ArticlePloS one2013
An inducible, isogenic cancer cell line system for targeting the state of mismatch repair deficiency.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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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
8 citing papers in PubMed, 13 citations in OpenAlex.
- Cancer models in preclinical research: A chronicle review of advancement in effective cancer research.Animal models and experimental medicine · 2021Review
- Werner Syndrome Helicase Is Required for the Survival of Cancer Cells with Microsatellite Instability.iScience · 2019Article
- A Family of Rhodium Complexes with Selective Toxicity toward Mismatch Repair-Deficient Cancers.Journal of the American Chemical Society · 2018Article
- Selective tumor cell death induced by irradiated riboflavin through recognizing DNA G-T mismatch.Nucleic acids research · 2017Article
- Rhodium metalloinsertor binding generates a lesion with selective cytotoxicity for mismatch repair-deficient cells.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Targeting DNA Mismatches with Rhodium Metalloinsertors.Inorganica chimica acta · 2016Article
- miR-15b regulates cisplatin resistance and metastasis by targeting PEBP4 in human lung adenocarcinoma cells.Cancer gene therapy · 2015Article
- Targeted Chemotherapy with Metal Complexes.Comments on modern chemistry. Part A, Comments on inorganic chemistry : a journal of critical discussion of the current literature · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The DNA mismatch repair system (MMR) maintains genome stability through recognition and repair of single-base mismatches and small insertion-deletion loops. Inactivation of the MMR pathway causes microsatellite instability and the accumulation of genomic mutations that can cause or contribute to cancer. In fact, 10-20% of certain solid and hematologic cancers are MMR-deficient. MMR-deficient cancers do not respond to some standard of care chemotherapeutics because of presumed increased tolerance of DNA damage, highlighting the need for novel therapeutic drugs. Toward this goal, we generated isogenic cancer cell lines for direct comparison of MMR-proficient and MMR-deficient cells. We engineered NCI-H23 lung adenocarcinoma cells to contain a doxycycline-inducible shRNA designed to suppress the expression of the mismatch repair gene MLH1, and compared single cell subclones that were uninduced (MLH1-proficient) versus induced for the MLH1 shRNA (MLH1-deficient). Here we present the characterization of these MMR-inducible cell lines and validate a novel class of rhodium metalloinsertor compounds that differentially inhibit the proliferation of MMR-deficient cancer cells.
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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.