Evidence map›Paper›PMID 33572196›Full record

ReviewVaccines2021

Targeting Innate Immunity in Cancer Therapy.

Srikrishnan Rameshbabu, Brian W Labadie, Anna Argulian, Akash Patnaik

Open access · goldAbstract readReview
In one paragraph

Review in Vaccines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 112 citations in OpenAlex.

  1. Trial
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  6. Anti-tumor analysis of the RIG-I agonist inBiochemistry and biophysics reports · 2025
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  8. Review
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  15. Potential prognostic biomarker SERPINA12: implications for hepatocellular carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
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8 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Srikrishnan RameshbabuSection of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, IL 60637, USA.
Brian W LabadieSection of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, IL 60637, USA.
Anna ArgulianSection of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, IL 60637, USA.
Akash PatnaikSection of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, IL 60637, USA.
University of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The majority of current cancer immunotherapy strategies target and potentiate antitumor adaptive immune responses. Unfortunately, the efficacy of these treatments has been limited to a fraction of patients within a subset of tumor types, with an aggregate response rate of approximately 20% to date across all malignancies. The success of therapeutic inhibition of programmed death protein 1 (PD-1), protein death ligand 1 (PD-L1) and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) with immune checkpoint inhibitors (ICI) has been limited to "hot" tumors characterized by preexisting T cell infiltration, whereas "cold" tumors, which lack T cell infiltration, have not achieved durable benefit. There are several mechanisms by which "cold" tumors fail to generate spontaneous immune infiltration, which converge upon the generation of an immunosuppressive tumor microenvironment (TME). The role of the innate immune system in tumor immunosurveillance and generation of antitumor immune responses has been long recognized. In recent years, novel strategies to target innate immunity in cancer therapy have emerged, including therapeutic stimulation of pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs); the DNA sensing cGAS/STING pathway; nucleotide-binding oligomerization domain-like receptors (NLRs), such as NLRP3; and the retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs). In addition, therapeutic modulation of key innate immune cell types, such as macrophages and natural killer cells, has been investigated. Herein, we review therapeutic approaches to activate innate immunity within the TME to enhance antitumor immune responses, with the goal of disease eradication in "cold" tumors. In addition, we discuss rational immune-oncology combination strategies that activate both innate and adaptive immunity, with the potential to enhance the efficacy of current immunotherapeutic approaches.

Indexed as

cancercancer immunotherapyCD40innate immunityNK cellsNLRP3oncolytic virusespattern recognition receptorsRIG-ISTINGTLRstumor-associated macrophages

Identifiers

PMID33572196
PMCPMC7916062
OpenAlexW3128268273

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.