Evidence map›Paper›PMID 32913891›Full record

ArticleMolecular therapy oncolytics2020

Development of a Novel Class of Self-Assembling dsRNA Cancer Therapeutics: A Proof-of-Concept Investigation.

Vishwaratn Asthana, Brett S Stern, Yuqi Tang, Pallavi Bugga, Ang Li, Adam Ferguson, Anantratn Asthana, Gang Bao, Rebekah A Drezek

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy oncolytics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 58% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Perturbation of RNA homeostasis impairs mitochondrial respiration during poxvirus infection through excess RNA accumulation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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

9 authors at 1 institution in 1 country.

Vishwaratn AsthanaDepartment of Bioengineering, Rice University, Houston, TX 77030, USA.
Brett S SternDepartment of Bioengineering, Rice University, Houston, TX 77030, USA.
Yuqi TangDepartment of Bioengineering, Rice University, Houston, TX 77030, USA.
Pallavi BuggaDepartment of Bioengineering, Rice University, Houston, TX 77030, USA.
Ang LiDepartment of Bioengineering, Rice University, Houston, TX 77030, USA.
Adam FergusonDepartment of Bioengineering, Rice University, Houston, TX 77030, USA.
Anantratn AsthanaDepartment of Bioengineering, Rice University, Houston, TX 77030, USA.
Gang BaoDepartment of Bioengineering, Rice University, Houston, TX 77030, USA.
Rebekah A DrezekDepartment of Bioengineering, Rice University, Houston, TX 77030, USA.
Rice University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer has proven to be an extremely difficult challenge to treat. Several fundamental issues currently underlie cancer treatment, including differentiating self from nonself, functional coupling of the recognition and therapeutic components of various therapies, and the propensity of cancerous cells to develop resistance to common treatment modalities via evolutionary pressure. Given these limitations, there is an increasing need to develop an all-encompassing therapeutic that can uniquely target malignant cells, decouple recognition from treatment, and overcome evolutionarily driven cancer resistance. We describe herein a new class of programmable self-assembling double-stranded RNA (dsRNA)-based cancer therapeutics that uniquely targets aberrant genetic sequences and in a functionally decoupled manner, undergoes oncogenic RNA-activated displacement (ORAD), initiating a therapeutic cascade that induces apoptosis and immune activation. As a proof of concept, we show that RNA strands targeting the EWS/Fli1 fusion gene in Ewing sarcoma cells that are end blocked with phosphorothioate bonds and additionally sealed with a 2'-deoxyuridine (2'-U)-modified DNA protector can be used to induce specific and potent killing of cells containing the target oncogenic sequence but not wild type.

Identifiers

PMID32913891
PMCPMC7452102
OpenAlexW3046897916

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.