ArticleOncology reports2008
DNA methylotype analysis in colorectal cancer.
Article in Oncology reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed, 7 citations in OpenAlex.
- IncreasedMolecular & cellular oncology · 2025Article
- Frequent intragenic rearrangements of DPYD in colorectal tumours.The pharmacogenomics journal · 2015Article
- Genetic and epigenetic regulation of the organic cation transporter 3, SLC22A3.The pharmacogenomics journal · 2013Article
- Stratification and Prognostic Relevance of Jass's Molecular Classification of Colorectal Cancer.Frontiers in oncology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The methylation status of a gene promoter is considered to be an important mechanism for the development of many tumors, including colorectal cancer. Recent studies have shown that specific patterns of DNA methylation across multiple CpG loci in some human tumors are more informative than the detection of one single CpG locus in tumor genomes. In the present study, multiple CpG methylations of three genes (CDKN2A, DPYD and MLH1) were detected in DNA samples from patients with colorectal cancer using Pyrosequencing(R) technology. The bisulfite-converted DNA was amplified with a nested PCR and five or six CpG loci of each gene were assessed to determine DNA methylotype. Our data showed that 10/49 (20.4%), 6/48 (12.5%) and 14/49 (28.6%) of tumors were methylated with a DNA methylation level >0.2 in CDKN2A, DPYD and MLH1, respectively. Our study indicated a similar DNA methylation level across the multiple CpG loci for all three genes in the methylated tumor DNA samples, demonstrating a dichotomous trait in DNA methylation. The tumor DNA samples had unique DNA methylation patterns, which were high-degree and multiple-site methylation, but the normal DNA samples had no or a low-degree and dispersed single-site methylation. In addition, an inverse correlation in those methylated tumors was observed between DNA methylation and RNA expression for MLH1 (RS=-0.62, P=0.003), but not for CDKN2A and DPYD. In conclusion, distinctive DNA methylotypes exist in colorectal cancer and may depict a distinct biology in apparently homogeneous tumors.
Indexed as
Identifiers
18813836PMC4294550W2126340266What 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.