Article
- New methods to assess 6-thiopurine toxicity and expanding its therapeutic application to pancreatic cancerMedChemComm · 2019Article
- Exploiting DNA repair defects in colorectal cancer.Molecular oncology · 2019Review
- Efforts in redesigning the antileukemic drug 6-thiopurine: decreasing toxic side effects while maintaining efficacy.MedChemComm · 2019Article
- Recent progress in Lynch syndrome and other familial colorectal cancer syndromes.CA: a cancer journal for clinicians · 2018Review
- Methylation and expression of mismatch repair gene human mutS homolog 2 in myelodysplastic syndromes.Experimental and therapeutic medicine · 2018Article
- The colorectal cancer immune microenvironment and approach to immunotherapies.Future oncology (London, England) · 2017Review
- Human MLH1 suppresses the insertion of telomeric sequences at intra-chromosomal sites in telomerase-expressing cells.Nucleic acids research · 2017Article
- Role of Deficient Mismatch Repair in the Personalized Management of Colorectal Cancer.International journal of environmental research and public health · 2016Review
- GRG Profiles: John M. Carethers.Digestive diseases and sciences · 2016Article
- HEREDITARY, SPORADIC AND METASTATIC COLORECTAL CANCER ARE COMMONLY DRIVEN BY SPECIFIC SPECTRUMS OF DEFECTIVE DNA MISMATCH REPAIR COMPONENTS.Transactions of the American Clinical and Climatological Association · 2016Article
- A monofunctional platinum complex coordinated to a rhodium metalloinsertor selectively binds mismatched DNA in the minor groove.Inorganic chemistry · 2015Article
- Lynch syndrome and Lynch syndrome mimics: The growing complex landscape of hereditary colon cancer.World journal of gastroenterology · 2015Review
- An unusual ligand coordination gives rise to a new family of rhodium metalloinsertors with improved selectivity and potency.Journal of the American Chemical Society · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The phenomenon of alkylation tolerance has been observed in cells that are deficient in some component of the DNA mismatch repair (MMR) system. An alkylation-induced cell cycle arrest had been reported previously in one MMR-proficient cell line, whereas a MMR-defective clone derived from this line escapes from this arrest. We examined human cancer cell lines to determine if the cell cycle arrest were dependent upon the MMR system. Growth characteristics and cell cycle analysis after MNNG treatment were ascertained in seven MMR-deficient and proficient cell lines, with and without confirmed mutations in hMLH1 or hMSH2 by an in vitro transcription/translation assay. MMR-proficient cells underwent growth arrest in the G2 phase of the cell cycle after the first S phase, whereas MMR-deficient cells escaped an initial G2 delay and resumed a normal growth pattern. In the HCT116 line corrected for defective MMR by chromosome 3 transfer, the G2 phase arrest lasted more than five days. In another MMR-proficient colon cancer cell line, SW480, cell death occurred five days after MNNG treatment. A competent MMR system appears to be necessary for G2 arrest or cell death after alkylation damage, and this cell cycle checkpoint may allow the cell to repair damaged DNA, or prevent the replication of mutated DNA by prohibiting clonal expansion.
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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.