Evidence map›Paper›PMID 23824064›Full record

ArticleJournal of cancer research and clinical oncology2013

Belinostat and panobinostat (HDACI): in vitro and in vivo studies in thyroid cancer.

Daniel Chan, Yun Zheng, Jeffrey W Tyner, Wee Joo Chng, Wen Wen Chien, Sigal Gery, Geraldine Leong, Glenn D Braunstein, H Phillip Koeffler

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Journal of cancer research and clinical oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-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

22 citing papers in PubMed, 46 citations in OpenAlex.

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  13. Mechanism of Action for HDAC Inhibitors-Insights from Omics Approaches.International journal of molecular sciences · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 3 countries.

Daniel ChanNational University Hospital, National University Cancer Institute Singapore, 1E Kent Ridge Road, Singapore, 119228, Singapore.
Yun Zheng
Jeffrey W Tyner
Wee Joo Chng
Wen Wen Chien
Sigal Gery
Geraldine Leong
Glenn D Braunstein
H Phillip Koeffler
National Cancer Centre Singapore · SGNational University Cancer Institute, Singapore · SGUniversity of California, Los Angeles · USCedars-Sinai Medical Center · USOregon Health & Science University · US

Funding

Oregon Clinical and Translational Research InstituteUL1TR000128 · NCATS · OREGON HEALTH & SCIENCE UNIVERSITY · PI ELLISON, DAVID H · 2012 to 2015
$28.7M
REGULATION OF HEMATOPOIETIC CYTOKINESR01CA026038 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KOEFFLER, HAROLD PHILLIP · 1985 to 2013
$4.7M
Medical Research CouncilNCATS NIH HHS UL1 TR000128NCI NIH HHS R01 CA026038NCI NIH HHS R01CA026038-32NCI NIH HHS U54CA137785-01
6 · The paper itself

Abstract

purposeAdvanced thyroid cancer responds poorly to most therapies. New therapies and combinations are needed. The aim of this study was to examine both in vitro and in vivo activity of two relatively new histone deacetylase inhibitors (HDACIs), belinostat and panobinostat, and a variety of tyrosine kinase inhibitors (TKIs) against a panel of nine human thyroid cancer cell lines.

methodsThe anti-proliferative activity and the effects of HDACIs, TKIs and their combinations on thyroid cancer cells were determined by cytotoxicity assays, microarray and immunoblot analyses. Synergism between HDACIs and TKIs was assessed by the median effects model of Chou-Talalay (Calcusyn(®)).

resultsBelinostat and panobinostat were active against the thyroid cancer cell lines irrespective of their mutational composition, and belinostat was effective in preventing growth of human thyroid cancer xenografts in immunodeficient mice. Further studies showed that both HDACIs induced apoptosis. HDACI also elevated acetylated histone 3, p21(Waf), and PARP, and decreased levels of phosphorylated ERK and AKT (Ser473). RNA assay analysis suggested both HDACIs modulated genes associated with the cell cycle, DNA damage and apoptosis. Most of the TKI (pazopanib, motesanib, sorafenib and dasatinib) were either inactive in vitro or were active only at high doses. However, the novel combinations of either pazopanib or dasatinib TKIs with either belinostat or panobinostat synergistically inhibited cell growth of thyroid cancer cells in vitro.

conclusionsIn summary, these HDACIs either alone or combined with selected TKIs may have a role in treatment of aggressive thyroid cancer.

Indexed as

AcetylationAnimalsApoptosisBlotting, WesternCell CycleCell Line, TumorCell ProliferationDrug SynergismDrug Therapy, CombinationFemaleHistone Deacetylase InhibitorsHumansHydroxamic AcidsIndolesIn Vitro TechniquesMicebelinostatHistone Deacetylase InhibitorsHydroxamic AcidsIndolesPanobinostatSulfonamides

Identifiers

PMID23824064
PMCPMC3742422
OpenAlexW2086720185

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.