Evidence map›Paper›PMID 29637478›Full record

ReviewBioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy2018

Overcoming Tumor-Induced Immune Suppression: From Relieving Inhibition to Providing Costimulation with T Cell Agonists.

Dana A Emerson, William L Redmond

Open access · greenAbstract readReview
In one paragraph

Review in BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Targeting Co-Stimulatory Receptors of the TNF Superfamily for Cancer Immunotherapy.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023
    Review
  7. Review
  8. Article
  9. CHI3L1 enhances melanoma lung metastasisFrontiers in immunology · 2022
    Article
  10. Article
  11. Review
  12. Targeted Delivery of CXCL9 and OX40L by Mesenchymal Stem Cells Elicits Potent Antitumor Immunity.Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  13. Article
  14. The Evolving Role of CD8International journal of molecular sciences · 2019
    Review
  15. Article
  16. 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

2 authors at 2 institutions in 1 country.

Dana A EmersonEarle A. Chiles Research Institute, Providence Portland Medical Center, 4805 NE Glisan St., 2N35, Portland, OR, 97213, USA.ORCID http://orcid.org/0000-0001-9515-9206
William L RedmondEarle A. Chiles Research Institute, Providence Portland Medical Center, 4805 NE Glisan St., 2N35, Portland, OR, 97213, USA. william.redmond@providence.org.ORCID http://orcid.org/0000-0002-2572-1731
Oregon Health & Science University · USProvidence Portland Medical Center · US

Funding

Ipilimumab plus a galectin-3 inhibitor for metastatic melanomaR21CA190790 · NCI · PROVIDENCE PORTLAND MEDICAL CENTER · PI CURTI, BRENDAN D, REDMOND, WILLIAM L · 2015 to 2016
$339k
NCI NIH HHS R21 CA190790NCI NIH HHS R21CA190790Susan G. Komen CCR15329664
6 · The paper itself

Abstract

Recent advancements in T-cell biology and antibody engineering have opened doors to significant improvements in cancer immunotherapy. Initial success with monoclonal antibodies targeting key receptors that inhibit T-cell function such as cytotoxic T lymphocyte antigen 4 (CTLA-4) and programmed death-ligand 1 (PD-1) have demonstrated the potency of this new class of therapy, highlighted by long-term complete responses for metastatic cancers once thought incurable. However, only a subset of patients responds to checkpoint blockade because of a multitude of factors, including an immunosuppressive tumor microenvironment and the mutational burden of the cancer. Novel antibodies, as well as ligand-immunoglobulin fusion proteins that target costimulatory immune receptors, are being developed and tested in clinical trials to further enhance the anti-tumor immune response. Many of these costimulatory receptors are in the tumor necrosis factor receptor superfamily (TNFRSF) and are expressed on multiple immune cell types, including inhibitory cells. While TNFRSFs signal through common pathways, the outcome of targeting different receptors depends on the functional status of the cell types expressing the relevant receptors. In this review, we discuss the current state of targeted costimulatory immunotherapy.

Indexed as

AnimalsAntibodies, MonoclonalAntigen-Presenting CellsClinical Trials as TopicCostimulatory and Inhibitory T-Cell ReceptorsCTLA-4 AntigenHumansImmunotherapyLymphocyte ActivationNeoplasmsProgrammed Cell Death 1 ReceptorReceptors, Tumor Necrosis FactorT-LymphocytesAntibodies, MonoclonalCostimulatory and Inhibitory T-Cell ReceptorsCTLA-4 AntigenCTLA4 protein, humanProgrammed Cell Death 1 ReceptorReceptors, Tumor Necrosis Factor

Identifiers

PMID29637478
PMCPMC7664461
OpenAlexW2799464107

What OpenQuestion holds

Textmetadata
LicenceTDM
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.