Evidence map›Paper›PMID 38023717›Full record

ArticleBioengineering & translational medicine2023

An engineered interleukin-11 decoy cytokine inhibits receptor signaling and proliferation in lung adenocarcinoma.

Brianna J McIntosh, Griffin G Hartmann, Sean A Yamada-Hunter, Phillip Liu, Camille F Williams, Julien Sage, Jennifer R Cochran

Open access · goldAbstract read
In one paragraph

Article in Bioengineering & translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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

7 authors at 2 institutions in 1 country.

Brianna J McIntoshCancer Biology Program Stanford University Stanford California USA.ORCID https://orcid.org/0000-0003-3626-625X
Griffin G HartmannCancer Biology Program Stanford University Stanford California USA.ORCID https://orcid.org/0000-0001-9213-8995
Sean A Yamada-HunterCenter for Cancer Cell Therapy, Stanford Cancer Institute Stanford University School of Medicine Stanford California USA.ORCID https://orcid.org/0000-0002-4372-6587
Phillip LiuBiophysics Program Stanford University Stanford California USA.ORCID https://orcid.org/0000-0002-7935-7912
Camille F WilliamsDepartment of Chemistry Stanford University Stanford California USA.
Julien SageDepartment of Pediatrics Stanford University Stanford California USA.
Jennifer R CochranCancer Biology Program Stanford University Stanford California USA.ORCID https://orcid.org/0000-0002-6532-9873
Stanford University · USCancer Prevention Institute of California · US

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Molecular Biophysics Training Program at StanfordT32GM008294 · NIGMS · STANFORD UNIVERSITY · PI HUANG, KERWYN C. · 1989 to 2019
$7.4M
Molecular Biophysics Training Program at StanfordT32GM136568 · NIGMS · STANFORD UNIVERSITY · PI Zev Bryant, KERWYN C. HUANG · 2021 to 2026
$3.7M
Development of novel protein-based therapeutics for lung cancerR01CA225103 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BASSIK, MICHAEL C, COCHRAN, JENNIFER R · 2018 to 2022
$2.8M
NCI NIH HHS R01 CA225103NCI NIH HHS T32 CA009302NIGMS NIH HHS T32 GM008294NIGMS NIH HHS T32 GM136568
6 · The paper itself

Abstract

The cytokine interleukin (IL)-11 has been shown to play a role in promoting fibrosis and cancer, including lung adenocarcinoma, garnering interest as an attractive target for therapeutic intervention. We used combinatorial methods to engineer an IL-11 variant that binds with higher affinity to the IL-11 receptor and stimulates enhanced receptor-mediated cell signaling. Introduction of two additional point mutations ablates IL-11 ligand/receptor association with the gp130 coreceptor signaling complex, resulting in a high-affinity receptor antagonist. Unlike wild-type IL-11, this engineered variant potently blocks IL-11-mediated cell signaling and slows tumor growth in a mouse model of lung cancer. Our approach highlights a strategy where native ligands can be engineered and exploited to create potent receptor antagonists.

Indexed as

cancer progressioncytokinesIL‐11ligand/receptor interactionprotein engineering

Identifiers

PMID38023717
PMCPMC10658506
OpenAlexW4384823990

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.