Evidence map›Paper›PMID 24398667›Full record

ArticleCarcinogenesis2014

Genome-wide unmasking of epigenetically silenced genes in lung adenocarcinoma from smokers and never smokers.

Mathewos Tessema, Christin M Yingling, Yushi Liu, Carmen S Tellez, Leander Van Neste, Stephen S Baylin, Steven A Belinsky

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Mathewos TessemaDepartment of Lung Cancer, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA, MDxHealth Inc., Irvine, CA 92618, USA, Department of Pathology, GROW - School for Oncology and Developmental Biology, Maastricht University Medical Center, 6200 MD, Maastricht, The Netherlands and Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA sbelinsk@LRRI.org mtessema@LRRI.org.
Christin M YinglingDepartment of Lung Cancer, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA, MDxHealth Inc., Irvine, CA 92618, USA, Department of Pathology, GROW - School for Oncology and Developmental Biology, Maastricht University Medical Center, 6200 MD, Maastricht, The Netherlands and Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA.
Yushi LiuDepartment of Lung Cancer, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA, MDxHealth Inc., Irvine, CA 92618, USA, Department of Pathology, GROW - School for Oncology and Developmental Biology, Maastricht University Medical Center, 6200 MD, Maastricht, The Netherlands and Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA.
Carmen S TellezDepartment of Lung Cancer, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA, MDxHealth Inc., Irvine, CA 92618, USA, Department of Pathology, GROW - School for Oncology and Developmental Biology, Maastricht University Medical Center, 6200 MD, Maastricht, The Netherlands and Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA.
Leander Van NesteMDxHealth Inc., Irvine, CA 92618, USA, Department of Pathology, GROW - School for Oncology and Developmental Biology, Maastricht University Medical Center, 6200 MD, Maastricht, The Netherlands and.
Stephen S BaylinDepartment of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA.
Steven A BelinskyDepartment of Lung Cancer, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA, MDxHealth Inc., Irvine, CA 92618, USA, Department of Pathology, GROW - School for Oncology and Developmental Biology, Maastricht University Medical Center, 6200 MD, Maastricht, The Netherlands and Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA sbelinsk@LRRI.org.
Lovelace Respiratory Research Institute · USSidney Kimmel Comprehensive Cancer Center · US

Funding

Biomarkers to Assess Selenium Chemoprevention for NSCLCR01CA095568 · NCI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI BELINSKY, STEVEN A · 2003 to 2012
$8.9M
TUMOR SUPPRESSOR GENE METHYLATION IN LUNG ADENOCARCINOMAR01ES008801 · NIEHS · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI BELINSKY, STEVEN A · 1998 to 2010
$3.9M
Gene Methylation and Therapeutic Response in Lung CancerR01CA089551 · NCI · LOVELACE BIOMEDICAL &ENVIRONMENTAL RES · PI BELINSKY, STEVEN A · 2001 to 2005
$3.1M
NCI NIH HHS R01 CA089551NCI NIH HHS R01CA089551NCI NIH HHS R01 CA095568NCI NIH HHS R01CA095568NIEHS NIH HHS R01 ES008801
6 · The paper itself

Abstract

Lung cancer in never smokers (NS) shows striking demographic, clinicopathological and molecular distinctions from the disease in smokers (S). Studies on selected genetic and epigenetic alterations in lung cancer identified that the frequency and profile of some abnormalities significantly differ by smoking status. This study compared the transcriptome of lung adenocarcinoma cell lines derived from S (n = 3) and NS (n = 3) each treated with vehicle (control), histone deacetylation inhibitor (trichostatin A) or DNA methylation inhibitor (5-aza-2'-deoxycytidine). Among 122 genes reexpressed following 5-aza-2'-deoxycytidine but not trichostatin A treatment in two or more cell lines (including 32 genes in S-only and 12 NS-only), methylation was validated for 80% (98/122 genes). After methylation analysis of 20 normal tissue samples and 14 additional non-small cell lung cancer cell lines (total 20), 39 genes frequently methylated in normal (>20%, 4/20) and 21 genes rarely methylated in non-small cell lung cancer (≤10%, 2/20) were excluded. The prevalence for methylation of the remaining 38 genes in lung adenocarcinomas from S (n = 97) and NS (n = 75) ranged from 8-89% and significantly differs between S and NS for CPEB1, CST6, EMILIN2, LAYN and MARVELD3 (P < 0.05). Furthermore, methylation of EMILIN2, ROBO3 and IGDCC4 was more prevalent in advanced (Stage II-IV, n = 61) than early (Stage I, n = 110) tumors. Knockdown of MARVELD3, one of the novel epigenetically silenced genes, by small interfering RNA significantly reduced anchorage-independent growth of lung cancer cells (P < 0.001). Collectively, this study has identified multiple, novel, epigenetically silenced genes in lung cancer and provides invaluable resources for the development of diagnostic and prognostic biomarkers.

Indexed as

Epigenesis, GeneticGene Expression Regulation, NeoplasticGene SilencingSmokingAdenocarcinomaAzacitidineCell Line, TumorCpG IslandsDecitabineDisease ProgressionDNA MethylationGenome-Wide Association StudyHumansLung NeoplasmsPromoter Regions, GeneticReproducibility of ResultsAzacitidineDecitabine

Identifiers

PMID24398667
PMCPMC4110480
OpenAlexW2099628341

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.