Evidence map›Paper›PMID 39097736›Full record

ArticleClinical epigenetics2024

Anti-tumour activity of Panobinostat in oesophageal adenocarcinoma and squamous cell carcinoma cell lines.

Nair Lopes, Sofia Salta, Bianca Troncarelli Flores, Vera Miranda-Gonçalves, Margareta P Correia, Davide Gigliano, Rita Guimarães, Rui Henrique, Carmen Jerónimo

Abstract read
In one paragraph

Article in Clinical epigenetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

9 authors.

Nair LopesCancer Biology and Epigenetics Group, Research Center of IPO Porto (CI-IPOP) - CI-IPOP@RISE (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Research Center-LAB 3, F Bdg, 1st Floor, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Sofia SaltaCancer Biology and Epigenetics Group, Research Center of IPO Porto (CI-IPOP) - CI-IPOP@RISE (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Research Center-LAB 3, F Bdg, 1st Floor, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Bianca Troncarelli FloresCancer Biology and Epigenetics Group, Research Center of IPO Porto (CI-IPOP) - CI-IPOP@RISE (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Research Center-LAB 3, F Bdg, 1st Floor, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Vera Miranda-GonçalvesCancer Biology and Epigenetics Group, Research Center of IPO Porto (CI-IPOP) - CI-IPOP@RISE (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Research Center-LAB 3, F Bdg, 1st Floor, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Margareta P CorreiaCancer Biology and Epigenetics Group, Research Center of IPO Porto (CI-IPOP) - CI-IPOP@RISE (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Research Center-LAB 3, F Bdg, 1st Floor, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Davide GiglianoDepartment of Pathology, Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Rita GuimarãesDepartment of Pathology, Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Rui HenriqueCancer Biology and Epigenetics Group, Research Center of IPO Porto (CI-IPOP) - CI-IPOP@RISE (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Research Center-LAB 3, F Bdg, 1st Floor, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Carmen JerónimoCancer Biology and Epigenetics Group, Research Center of IPO Porto (CI-IPOP) - CI-IPOP@RISE (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Research Center-LAB 3, F Bdg, 1st Floor, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal. cljeronimo@icbas.up.pt.

Funding

Fundação para a Ciência e a Tecnologia 10.544999/SFRH/BD/143717/2019Fundação para a Ciência e a Tecnologia CEECINST/00091/2018Fundação para a Ciência e a Tecnologia UID/DTP/0076/POCI-01-0145-FEDER-006868Fundação para a Ciência e a Tecnologia UIDP/00776/2020Instituto Português de Oncologia do Porto BF.CBEG CI-IPOP- 27-2016Instituto Português de Oncologia do Porto CI-IPOP/PD/Kymab
6 · The paper itself

Abstract

backgroundOesophageal cancer remains a challenging disease with high mortality rates and few therapeutic options. In view of these difficulties, epigenetic drugs have emerged as potential alternatives for patient care. The goal of this study was to evaluate the effect and biological consequences of Panobinostat treatment, an HDAC (histone deacetylase) inhibitor already approved for treatment of patients with multiple myeloma, in oesophageal cell lines of normal and malignant origin, with the latter being representative of the two main histological subtypes: adenocarcinoma and squamous cell carcinoma.

resultsPanobinostat treatment inhibited growth and hindered proliferation, colony formation and invasion of oesophageal cancer cells. Considering HDAC tissue expression, HDAC1 was significantly upregulated in normal oesophageal epithelium in comparison with tumour tissue, whereas HDAC3 was overexpressed in oesophageal cancer compared to non-malignant mucosa. No differences between normal and tumour tissue were observed for HDAC2 and HDAC8 expression.

conclusionsPanobinostat exposure effectively impaired malignant features of oesophageal cancer cells. Because HDAC3 was shown to be overexpressed in oesophageal tumour samples, this epigenetic drug may represent an alternative therapeutic option for oesophageal cancer patients.

Indexed as

AdenocarcinomaCarcinoma, Squamous CellCell ProliferationEsophageal NeoplasmsHistone Deacetylase InhibitorsHistone DeacetylasesPanobinostatAntineoplastic AgentsCell Line, TumorEpigenesis, GeneticEsophageal Squamous Cell CarcinomaGene Expression Regulation, NeoplasticHistone Deacetylase 1Histone Deacetylase 2Histone Deacetylase 3HumansAntineoplastic AgentsHDAC1 protein, humanHDAC2 protein, humanHDAC8 protein, humanHistone Deacetylase 1Histone Deacetylase 2Histone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsIndolesPanobinostatRepressor ProteinsHDACOesophageal cancerPanobinostat

Identifiers

PMID39097736
PMCPMC11297794

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Registered trials

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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.