Evidence map›Paper›PMID 19017733›Full record

ArticleProceedings of the American Thoracic Society2008

Mining the epigenome for methylated genes in lung cancer.

Mathewos Tessema, Steven A Belinsky

Abstract read
In one paragraph

Article in Proceedings of the American Thoracic Society, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

21 citing papers in PubMed, 44 citations in OpenAlex.

  1. Biomedicines · 2021
    Article
  2. MiR-338-3p improved lung adenocarcinoma byArchives of medical science : AMS · 2021
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Validation of SCT Methylation as a Hallmark Biomarker for Lung Cancers.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2016
    Article
  11. Article
  12. Epigenetic research in cancer epidemiology: trends, opportunities, and challenges.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2014
    Review
  13. Review
  14. Nesprins: from the nuclear envelope and beyond.Expert reviews in molecular medicine · 2013
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Mathewos TessemaLovelace Respiratory Research Institute, 2425 Ridgecrest Dr. SE, Albuquerque, NM 87108, USA.
Steven A Belinsky
Lovelace Respiratory Research Institute · US

Funding

TUMOR SUPPRESSOR GENE METHYLATION IN LUNG ADENOCARCINOMAR01ES008801 · NIEHS · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI BELINSKY, STEVEN A · 1998 to 2010
$3.9M
NIEHS NIH HHS R01 ES008801
6 · The paper itself

Abstract

Lung cancer has become a global public health burden, further substantiating the need for early diagnosis and more effective targeted therapies. The key to accomplishing both these goals is a better understanding of the genes and pathways disrupted during the initiation and progression of this disease. Gene promoter hypermethylation is an epigenetic modification of DNA at promoter CpG islands that together with changes in histone structure culminates in loss of transcription. The fact that gene promoter hypermethylation is a major mechanism for silencing genes in lung cancer has stimulated the development of screening approaches to identify additional genes and pathways that are disrupted within the epigenome. Some of these approaches include restriction landmark scanning, methylation CpG island amplification coupled with representational difference analysis, and transcriptome-wide screening. Genes identified by these approaches, their function, and prevalence in lung cancer are described. Recently, we used global screening approaches to interrogate 43 genes in and around the candidate lung cancer susceptibility locus, 6q23-25. Five genes, TCF21, SYNE1, AKAP12, IL20RA, and ACAT2, were methylated at 14 to 81% prevalence, but methylation was not associated with age at diagnosis or stage of lung cancer. These candidate tumor suppressor genes likely play key roles in contributing to sporadic lung cancer. The realization that methylation is a dominant mechanism in lung cancer etiology and its reversibility by pharmacologic agents has led to the initiation of translational studies to develop biomarkers in sputum for early detection and the testing of demethylating and histone deacetylation inhibitors for treatment of lung cancer.

Indexed as

Chromosomes, Human, Pair 6Epigenesis, GeneticHumansLung NeoplasmsMethylationPromoter Regions, Genetic

Identifiers

PMID19017733
PMCPMC2645235
OpenAlexW2148361096

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.