SynthesisPloS one2013
Association between P(16INK4a) promoter methylation and non-small cell lung cancer: a meta-analysis.
Synthesis in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 4 of them syntheses that pooled 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.
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.
Who cites it
11 citing papers in PubMed, 4 syntheses or guidelines pooled it, 30 citations in OpenAlex.
- APC gene promoter methylation as a potential biomarker for lung cancer diagnosis: A meta-analysis.Thoracic cancer · 2021Pooled it
- P16Thoracic cancer · 2018Pooled it
- Does adenomatous polyposis coli gene promoter 1A methylation increase non-small cell lung cancer risk? A meta-analysis.Thoracic cancer · 2017Pooled it
- A meta-analysis of the relationship between RARβ gene promoter methylation and non-small cell lung cancer.PloS one · 2014Pooled it
- Epigenetic regulation in lung cancer.MedComm · 2023Review
- Expression and role of p16 and GLUT1 in malignant diseases and lung cancer: A review.Thoracic cancer · 2020Review
- Upconversion Nanoparticle-Based Förster Resonance Energy Transfer for Detecting DNA Methylation.Sensors (Basel, Switzerland) · 2016Article
- Aberrant methylation ofJournal of Cancer · 2016Article
- Role ofOncoTargets and therapy · 2016Article
- Demonstration program of population-based lung cancer screening in China: Rationale and study design.Thoracic cancer · 2014Article
- Quantitative assessment of the diagnostic role of APC promoter methylation in non-small cell lung cancer.Clinical epigenetics · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAberrant methylation of CpG islands acquired in tumor cells in promoter regions plays an important role in carcinogenesis. Accumulated evidence demonstrates P(16INK4a) gene promoter hypermethylation is involved in non-small cell lung carcinoma (NSCLC), indicating it may be a potential biomarker for this disease. The aim of this study is to evaluate the frequency of P(16INK4a) gene promoter methylation between cancer tissue and autologous controls by summarizing published studies.
methodsBy searching Medline, EMBSE and CNKI databases, the open published studies about P(16INK4a) gene promoter methylation and NSCLC were identified using a systematic search strategy. The pooled odds of P(16INK4A) promoter methylation in lung cancer tissue versus autologous controls were calculated by meta-analysis method.
resultsThirty-four studies, including 2 652 NSCLC patients with 5 175 samples were included in this meta-analysis. Generally, the frequency of P(16INK4A) promoter methylation ranged from 17% to 80% (median 44%) in the lung cancer tissue and 0 to 80% (median 15%) in the autologous controls, which indicated the methylation frequency in cancer tissue was much higher than that in autologous samples. We also find a strong and significant correlation between tumor tissue and autologous controls of P(16INK4A) promoter methylation frequency across studies (Correlation coefficient 0.71, 95% CI:0.51-0.83, P<0.0001). And the pooled odds ratio of P(16INK4A) promoter methylation in cancer tissue was 3.45 (95% CI: 2.63-4.54) compared to controls under random-effect model.
conclusionFrequency of P(16INK4a) promoter methylation in cancer tissue was much higher than that in autologous controls, indicating promoter methylation plays an important role in carcinogenesis of the NSCLC. Strong and significant correlation between tumor tissue and autologous samples of P(16INK4A) promoter methylation demonstrated a promising biomarker for NSCLC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.