Evidence map›Paper›PMID 8790415›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1996

Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands.

J G Herman, J R Graff, S Myöhänen, B D Nelkin, S B Baylin

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,833 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,833citing papers in PubMed, 4 pooled it
19.6field-weighted citation impact, top 1% 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

1,833 citing papers in PubMed, 4 syntheses or guidelines pooled it, 5,649 citations in OpenAlex.

  1. Pooled it
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  4. Pooled it
  5. Trial
  6. IL-1β/IL-6 inflammatory crosstalk drives DNA methylation and histone remodeling associated with cytokine induced senescence in luminal breast cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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1,773 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

J G HermanOncology Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA.
J R Graff
S Myöhänen
B D Nelkin
S B Baylin
Johns Hopkins University · US

Funding

TARGETING EARLY CHANGES FOR NEW SCREENING STRATEGIESP50CA058184 · NCI · JOHNS HOPKINS UNIVERSITY · PI BISWAL, SHYAM · 1992 to 2013
$30.5M
METHYLATION OF THE CALCITONIN GENE IN HUMAN TUMORSR01CA043318 · NCI · JOHNS HOPKINS UNIVERSITY · PI BAYLIN, STEPHEN B. · 1986 to 2013
$6.0M
NCI NIH HHS 5P5-CA58184-03S1NCI NIH HHS 5R01 CA43318-10
6 · The paper itself

Abstract

Precise mapping of DNA methylation patterns in CpG islands has become essential for understanding diverse biological processes such as the regulation of imprinted genes, X chromosome inactivation, and tumor suppressor gene silencing in human cancer. We describe a new method, MSP (methylation-specific PCR), which can rapidly assess the methylation status of virtually any group of CpG sites within a CpG island, independent of the use of methylation-sensitive restriction enzymes. This assay entails initial modification of DNA by sodium bisulfite, converting all unmethylated, but not methylated, cytosines to uracil, and subsequent amplification with primers specific for methylated versus unmethylated DNA. MSP requires only small quantities of DNA, is sensitive to 0.1% methylated alleles of a given CpG island locus, and can be performed on DNA extracted from paraffin-embedded samples. MSP eliminates the false positive results inherent to previous PCR-based approaches which relied on differential restriction enzyme cleavage to distinguish methylated from unmethylated DNA. In this study, we demonstrate the use of MSP to identify promoter region hypermethylation changes associated with transcriptional inactivation in four important tumor suppressor genes (p16, p15, E-cadherin, and von Hippel-Lindau) in human cancer.

Indexed as

Cell Cycle ProteinsCpG IslandsLigasesTumor Suppressor ProteinsUbiquitin-Protein LigasesAntisense Elements (Genetics)Base SequenceCadherinsCarrier ProteinsCell LineCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16DNA PrimersGenes, Tumor SuppressorHumansMethylationAntisense Elements (Genetics)CadherinsCarrier ProteinsCDKN2B protein, humanCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16DNA PrimersLigasesProteinsTumor Suppressor ProteinsUbiquitin-Protein LigasesVHL protein, humanVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID8790415
PMCPMC38513
OpenAlexW1994465394

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.