ArticlePloS one2011
Inhibition of cell proliferation by an anti-EGFR aptamer.
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 93 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
93 citing papers in PubMed, 199 citations in OpenAlex.
- Molecular Engineering of Aptamers for Glioblastoma Therapy: From Simple Antagonists to AI-Driven Approaches, a Narrative Review.International journal of molecular sciences · 2026Review
- Innovative aptamer approaches in glial tumor diagnostics and therapy: Progress and future directions.Molecular therapy. Nucleic acids · 2025Review
- Comprehensive advances in HER2-positive and HER2-negative breast cancer: unveiling molecular mechanisms and exploring cutting-edge targeted therapies for enhanced patient outcomes.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Plasmonic Nanosensors for EGFR Detection: Optimizing Aptamer-Based Competitive Displacement Assays.Biosensors · 2025Article
- Real-Time Kinetics of Internalization of Anti-EGFR DNA Aptamers and Aptamer Constructs into Cells Derived from Glioblastoma Patients as Indicated by Doxorubicin.International journal of molecular sciences · 2025Article
- Aptamer-based applications in delivering cancer gene therapies and beyond: state of the art and the missing links to clinical translation.Advanced drug delivery reviews · 2025Review
- Surface Functionalization of Nanocarriers with Anti-EGFR Ligands for Cancer Active Targeting.Nanomaterials (Basel, Switzerland) · 2025Review
- Anti-EGFR aptamer exhibits direct anti-cancer effects in NSCLC cells harboring EGFR L858R mutations.NPJ precision oncology · 2024Article
- Towards Aptamer-Targeted Drug Delivery to Brain Tumors: The Synthesis of Ramified Conjugates of an EGFR-Specific Aptamer with MMAE on a Cathepsin B-Cleavable Linker.Pharmaceutics · 2024Article
- Reversible Aptamer Staining, Sorting, and Cleaning of Cells (Clean FACS) with Antidote Oligonucleotide or Nuclease Yields Fully Responsive Cells.Nucleic acid therapeutics · 2024Article
- MultiplexedNucleic acid therapeutics · 2024Article
- Targeting lung cancer with clinically relevant EGFR mutations using anti-EGFR RNA aptamer.Molecular therapy. Nucleic acids · 2023Article
- Selection of optimised ligands by fluorescence-activated bead sorting.Chemical science · 2023Article
- Development and classification of RNA aptamers for therapeutic purposes: an updated review with emphasis on cancer.Molecular and cellular biochemistry · 2023Review
- DNA-Based Nanomaterials as Drug Delivery Platforms for Increasing the Effect of Drugs in Tumors.Cancers · 2023Review
- Bioimaging Nucleic-Acid Aptamers with Different Specificities in Human Glioblastoma Tissues Highlights Tumoral Heterogeneity.Pharmaceutics · 2022Article
- EGFR-Targeted Photodynamic Therapy.Pharmaceutics · 2022Review
- Recent advances in aptamer-based targeted drug delivery systems for cancer therapy.Frontiers in bioengineering and biotechnology · 2022Review
- Aptamer nucleotide analog drug conjugates in the targeting therapy of cancers.Frontiers in cell and developmental biology · 2022Review
- Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Aptamers continue to receive interest as potential therapeutic agents for the treatment of diseases, including cancer. In order to determine whether aptamers might eventually prove to be as useful as other clinical biopolymers, such as antibodies, we selected aptamers against an important clinical target, human epidermal growth factor receptor (hEGFR). The initial selection yielded only a single clone that could bind to hEGFR, but further mutation and optimization yielded a family of tight-binding aptamers. One of the selected aptamers, E07, bound tightly to the wild-type receptor (K(d) = 2.4 nM). This aptamer can compete with EGF for binding, binds to a novel epitope on EGFR, and also binds a deletion mutant, EGFRvIII, that is commonly found in breast and lung cancers, and especially in grade IV glioblastoma multiforme, a cancer which has for the most part proved unresponsive to current therapies. The aptamer binds to cells expressing EGFR, blocks receptor autophosphorylation, and prevents proliferation of tumor cells in three-dimensional matrices. In short, the aptamer is a promising candidate for further development as an anti-tumor therapeutic. In addition, Aptamer E07 is readily internalized into EGFR-expressing cells, raising the possibility that it might be used to escort other anti-tumor or contrast agents.
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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.