Evidence map›Paper›PMID 30899360›Full record

ReviewAmerican journal of translational research2019

Therapeutic targeting of immune checkpoints with small molecule inhibitors.

Wade M Smith, Ian J Purvis, Colin N Bomstad, Collin M Labak, Kiran K Velpula, Andrew J Tsung, Jenna N Regan, Sujatha Venkataraman, Rajeev Vibhakar, Swapna Asuthkar

Open access · greenAbstract readReview
In one paragraph

Review in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

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  14. Dual Effect of the Extract from the FungusJournal of inflammation research · 2022
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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

10 authors at 2 institutions in 1 country.

Wade M SmithDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine Peoria, IL.
Ian J PurvisDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine Peoria, IL.
Colin N BomstadDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine Peoria, IL.
Collin M LabakDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine Peoria, IL.
Kiran K VelpulaDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine Peoria, IL.
Andrew J TsungDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine Peoria, IL.
Jenna N ReganDepartment of Health Sciences Education, University of Illinois College of Medicine Peoria, IL.
Sujatha VenkataramanDepartment of Pediatrics, University of Colorado School of Medicine Aurora, CO.
Rajeev VibhakarDepartment of Pediatrics, University of Colorado School of Medicine Aurora, CO.
Swapna AsuthkarDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine Peoria, IL.
University of Colorado Denver · USIllinois College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune checkpoints are known to contribute to tumor progression by enhancing cancer's ability to evade the immune system and metastasize. Immunotherapies, including monoclonal antibodies, have been developed to target specific immunosuppressive molecules on the membranes of cancer cells and have proven revolutionary in the field of oncology. Recently, small molecule inhibitors (SMIs) have gained increased attention in cancer research with potential applications in immunotherapy. SMIs have desirable benefits over large-molecule inhibitors, such as monoclonal antibodies, including greater cell permeability, organ specificity, longer half-lives, cheaper production costs, and the possibility for oral administration. This paper will review the mechanisms by which noteworthy and novel immune checkpoints contribute to tumor progression, and how they may be targeted by SMIs and epigenetic modifiers to offer possible adjuvants to established therapeutic regimens. SMIs target immune checkpoints in several ways, such as blocking signaling between tumorigenic factors, building immune tolerance, and direct inhibition via epigenetic repression of immune inhibitory molecules. Further investigation into combination therapies utilizing SMIs and conventional cancer therapies will uncover new treatment options that may provide better patient outcomes across a range of cancers.

Indexed as

cancer progressionepigeneticsimmune checkpointsSmall molecule inhibitorstumor microenvironment

Identifiers

PMID30899360
PMCPMC6413273
OpenAlexW2993631402

What OpenQuestion holds

Textmetadata
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.