ArticleCarcinogenesis2006
Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6.
Article in Carcinogenesis, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed.
- Divergent accumulation patterns of SNVs and INDELs reveal negative selection in noncancerous cells.Innovation (Cambridge (Mass.)) · 2025Article
- Targeting DNA damage in ageing: towards supercharging DNA repair.Nature reviews. Drug discovery · 2025Review
- Advances in diagnostic and therapeutic applications of mismatch repair loss in cancer.DNA repair · 2025Review
- Efficient prime editing in two-cell mouse embryos using PEmbryo.Nature biotechnology · 2024Article
- Somatic mutations in aging and disease.GeroScience · 2024Review
- Homopolymer switches mediate adaptive mutability in mismatch repair-deficient colorectal cancer.Nature genetics · 2024Article
- PMS2 amplification contributes brain metastasis from lung cancer.Biological procedures online · 2024Article
- Negative Selection Allows DNA Mismatch Repair-Deficient Mouse FibroblastsbioRxiv : the preprint server for biology · 2024Article
- Dose-dependent reduction of somatic expansions but not Htt aggregates by di-valent siRNA-mediated silencing of MSH3 in HdhQ111 mice.Scientific reports · 2024Article
- Mitigating age-related somatic mutation burden.Trends in molecular medicine · 2023Review
- MutSα and MutSβ as size-dependent cellular determinants for prime editing in human embryonic stem cells.Molecular therapy. Nucleic acids · 2023Article
- A Human MSH6 Germline Variant Associated With Systemic Lupus Erythematosus Induces Lupus-like Disease in Mice.ACR open rheumatology · 2022Article
- Significance of rare variants in genes involved in the pathogenesis of Lynch syndrome.International journal of molecular medicine · 2022Article
- Spectrum of DNA mismatch repair failures viewed through the lens of cancer genomics and implications for therapy.Clinical science (London, England : 1979) · 2022Article
- Characteristic mutations induced in the small intestine of Msh2-knockout gpt delta mice.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2021Article
- Comprehensive Genomic Characterization of Fifteen Early-Onset Lynch-Like Syndrome Colorectal Cancers.Cancers · 2021Article
- The multifaceted roles of DNA repair and replication proteins in aging and obesity.DNA repair · 2021Review
- Variant profiling of colorectal adenomas from three patients of two families with MSH3-related adenomatous polyposis.PloS one · 2021Article
- A point mutation in the nuclease domain of MLH3 eliminates repeat expansions in a mouse stem cell model of the Fragile X-related disorders.Nucleic acids research · 2020Article
- Genetic instability as a driver for immune surveillance.Journal for immunotherapy of cancer · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Defects in genes associated with DNA mismatch repair (MMR) have been linked to hereditary colon cancer. Because the MMR pathway includes multiple factors with both overlapping and divergent functions, we sought to compare the impact of deficiencies in each of several MMR genes on genetic instability using a collection of knock-out mouse models. We investigated mutation frequencies and patterns in MMR-deficient mice using two transgenic reporter genes, supFG1 and cII, in the context of mice deficient for Pms2, Mlh1, Msh2, Msh3 or Msh6 or both Msh2 and Msh3 or both Msh3 and Msh6. We found that the mean mutation frequencies of all of the MMR-deficient mice were significantly higher than the mean mutation frequencies of wild-type mice. Mlh1-deficient mice and Msh2-deficient mice had the highest mutation frequencies in a comparison of the single nullizygous mice. Of all the mice studied, mice nullizygous for both Msh2 and Msh3 and those nullizygous for both Msh3 and Msh6 displayed the greatest overall increases in mutation frequencies compared with wild-type mice. Sequence analysis of the mutated reporter genes revealed significant differences between the individual groups of MMR-deficient mice. Taken together, our results further characterize the functions of the MMR factors in mutation avoidance and provide in vivo correlation to biochemical models of the MMR pathway.
Indexed as
Identifiers
What OpenQuestion holds
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.