Evidence map›Paper›PMID 30222359›Full record

ArticleMolecular pharmaceutics2018

Synergistic Targeting HER2 and EGFR with Bivalent Aptamer-siRNA Chimera Efficiently Inhibits HER2-Positive Tumor Growth.

Lu Xue, Nita J Maihle, Xiaolin Yu, Shou-Ching Tang, Hong Yan Liu

Open access · greenAbstract read
In one paragraph

Article in Molecular pharmaceutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 45 citations in OpenAlex.

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  15. Aptamers, the Nucleic Acid Antibodies, in Cancer Therapy.International journal of molecular sciences · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Lu XueGeorgia Cancer Center, Department of Biochemistry and Molecular Biology, Medical College of Georgia , Augusta University , Augusta , Georgia 30912 , United States.
Nita J MaihleGeorgia Cancer Center, Department of Biochemistry and Molecular Biology, Medical College of Georgia , Augusta University , Augusta , Georgia 30912 , United States.
Xiaolin YuGeorgia Cancer Center, Department of Biochemistry and Molecular Biology, Medical College of Georgia , Augusta University , Augusta , Georgia 30912 , United States.
Shou-Ching TangUniversity of Mississippi Medical Center Cancer Institute , Jackson , Mississippi 39216 , United States.
Hong Yan LiuGeorgia Cancer Center, Department of Biochemistry and Molecular Biology, Medical College of Georgia , Augusta University , Augusta , Georgia 30912 , United States.ORCID 0000-0001-6484-9896
Augusta University · USJilin University · CNUniversity of Mississippi Medical Center · US

Funding

Quantitative molecular profiling of tumor biomarkers with multi-color monovalentF32CA150301 · NCI · UNIVERSITY OF WASHINGTON · PI LIU, HONG YAN · 2010 to 2012
$183k
NCI NIH HHS F32 CA150301
6 · The paper itself

Abstract

HER2 overexpression is identified on 20-30% breast cancer and other cancers at different levels. Although HER2 targeted monoclonal antibody combined with chemical drugs has shown improved outcomes in HER2 expressing patients, drug resistance and toxicity have limited their efficacy. To overcome drug resistance, cotargeting  multiple HER receptors was proven to be effective. EGFR/HER2 dimerization can active PI3K/AKT pathway, and resistance to HER2-targeted drugs is associated with upregulation of EGFR. Here, we developed a novel HER2/EGFR targeted nucleic acid therapeutic to address current drug limits. The new therapeutic is constructed by fusing HER2 aptamer-EGFR siRNA sense strand with HER2 aptamer-EGFR siRNA antisense strand into one molecule: a bivalent HER2 aptamer-EGFR siRNA aptamer chimera (HEH). In breast cancer cell lines, HEH can be selectively taken up into HER2 expressing cells and successfully silence EGFR gene and down regulate HER2 expression. In breast cancer xenograft models, HEH is capable of triggering cell apoptosis, decreasing HER2 and EGFR expression, and suppressing tumor growth. The therapeutic efficacy of HEH is superior to HER2 aptamer only, which suggests that HEH has synergistic effect by targeting HER2 and EGFR. This study demonstrated that HEH has great potential as a new HER2 targeted drug to address toxicity and resistance of current drugs and may provide a cure for many HER2 positive cancers.

Indexed as

AnimalsAntineoplastic AgentsAptamers, NucleotideBreast NeoplasmsCell Line, TumorErb-b2 Receptor Tyrosine KinasesErbB ReceptorsFemaleHumansMiceMice, NudeRNA, Small InterferingTreatment OutcomeXenograft Model Antitumor AssaysAntineoplastic AgentsAptamers, NucleotideEGFR protein, humanERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesErbB ReceptorsRNA, Small InterferingaptamerbivalentHER2siRNAsiRNA deliverysynergistic treatmenttargeted therapeutic

Identifiers

PMID30222359
PMCPMC6220360
OpenAlexW2890535040

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.