Evidence map›Paper›PMID 31640185›Full record

ReviewCancers2019

Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer.

Alice Blondel, Amine Benberghout, Rémy Pedeux, Charles Ricordel

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. [Luteolin reverses OPCML methylation to inhibit proliferation of breast cancer MDA-MB-231 cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
    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

4 authors at 1 institution in 1 country.

Alice BlondelINSERM U1242, Chemistry Oncogenesis Stress and Signaling, CLCC Eugène Marquis, 35033 Rennes, France. alice.blondel@univ-rennes1.fr.
Amine BenberghoutINSERM U1242, Chemistry Oncogenesis Stress and Signaling, CLCC Eugène Marquis, 35033 Rennes, France. benberghout.amine@gmail.com.ORCID 0000-0003-4439-4462
Rémy PedeuxINSERM U1242, Chemistry Oncogenesis Stress and Signaling, CLCC Eugène Marquis, 35033 Rennes, France. remy.pedeux@univ-rennes1.fr.ORCID 0000-0002-2553-7934
Charles RicordelINSERM U1242, Chemistry Oncogenesis Stress and Signaling, CLCC Eugène Marquis, 35033 Rennes, France. charles.ricordel@chu-rennes.fr.
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) has been the leading cause of cancer-related death worldwide, over the last few decades. Survival remains extremely poor in the metastatic setting and, consequently, innovative therapeutic strategies are urgently needed. Inhibitor of Growth Gene 2 (ING2) is a core component of the mSin3A/Histone deacetylases complex (HDAC), which controls the chromatin acetylation status and modulates gene transcription. This gene has been characterized as a tumor suppressor gene and its status in cancer has been scarcely explored. In this review, we focused on ING2 and other mSin3A/HDAC member statuses in NSCLC. Taking advantage of existing public databases and known pharmacological properties of HDAC inhibitors, finally, we proposed a therapeutic model based on an ING2 biomarker-guided strategy.

Indexed as

chromatin remodelingHDAC inhibitorsING1ING2ING3ING4ING5mSin3A/HDAC complexnon-small cell lung cancerNSCLCtherapeutic approach

Identifiers

PMID31640185
PMCPMC6827349
OpenAlexW2980659225

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.