Evidence map›Paper›PMID 18308762›Full record

ArticleCarcinogenesis2008

Epigenetic alteration of Wnt pathway antagonists in progressive glandular neoplasia of the lung.

Julien D F Licchesi, William H Westra, Craig M Hooker, Emi O Machida, Stephen B Baylin, James G Herman

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 2 pooled it
6.1field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. International association for the study of lung cancer/american thoracic society/european respiratory society international multidisciplinary classification of lung adenocarcinoma.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2011
    Pooled it
  3. Article
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  7. Frontiers in immunology · 2023
    Article
  8. Review
  9. Review
  10. Article
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  13. Epigenetics of lung cancer: a translational perspective.Cellular oncology (Dordrecht, Netherlands) · 2019
    Review
  14. Long noncoding RNA LINC00673-v4 promotes aggressiveness of lung adenocarcinoma via activating WNT/β-catenin signaling.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
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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

6 authors at 2 institutions in 1 country.

Julien D F LicchesiCancer Biology Program, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21231, USA.
William H Westra
Craig M Hooker
Emi O Machida
Stephen B Baylin
James G Herman
Sidney Kimmel Comprehensive Cancer Center · USJohns Hopkins University · US

Funding

TARGETING EARLY CHANGES FOR NEW SCREENING STRATEGIESP50CA058184 · NCI · JOHNS HOPKINS UNIVERSITY · PI BISWAL, SHYAM · 1992 to 2013
$30.5M
NCI NIH HHS CA058184
6 · The paper itself

Abstract

backgroundAtypical adenomatous hyperplasia (AAH) is now recognized as a precursor lesion from which lung adenocarcinomas arise and thus represents an ideal target for studying the early genetic and epigenetic alterations associated with lung tumorigenesis such as alterations of the Wnt pathway.

methodsWe assessed the level of Wnt signaling activity in lung cancer cell lines by determining the level of active beta-catenin and determined the level of expression of Wnt antagonists APC, DKK1, DKK3, LKB1, SFRP1, 2, 4, 5, WIF1 and RUNX3 using reverse transcription-polymerase chain reaction. Using multiplex nested methylation-specific polymerase chain reaction, we analyzed promoter region methylation of these genes in resected lung tissue in the histopathologic sequence of glandular neoplasia (normal lung parenchyma, low-grade and high-grade AAH, adenocarcinoma).

resultsThe majority of non-small cell lung cancer cell lines (11 of 16, 69%) have evidence of active Wnt signaling and silencing of Wnt antagonists correlated with promoter hypermethylation. Promoter region methylation of Wnt antagonists was common in primary lung adenocarcinoma and there was a significant increase in the frequency of methylation for Wnt antagonist genes and the number of genes methylated with each stage of tumorigenesis (test for rend P <or= 0.01). Additionally, odds ratios for promoter hypermethylation of individual or multiple Wnt antagonist genes and adenocarcinomas were statistically significantly elevated and ranged between 3.64 and 48.17.

conclusionThese results show that gene silencing of Wnt antagonists by promoter hypermethylation occurs during the earliest stages of glandular neoplasia of the lung and accumulates with progression toward malignancy.

Indexed as

AdenocarcinomaCarcinoma, Non-Small-Cell LungCell Line, TumorColonic NeoplasmsCore Binding Factor Alpha 3 SubunitDisease ProgressionDNA, NeoplasmHumansLung NeoplasmsMutationNeoplasms, Glandular and EpithelialProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsRepressor ProteinsReverse Transcriptase Polymerase Chain ReactionCore Binding Factor Alpha 3 SubunitDMAP1 protein, humanDNA, NeoplasmKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsRepressor ProteinsRNA, NeoplasmWnt Proteins

Identifiers

PMID18308762
PMCPMC3312609
OpenAlexW2096865440

What OpenQuestion holds

Textmetadata
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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.