ArticlePloS one2011
Loss of DNA mismatch repair imparts a selective advantage in planarian adult stem cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Evaluation of Mutation Risk Using Patient-Derived Organoids in Patients With Lynch Syndrome.International journal of cancer · 2026Article
- Evolutionary origin of germline pathogenic variants in human DNA mismatch repair genes.Human genomics · 2024Article
- Loss of mismatch repair promotes a direct selective advantage in human stem cells.Stem cell reports · 2022Article
- Ethanol-induced formation of colorectal tumours and precursors in a mouse model of Lynch syndrome.The Journal of pathology · 2021Article
- Neoblast-enriched zinc finger protein FIR1 triggers local proliferation during planarian regeneration.Protein & cell · 2019Article
- A carcinogenic trigger to study the function of tumor suppressor genes inDisease models & mechanisms · 2018Article
- Protein expression profiling in head fragments during planarian regeneration after amputation.Development genes and evolution · 2015Article
- Curcumin chemosensitizes 5-fluorouracil resistant MMR-deficient human colon cancer cells in high density cultures.PloS one · 2014Article
- Determining the functional significance of mismatch repair gene missense variants using biochemical and cellular assays.Hereditary cancer in clinical practice · 2012Article
- Transcriptome analysis reveals strain-specific and conserved stemness genes in Schmidtea mediterranea.PloS one · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lynch syndrome (LS) leads to an increased risk of early-onset colorectal and other types of cancer and is caused by germline mutations in DNA mismatch repair (MMR) genes. Loss of MMR function results in a mutator phenotype that likely underlies its role in tumorigenesis. However, loss of MMR also results in the elimination of a DNA damage-induced checkpoint/apoptosis activation barrier that may allow damaged cells to grow unchecked. A fundamental question is whether loss of MMR provides pre-cancerous stem cells an immediate selective advantage in addition to establishing a mutator phenotype. To test this hypothesis in an in vivo system, we utilized the planarian Schmidtea mediterranea which contains a significant population of identifiable adult stem cells. We identified a planarian homolog of human MSH2, a MMR gene which is mutated in 38% of LS cases. The planarian Smed-msh2 is expressed in stem cells and some progeny. We depleted Smed-msh2 mRNA levels by RNA-interference and found a striking survival advantage in these animals treated with a cytotoxic DNA alkylating agent compared to control animals. We demonstrated that this tolerance to DNA damage is due to the survival of mitotically active, MMR-deficient stem cells. Our results suggest that loss of MMR provides an in vivo survival advantage to the stem cell population in the presence of DNA damage that may have implications for tumorigenesis.
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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.