Evidence map›Paper›PMID 34353435›Full record

ReviewAdvances in cancer research2021

Acetylcholinesterase and human cancers.

Stephen D Richbart, Justin C Merritt, Nicholas A Nolan, Piyali Dasgupta

Open access · greenAbstract readReview
In one paragraph

Review in Advances in cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
36.2field-weighted citation impact, top 1% 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

20 citing papers in PubMed, 57 citations in OpenAlex.

  1. Uncovering hypothesis-generating associations between prescription drugs and digestive cancer risk: a case-control drug-wide association study (DWAS).Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
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  6. Mangrove Against Invasive Snails:Plants (Basel, Switzerland) · 2025
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  20. Foods (Basel, Switzerland) · 2022
    Review
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 2 institutions in 1 country.

Stephen D RichbartDepartment of Biomedical Sciences, Toxicology Research Cluster, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, United States.
Justin C MerrittDepartment of Biomedical Sciences, Toxicology Research Cluster, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, United States.
Nicholas A NolanWest Virginia University Medical School, Morgantown, WV, United States.
Piyali DasguptaDepartment of Biomedical Sciences, Toxicology Research Cluster, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, United States. Electronic address: dasgupta@marshall.edu.
Marshall University · USWest Virginia University · US

Funding

WV INBRE: The Inhibitor of Growth Family Member 4 (ING4) inhibits L-Type Amino Acid Transporter 1 (LAT1) expression to suppress Breast CancerP20GM103434 · NIGMS · MARSHALL UNIVERSITY · PI Travis Salisbury · 2012 to 2026
$61.1M
Capsaicin and Small cell Lung Cancer TherapyR15CA161491 · NCI · MARSHALL UNIVERSITY · PI DASGUPTA, PIYALI · 2012 to 2021
$1.3M
NCI NIH HHS R15 CA161491NIGMS NIH HHS P20 GM103434
6 · The paper itself

Abstract

The enzyme acetylcholinesterase (AChE) is a serine hydrolase whose primary function is to degrade acetylcholine (ACh) and terminate neurotransmission. Apart from its role in synaptic transmission, AChE has several "non-classical" functions in non-neuronal cells. AChE is involved in cellular growth, apoptosis, drug resistance pathways, response to stress signals and inflammation. The observation that the functional activity of AChE is altered in human tumors (relative to adjacent matched normal tissue) has raised several intriguing questions about its role in the pathophysiology of human cancers. Published reports show that AChE is a vital regulator of oncogenic signaling pathways involving proliferation, differentiation, cell-cell adhesion, migration, invasion and metastasis of primary tumors. The objective of this book chapter is to provide a comprehensive overview of the contributions of the AChE-signaling pathway in the growth of progression of human cancers. The AChE isoforms, AChE-T, AChE-R and AChE-S are robustly expressed in human cancer cell lines as well in human tumors (isolated from patients). Traditionally, AChE-modulators have been used in the clinic for treatment of neurodegenerative disorders. Emerging studies reveal that these drugs could be repurposed for the treatment of human cancers. The discovery of potent, selective AChE ligands will provide new knowledge about AChE-regulatory pathways in human cancers and foster the hope of novel therapies for this disease.

Indexed as

AcetylcholinesteraseNeoplasmsApoptosisCell ProliferationHumansOncogenesAcetylcholinesteraseAcetylcholinesteraseAChE-modulatorsAnti-cancer drugCancerExpressionIsoforms

Identifiers

PMID34353435
PMCPMC12752484
OpenAlexW3190014273

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.