ArticleOncotarget2015
Mutational profiling of colorectal cancers with microsatellite instability.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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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.
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
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Signal transduction pathway mutations in gastrointestinal (GI) cancers: a systematic review and meta-analysis.Scientific reports · 2020Pooled it
- Mutation enrichment in targeted panels flags immunotherapy-responsive POLE-driven hypermutated microsatellite-stable colorectal cancers.NPJ precision oncology · 2026Article
- TP53 mutation is associated with improved disease control in patients with advanced RAS wild-type colorectal adenocarcinoma treated with cetuximab and pembrolizumab.International journal of cancer · 2026Article
- Increased vulnerability of colorectal cancer models with high alkylation damage to NTHL1 inactivation.Scientific reports · 2026Article
- DNA polymerase epsilon-mutant colorectal cancers: Insights into non-exonuclease domain mutation variants, microsatellite instability status, and co-mutation profiles.World journal of gastroenterology · 2025Article
- Dipeptidase-1-knockout mice develop invasive tumors with features of microsatellite-unstable colorectal cancer.JCI insight · 2025Article
- The single-cell spatial landscape of stage III colorectal cancers.NPJ precision oncology · 2025Article
- From whole-slide image to biomarker prediction: end-to-end weakly supervised deep learning in computational pathology.Nature protocols · 2025Article
- Astilbin Induces Apoptosis in Oral Squamous Cell Carcinoma through p53 Reactivation and Mdm-2 Inhibition.Doklady. Biochemistry and biophysics · 2024Article
- Prognostic biomarkers for immunotherapy in esophageal cancer.Frontiers in immunology · 2024Review
- Microsatellite Instability: A Review of Molecular Epidemiology and Implications for Immune Checkpoint Inhibitor Therapy.Cancers · 2023Review
- Germline Variants in MLH1 and ATM Genes in a Young Patient with MSI-H in a Precancerous Colonic Lesion.International journal of molecular sciences · 2023Article
- Genomic landscape and survival analysis of ctDNA "neo-Frontiers in oncology · 2023Article
- Genomic signature of MTOR could be an immunogenicity marker in human colorectal cancer.BMC cancer · 2022Article
- Significance of rare variants in genes involved in the pathogenesis of Lynch syndrome.International journal of molecular medicine · 2022Article
- Concurrent loss of MLH1, PMS2 and MSH6 immunoexpression in digestive system cancers indicating a widespread dysregulation in DNA repair processes.Frontiers in oncology · 2022Article
- Article
- Distinct mutational profile and immune microenvironment in microsatellite-unstable andJournal for immunotherapy of cancer · 2021Article
- Characterization and clinical evaluation of microsatellite instability and loss of heterozygosity within tumor-related genes in colorectal cancer.BMC medical genomics · 2021Article
- Andrographolide Induces Apoptosis in Gastric Cancer Cells through Reactivation of p53 and Inhibition of Mdm-2.Doklady. Biochemistry and biophysics · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Microsatellite instability (MSI) is caused by defective mismatch repair in 15-20% of colorectal cancers (CRCs). Higher mutation loads in tumors with mismatch repair deficiency can predict response to pembrolizumab, an anti-programmed death 1 (PD-1) immune checkpoint inhibitor. We analyzed the mutations in 113 CRCs without MSI (MSS) and 29 CRCs with MSI-High (MSI-H) using the 50-gene AmpliSeq cancer panel. Overall, MSI-H CRCs showed significantly higher mutations than MSS CRCs, including insertion/deletion mutations at repeat regions. MSI-H CRCs showed higher incidences of mutations in the BRAF, PIK3CA, and PTEN genes as well as mutations in the receptor tyrosine kinase families. While the increased mutations in BRAF and PTEN in MSI-H CRCs are well accepted, we also support findings of mutations in the mTOR pathway and receptor tyrosine kinase family genes. MSS CRCs showed higher incidences of mutations in the APC, KRAS and TP53 genes, confirming previous findings. NGS assays may be designed to detect driver mutations for targeted therapeutics and to identify tumors with high mutation loads for potential treatment with immune checkpoint blockade therapies. Further studies may be warranted to elucidate potential targeted therapeutics against mutations in the mTOR pathway and the receptor tyrosine kinase family in MSI-H CRCs as well as the benefit of anti-PD-1 immunotherapy in hypermutated MSS CRCs or other cancers.
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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.