ArticleNeoplasia (New York, N.Y.)2014
Efficacy of an EGFR-specific peptide against EGFR-dependent cancer cell lines and tumor xenografts.
Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Integrated meta-analysis and network pharmacology analysis: evaluation of Zhigancao decoction as treatment for diabetic cardiomyopathy.Frontiers in cardiovascular medicine · 2025Pooled it
- An MIEN1-based hexamer peptide (LA3IK) inhibits EGF-driven oncogenic signaling in prostate cancer by disrupting EGFR-ERBB2 heterodimerization.Scientific reports · 2026Article
- From Mechanism to Medicine: Peptide-Based Approaches for Cancer Diagnosis and Therapy.Biomolecules · 2025Review
- Design and investigation of novel iridoid-based peptide conjugates for targeting EGFR and its mutants L858R and T790M/L858R/C797S: an in silico study.Molecular diversity · 2025Article
- Peptide-Drug Conjugates as Next-Generation Therapeutics: Exploring the Potential and Clinical Progress.Bioengineering (Basel, Switzerland) · 2025Review
- Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreatic Ductal Adenocarcinoma Cells.Pharmaceutics · 2023Article
- Current and emerging therapeutic approaches for colorectal cancer: A comprehensive review.World journal of gastrointestinal surgery · 2023Review
- Novel Cyclic Peptides for Targeting EGFR and EGRvIII Mutation for Drug Delivery.Pharmaceutics · 2022Article
- Peptide-Based Drug Delivery Systems.Medicina (Kaunas, Lithuania) · 2021Review
- Personalized Immunotherapy in Colorectal Cancers: Where Do We Stand?Frontiers in oncology · 2021Review
- Targeting and therapeutic peptide-based strategies for polycystic kidney disease.Advanced drug delivery reviews · 2020Review
- Understanding Cell Penetration of Cyclic Peptides.Chemical reviews · 2019Review
- Peptide-based materials for cancer immunotherapy.Theranostics · 2019Review
- Updates on immunotherapy for colorectal cancer.Journal of gastrointestinal oncology · 2018Review
- Differential protein stability of EGFR mutants determines responsiveness to tyrosine kinase inhibitors.Oncotarget · 2016Article
- AZD9291 overcomes T790 M-mediated resistance through degradation of EGFR(L858R/T790M) in non-small cell lung cancer cells.Investigational new drugs · 2016Article
- Armored long non-coding RNA MEG3 targeting EGFR based on recombinant MS2 bacteriophage virus-like particles against hepatocellular carcinoma.Oncotarget · 2016Article
- EGFR targeted therapies and radiation: Optimizing efficacy by appropriate drug scheduling and patient selection.Pharmacology & therapeutics · 2015Review
- Inducing Oncoprotein Degradation to Improve Targeted Cancer Therapy.Neoplasia (New York, N.Y.) · 2015Review
- Peptide-Based Treatment: A Promising Cancer Therapy.Journal of immunology research · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
We have recently synthesized a peptide called Disruptin, which comprised the SVDNPHVC segment of the epidermal growth factor receptor (EGFR) that inhibits binding of heat shock protein 90 (Hsp90) to the EGFR and EGF-dependent EGFR dimerization to cause EGFR degradation. The effect is specific for EGFR versus other Hsp90 client proteins [Ahsan et al.: (2013). Destabilization of the epidermal growth factor receptor (EGFR) by a peptide that inhibits EGFR binding to heat shock protein 90 and receptor dimerization. J Biol Chem288, 26879-26886]. Here, we show that Disruptin decreases the clonogenicity of a variety of EGFR-dependent cancer cells in culture but not of EGFR-independent cancer or noncancerous cells. The selectivity of Disruptin toward EGFR-driven cancer cells is due to the high level of EGF stimulation of EGFR in EGFR-dependent tumor cells relative to normal cells. When administered by intraperitoneal injection into nude mice bearing EGFR-driven human tumor xenografts, Disruptin causes extensive degradation of EGFR in the tumor but not in adjacent host tissue. Disruptin markedly inhibits the growth of EGFR-driven tumors without producing the major toxicities caused by the Hsp90 inhibitor geldanamycin or by cisplatin. These findings provide proof of concept for development of a new Disruptin-like class of antitumor drugs that are directed specifically against EGFR-driven tumors.
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What OpenQuestion holds
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.