Evidence map›Paper›PMID 33114147›Full record

ArticleCancers2020

Liver-Targeting Class I Selective Histone Deacetylase Inhibitors Potently Suppress Hepatocellular Tumor Growth as Standalone Agents.

Subhasish Tapadar, Shaghayegh Fathi, Bocheng Wu, Carrie Q Sun, Idris Raji, Samuel G Moore, Rebecca S Arnold, David A Gaul, John A Petros, Adegboyega K Oyelere

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

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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 2 countries.

Subhasish TapadarSchool of Chemistry and Biochemistry, Georgia Institute of Technology, 901 Atlantic Drive, Atlanta, GA 30332, USA.
Shaghayegh FathiSchool of Chemistry and Biochemistry, Georgia Institute of Technology, 901 Atlantic Drive, Atlanta, GA 30332, USA.
Bocheng WuSchool of Chemistry and Biochemistry, Georgia Institute of Technology, 901 Atlantic Drive, Atlanta, GA 30332, USA.ORCID 0000-0002-7381-9506
Carrie Q SunDepartment of Urology, Emory University School of Medicine, 1365 Clifton Road NE, Atlanta, GA 30322, USA.
Idris RajiSchool of Chemistry and Biochemistry, Georgia Institute of Technology, 901 Atlantic Drive, Atlanta, GA 30332, USA.ORCID 0000-0001-5697-6422
Samuel G MooreSchool of Chemistry and Biochemistry, Georgia Institute of Technology, 901 Atlantic Drive, Atlanta, GA 30332, USA.
Rebecca S ArnoldDepartment of Urology, Emory University School of Medicine, 1365 Clifton Road NE, Atlanta, GA 30322, USA.
David A GaulSophia Bioscience, Inc. 311 Ferst Drive NW, Ste. L1325A, Atlanta, GA 30332, USA.ORCID 0000-0002-9308-1895
John A PetrosDepartment of Urology, Emory University School of Medicine, 1365 Clifton Road NE, Atlanta, GA 30322, USA.
Adegboyega K OyelereSchool of Chemistry and Biochemistry, Georgia Institute of Technology, 901 Atlantic Drive, Atlanta, GA 30332, USA.
Georgia Institute of Technology · USEmory University · US

Funding

Development of Novel Targeted Therapy for Hepatocellular CarcinomaR43CA224642 · NCI · SOPHIA BIOSCIENCE, INC. · PI TAPADAR, SUBHASISH · 2018 to 2018
$300k
NCI NIH HHS R43 CA224642NIH HHS 1R43CA224642
6 · The paper itself

Abstract

Dysfunctions in epigenetic regulation play critical roles in tumor development and progression. Histone deacetylases (HDACs) and histone acetyl transferase (HAT) are functionally opposing epigenetic regulators, which control the expression status of tumor suppressor genes. Upregulation of HDAC activities, which results in silencing of tumor suppressor genes and uncontrolled proliferation, predominates in malignant tumors. Inhibition of the deacetylase activity of HDACs is a clinically validated cancer therapy strategy. However, current HDAC inhibitors (HDACi) have elicited limited therapeutic benefit against solid tumors. Here, we disclosed a class of HDACi that are selective for sub-class I HDACs and preferentially accumulate within the normal liver tissue and orthotopically implanted liver tumors. We observed that these compounds possess exquisite on-target effects evidenced by their induction of dose-dependent histone H4 hyperacetylation without perturbation of tubulin acetylation status and G0/G1 cell cycle arrest. Representative compounds

Indexed as

hepatocellular cancerhistone deacetylasehistone deacetylase inhibitorshistone deacetylase isoformsimmunoblotliver tissue accumulationmacrolidemolecular dockingorthotopic modelzinc binding group

Identifiers

PMID33114147
PMCPMC7690782
OpenAlexW3094483489

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.