Evidence map›Paper›PMID 26251030›Full record

ArticleCancer gene therapy2015

Novel analogs targeting histone deacetylase suppress aggressive thyroid cancer cell growth and induce re-differentiation.

S Jang, X-M Yu, S Odorico, M Clark, R Jaskula-Sztul, C M Schienebeck, K R Kupcho, A D Harrison, G N Winston-McPherson, W Tang and 1 more

Open access · bronzeAbstract read
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In one paragraph

Article in Cancer gene therapy, 2015. 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
1.4field-weighted citation impact, top 19% 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, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Notch Signaling in Thyroid Cancer.Advances in experimental medicine and biology · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. 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

11 authors at 2 institutions in 1 country.

S JangDepartment of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
X-M YuDepartment of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
S OdoricoDepartment of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
M ClarkDepartment of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
R Jaskula-SztulDepartment of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
C M SchienebeckDepartment of Chemistry, University of Wisconsin School of Pharmacy, Madison, WI, USA.
K R KupchoPromega Corporation, Madison, WI, USA.
A D HarrisonDepartment of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
G N Winston-McPhersonDepartment of Chemistry, University of Wisconsin School of Pharmacy, Madison, WI, USA.
W TangDepartment of Chemistry, University of Wisconsin School of Pharmacy, Madison, WI, USA.
H ChenDepartment of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
University of Wisconsin–Madison · USPromega (United States) · US

Funding

GSK3-beta Signaling in Medullary Thyroid CancerR01CA121115 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI CHEN, HERBERT · 2009 to 2013
$1.5M
NCI NIH HHS R01 CA121115
6 · The paper itself

Abstract

To develop novel therapies for aggressive thyroid cancers, we have synthesized a collection of histone deacetylase (HDAC) inhibitor analogs named AB1 to AB13, which have different linkers between a metal chelating group and a hydrophobic cap. The purpose of this study was to screen out the most effective compounds and evaluate the therapeutic efficacy. AB2, AB3 and AB10 demonstrated the lowest half-maximal inhibitory concentration (IC50) values in one metastatic follicular and two anaplastic thyroid cancer cell lines. Treatment with each of the three ABs resulted in an increase in apoptosis markers, including cleaved poly adenosine diphosphate ribose polymerase (PARP) and cleaved caspase 3. Additionally, the expression of cell-cycle regulatory proteins p21(WAF1) and p27(Kip1) increased with the treatment of ABs while cyclin D1 decreased. Furthermore, AB2, AB3 and AB10 were able to induce thyrocyte-specific genes in the three thyroid cancer cell lines indicated by increased expression levels of sodium iodide symporter, paired box gene 8, thyroid transcription factor 1 (TTF1), TTF2 and thyroid-stimulating hormone receptors. AB2, AB3 and AB10 suppress thyroid cancer cell growth via cell-cycle arrest and apoptosis. They also induce cell re-differentiation, which could make aggressive cancer cells more susceptible to radioactive iodine therapy.

Indexed as

Antineoplastic AgentsApoptosisCaspase 3Cell Cycle CheckpointsCell DifferentiationCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Drug Screening Assays, AntitumorGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHumansInhibitory Concentration 50Molecular Targeted TherapyThyroid Carcinoma, AnaplasticThyroid NeoplasmsAntineoplastic AgentsCaspase 3CDKN1A protein, humanCDKN1B protein, humanCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Histone Deacetylase Inhibitors

Identifiers

PMID26251030
OpenAlexW2200241869

What OpenQuestion holds

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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.