ArticleOncology letters2014
Epigenetic silencing of checkpoint with fork-head associated and ring finger gene expression in esophageal cancer.
Article in Oncology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed, 2 citations in OpenAlex.
- Chromatin Memory in the Development of Human Cancers.Gene technology · 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
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Checkpoint with fork-head associated and ring finger (CHFR) is a mitotic checkpoint gene with tumor-suppressor functions. Previous studies have described the hypermethylation of the CpG island in the promoter region as a key mechanism involved in silencing tumor suppressor genes. The epigenetic alterations regulating CHFR expression and the clinical significance of CHFR downregulation remain unclear. A total of 40 patients with esophageal squamous cell carcinoma who underwent primary resection were enrolled in this study. CHFR mRNA expression was quantified, followed by an evaluation of the methylation status using methylation-specific polymerase chain reaction (MSP) techniques in 29 patients. The correlation between CHFR expression and MSP status was then analyzed. In addition, the significance of CHFR expression was determined, with respect to clinicopathological features and overall survival. Aberrant hypermethylation of the CHFR gene was observed in 13 of 29 primary esophageal cancers. The CHFR expression levels of the methylated status samples was significantly lower than that of the unmethylated status samples (P=0.014). CHFR expression levels did not exhibit clinical significance with respect to the patient characteristics or overall survival. Hypermethylation of the CHFR gene is a common event in the development of primary esophageal cancer. CpG island hypermethylation of the promoter region in the CHFR gene is a key mechanism involved in silencing the CHFR gene in patients with esophageal cancer.
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.