Evidence map›Paper›PMID 21799651›Full record

SynthesisWorld journal of gastroenterology2011

P16 gene hypermethylation and hepatocellular carcinoma: a systematic review and meta-analysis.

Jia-Jie Zang, Feng Xie, Jin-Fang Xu, Ying-Yi Qin, Rong-Xi Shen, Jia-Mei Yang, Jia He

Open access · hybridAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in World journal of gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. BRAF inhibition increases TGFβ2 production and stimulates metastasis in mice with endogenous BRAFProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Mallory-Denk bodies and hepatocellular senescence: a causal relationship?Virchows Archiv : an international journal of pathology · 2024
    Article
  4. Review
  5. Article
  6. P16INK4A-More Than a Senescence Marker.Life (Basel, Switzerland) · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Sex and Race-Related DNA Methylation Changes in Hepatocellular Carcinoma.International journal of molecular sciences · 2021
    Review
  11. Hypomethylation ofJournal of biosciences · 2021
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. The Correlation Relationship between P14ARF Gene DNA Methylation and Primary Liver Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Article
  19. Review
  20. Article
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 1 institution in 1 country.

Jia-Jie ZangDepartment of Health Statistics, Second Military Medical University, Shanghai 200433, China.
Feng Xie
Jin-Fang Xu
Ying-Yi Qin
Rong-Xi Shen
Jia-Mei Yang
Jia He
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo quantitatively investigate the effect of p16 hypermethylation on hepatocellular carcinoma (HCC) and hepatocirrhosis using a meta-analysis of available case-control studies.

methodsPrevious studies have primarily evaluated the incidence of p16 hypermethylation in HCC and corresponding control groups, and compared the incidence of p16 hypermethylation in tumor tissues, pericancer liver tissues, normal liver tissues and non-tumor liver tissues with that in other diseases. Data regarding publication information, study characteristics, and incidence of p16 hypermethylation in both groups were collected from these studies and summarized.

resultsFifteen studies, including 744 cases of HCC and 645 non-tumor cases, were identified for meta-analysis. Statistically significant odds ratios (ORs) of p16 hypermethylation were obtained from tumor tissues and non-tumorous liver tissues of HCC patients (OR 7.04, 95% CI: 3.87%-12.78%, P < 0.0001), tumor tissues of HCC patients and healthy liver tissues of patients with other diseases (OR 12.17, 95% CI: 6.64%-22.31%, P < 0.0001), tumor tissues of HCC patients and liver tissues of patients with non-tumorous liver diseases (OR 6.82, 95% CI: 4.31%-10.79%, P < 0.0001), and cirrhotic liver tissues and non-cirrhotic liver tissues (OR 4.96, 95% CI: 1.45%-16.96%, P = 0.01). The pooled analysis showed significantly increased ORs of p16 hypermethylation (OR 6.98, 95% CI: 4.64%-10.49%, P < 0.001) from HCC tissues and cirrhotic tissues.

conclusionP16 hypermethylation induces the inactivation of p16 gene, plays an important role in hepatocarcinogenesis, and is associated with an increased risk of HCC and liver cirrhosis.

Indexed as

DNA MethylationGenes, p16Carcinoma, HepatocellularHumansLiverLiver CirrhosisLiver NeoplasmsOdds RatioHepatocellular carcinomaLiver cirrhosisMeta-analysisOdds ratioP16 hypermethylation

Identifiers

PMID21799651
PMCPMC3132256
OpenAlexW2105581630

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.