ArticleNeoplasia (New York, N.Y.)2018
Characterizing Microsatellite Instability and Chromosome Instability in Interval Colorectal Cancers.
Article in Neoplasia (New York, N.Y.), 2018. 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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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
17 citing papers in PubMed, 33 citations in OpenAlex.
- Targeting the cGAS-STING Pathway in Gastrointestinal Cancers: Modulating Tumor-associated Inflammation for Therapeutic Effect.Current drug targets · 2026Review
- Application of low-coverage whole-genome sequencing technology in risk stratification of colorectal adenomas.Frontiers in oncology · 2025Article
- Article
- Detecting colorectal cancer using genetic and epigenetic biomarkers: screening and diagnosis.Journal of medicine and life · 2024Review
- Molecular subtyping in colorectal cancer: A bridge to personalized therapy (Review).Oncology letters · 2023Review
- Transcriptomes of the tumor-adjacent normal tissues are more informative than tumors in predicting recurrence in colorectal cancer patients.Journal of translational medicine · 2023Article
- The Importance of Immunohistochemical Heterogeneous Expression of MMR Protein in Patients with Colorectal Cancer in Stage II and III of the Disease.Medicina (Kaunas, Lithuania) · 2023Article
- Mesothelioma Mouse Models with Mixed Genomic States of Chromosome and Microsatellite Instability.Cancers · 2022Article
- Most large colorectal polyps missed by gastroenterology fellows at colonoscopy are sessile serrated lesions.Endoscopy international open · 2022Article
- Molecular pathways in post-colonoscopy versus detected colorectal cancers: results from a nested case-control study.British journal of cancer · 2022Article
- Comprehensive characterization of PTEN mutational profile in a series of 34,129 colorectal cancers.Nature communications · 2022Article
- Aberrant SKP1 Expression: Diverse Mechanisms Impacting Genome and Chromosome Stability.Frontiers in cell and developmental biology · 2022Review
- Profiling diverse sequence tandem repeats in colorectal cancer reveals co-occurrence of microsatellite and chromosomal instability involving Chromosome 8.Genome medicine · 2021Article
- Microsatellite Instability in Colorectal Cancers: Carcinogenesis, Neo-Antigens, Immuno-Resistance and Emerging Therapies.Cancers · 2021Review
- Poly adenosine diphosphate-ribosylation, a promising target for colorectal cancer treatment.World journal of gastrointestinal oncology · 2021Review
- Review
- Evaluation of the effects of sequence length and microsatellite instability on single-guide RNA activity and specificity.International journal of biological sciences · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There are a substantial portion of colorectal cancers (CRCs), termed interval CRCs (I-CRCs), that are diagnosed shortly after a negative colonoscopy (i.e., no detectable polyps or CRC) and before recommended follow-up screening. The underlying cause(s) accounting for I-CRCs remain poorly understood, but may involve aberrant biology that drives genome instability. Genetic defects inducing genome instability are pathogenic events that lead to the development and progression of traditional sporadic (Sp-) CRCs. Classically, there are two genome instability pathways that give rise to virtually all Sp-CRCs, chromosome instability (CIN; ~85% of Sp-CRCs) and microsatellite instability (MSI; ~15% of Sp-CRCs); however, the contribution MSI and CIN have in I-CRCs is only beginning to emerge. To date, no study has simultaneously evaluated both MSI and CIN within an I-CRC cohort, and thus we sought to determine and compare the prevalence of MSI and/or CIN within population-based I-CRC and matched Sp-CRC cohorts. MSI status was established using a clinically validated, immunohistochemical approach that assessed the presence or absence of four proteins (MLH1, MSH2, MSH6 and PMS2) implicated in MSI. By combining the MSI results of the current study with those of our previous CIN study, we provide unprecedented insight into the prevalence of MSI and/or CIN between and within Sp- and I-CRCs. Our data show that MSI
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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.