Evidence map›Paper›PMID 27186511›Full record

ReviewTranslational lung cancer research2016

Epigenetics in non-small cell lung cancer: from basics to therapeutics.

Junaid Ansari, Rodney E Shackelford, Hazem El-Osta

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Translational lung cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 2 pooled it
11.1field-weighted citation impact, top 1% 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

92 citing papers in PubMed, 2 syntheses or guidelines pooled it, 161 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Entinostat plus Pembrolizumab in Patients with Metastatic NSCLC Previously Treated with Anti-PD-(L)1 Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
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  16. Getting the right combination to break the epigenetic code.Nature reviews. Clinical oncology · 2025
    Review
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32 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Junaid Ansari1 Department of Medicine, Feist-Weiller Cancer Center, LSU Health, Shreveport, LA, USA ; 2 Department of Pathology, LSU Health Shreveport, Shreveport, LA, USA.
Rodney E Shackelford1 Department of Medicine, Feist-Weiller Cancer Center, LSU Health, Shreveport, LA, USA ; 2 Department of Pathology, LSU Health Shreveport, Shreveport, LA, USA.
Hazem El-Osta1 Department of Medicine, Feist-Weiller Cancer Center, LSU Health, Shreveport, LA, USA ; 2 Department of Pathology, LSU Health Shreveport, Shreveport, LA, USA.
Louisiana State University Health Sciences Center Shreveport · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer remains the number one cause of cancer-related deaths worldwide with 221,200 estimated new cases and 158,040 estimated deaths in 2015. Approximately 80% of cases are non-small cell lung cancer (NSCLC). The diagnosis is usually made at an advanced stage where the prognosis is poor and therapeutic options are limited. The evolution of lung cancer is a multistep process involving genetic, epigenetic, and environmental factor interactions that result in the dysregulation of key oncogenes and tumor suppressor genes, culminating in activation of cancer-related signaling pathways. The past decade has witnessed the discovery of multiple molecular aberrations that drive lung cancer growth, among which are epidermal growth factor receptor (EGFR) mutations and translocations involving the anaplastic lymphoma kinase (ALK) gene. This has translated into therapeutic agent developments that target these molecular alterations. The absence of targetable mutations in 50% of NSCLC cases and targeted therapy resistance development underscores the importance for developing alternative therapeutic strategies for treating lung cancer. Among these strategies, pharmacologic modulation of the epigenome has been used to treat lung cancer. Epigenetics approaches may circumvent the problem of tumor heterogeneity by affecting the expression of multiple tumor suppression genes (TSGs), halting tumor growth and survival. Moreover, it may be effective for tumors that are not driven by currently recognized druggable mutations. This review summarizes the molecular pathology of lung cancer epigenetic aberrations and discusses current efforts to target the epigenome with different pharmacological approaches. Our main focus will be on hypomethylating agents, histone deacetylase (HDAC) inhibitors, microRNA modulations, and the role of novel epigenetic biomarkers. Last, we will address the challenges that face this old-new strategy in treating lung cancer.

Indexed as

biomarkersDNA methylationepigenetic therapyhistone deacetylases (HDACs)Lung cancermicroRNA

Identifiers

PMID27186511
PMCPMC4858572
OpenAlexW2342551435

What OpenQuestion holds

Textmetadata
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.