Evidence map›Paper›PMID 35626710›Full record

ReviewCells2022

Interleukin-1 and Nuclear Factor Kappa B Signaling Promote Breast Cancer Progression and Treatment Resistance.

Sydney Diep, Mahita Maddukuri, Stephanie Yamauchi, Ganamee Geshow, Nikki A Delk

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 60 citations in OpenAlex.

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  20. Inflammatory factors collaboratively linkFrontiers in immunology · 2025
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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 1 institution in 1 country.

Sydney DiepBiological Sciences Department, The University of Texas at Dallas, 800 West Campbell Road, FO-1, Richardson, TX 75080, USA.
Mahita MaddukuriBiological Sciences Department, The University of Texas at Dallas, 800 West Campbell Road, FO-1, Richardson, TX 75080, USA.
Stephanie YamauchiBiological Sciences Department, The University of Texas at Dallas, 800 West Campbell Road, FO-1, Richardson, TX 75080, USA.
Ganamee GeshowBiological Sciences Department, The University of Texas at Dallas, 800 West Campbell Road, FO-1, Richardson, TX 75080, USA.
Nikki A DelkBiological Sciences Department, The University of Texas at Dallas, 800 West Campbell Road, FO-1, Richardson, TX 75080, USA.ORCID 0000-0001-9482-3830
The University of Texas at Dallas · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While meant for wound healing and immunity in response to injury and infection, inflammatory signaling is usurped by cancerous tumors to promote disease progression, including treatment resistance. The interleukin-1 (IL-1) inflammatory cytokine family functions in wound healing and innate and adaptive immunity. Two major, closely related IL-1 family members, IL-1α and IL-1β, promote tumorigenic phenotypes and contribute to treatment resistance in cancer. IL-1 signaling converges on transactivation of the Nuclear Factor Kappa B (NF-κB) and Activator protein 1 (AP-1) transcription factors. NF-κB and AP-1 signaling are also activated by the inflammatory cytokine Tumor Necrosis Factor Alpha (TNFα) and microbe-sensing Toll-Like Receptors (TLRs). As reviewed elsewhere, IL-1, TNFα, and TLR can promote cancer progression through NF-κB or AP-1. In this review, we focus on what is known about the role of IL-1α and IL-1β in breast cancer (BCa) progression and therapeutic resistance, and state evidence for the role of NF-κB in mediating IL-1-induced BCa progression and therapeutic resistance. We will present evidence that IL-1 promotes BCa cell proliferation, BCa stem cell expansion, angiogenesis, and metastasis. IL-1 also regulates intracellular signaling and BCa cell hormone receptor expression in a manner that confers a growth advantage to the tumor cells and allows BCa cells to evade therapy. As such, the IL-1 receptor antagonist, anakinra, is in clinical trials to treat BCa and multiple other cancer types. This article presents a review of the literature from the 1990s to the present, outlining the evidence supporting a role for IL-1 and IL-1-NF-κB signaling in BCa progression.

Indexed as

Breast NeoplasmsNF-kappa BCytokinesFemaleHumansInterleukin-1Transcription Factor AP-1Tumor Necrosis Factor-alphaCytokinesInterleukin-1NF-kappa BTranscription Factor AP-1Tumor Necrosis Factor-alphabreast cancerinterleukin-1NF-κB

Identifiers

PMID35626710
PMCPMC9139516
OpenAlexW4280622858

What Socratic 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 Socratic graph.